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"The Interplay Between Nutritional Deficiencies and Susceptibility to
Mycotoxicosis: Implications for Public Health and Food Safety"
David Chinonso Anih*1; Ugochukwu Cyrilgentle Okorocha2; Oluwadamisi Tayo-Ladega3; Joy Obinne
Onichabor4; Uzoegbo Helen Njideka5; Christiana Ozeiza Apata6 & Monday William Tarshi7
1Department of Biochemistry, Faculty of Biosciences, Federal University Wukari, Taraba, Nigeria.
2Department of Public health, Faculty of Health Sciences, Claretian University of Nigeria Maryland
Nekede Owerri Imo State.
3School of Health Sciences, Bangor University UK
4Department of Medical Biochemistry, College of Health Sciences, Delta State University, Nigeria
5Department of Nursing, Faculty- College of Nursing, Nnamdi Azikiwe University Teaching Hospital,
Anambra State Nigeria.
6Department of Public Health, Faculty of Basic Medical and Health Sciences, Thomas Adewumi
University Oko, Kwara State, Nigeria.
7Department of Medical Laboratory Science, Faculty of Health Sciences and Technology, University of
Jos, Nigeria.
*Corresponding author:
DOI: https://dx.doi.org/10.51244/IJRSI.2025.1210000242
Received: 22 October 2025; Accepted: 28 October 2025; Published: 17 November 2025
ABSTRACT
Mycotoxins are pervasive contaminants of staple crops in tropical and subtropical regions and pose a persistent
threat to food safety and public health, particularly among nutritionally vulnerable communities. This systematic
review synthesizes evidence published between 2020 and 2025 on the bidirectional relationship between
nutritional deficiencies and susceptibility to mycotoxicosis, integrating mechanistic, observational, and
intervention studies to provide an integrated perspective. We searched PubMed, Scopus, and Web of Science
and screened studies that examined nutrient status, absorption, detoxification, immune function, and health
outcomes associated with aflatoxins, fumonisins, ochratoxins, trichothecenes, and zearalenone. Results identify
several convergent mechanisms by which poor nutritional status amplifies mycotoxin harm. Protein energy
deficiency and inadequate micronutrients such as vitamins A, C, E, folate, selenium, zinc, and iron impair hepatic
Phase I and Phase II detoxification enzymes, reduce antioxidant defenses, and weaken immune competence.
Conversely, common mycotoxins damage intestinal architecture and downregulate nutrient transporters, creating
malabsorption syndromes that perpetuate nutrient loss. This reciprocal interaction generates a toxico nutritional
spiral that is most evident among children, pregnant women, and immunocompromised adults in low income
settings, with documented consequences including stunting, anemia, and adverse birth outcomes. The review
highlights the predictive value of nutritional biomarkers such as serum retinol, selenium dependent glutathione
peroxidase activity, plasma folate, serum zinc, and urinary oxidative damage markers to stratify vulnerability
and monitor interventions. Evidence for mitigation supports integrated approaches combining agricultural
measures to reduce contamination, biofortification, targeted micronutrient supplementation, improved post-
harvest storage, culturally appropriate food processing, and gut focused strategies such as probiotics. While
heterogeneity in study design limited meta-analysis, mechanistic findings from in vitro, animal, and human
studies converge to justify context specific trials of combined nutrition and food safety interventions. We
conclude that reducing the burden of mycotoxicosis requires coordinated multisectoral policies that link nutrition
programs with crop management and surveillance, and research that advances biomarker validation, omics based
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mechanistic discovery, and scalable delivery models. Implementing these strategies can disrupt the toxico
nutritional spiral, protect vulnerable populations, and strengthen food system resilience against a changing
climate. Policy makers, researchers, and communities must collaborate to translate evidence into action.
Keywords: Mycotoxicosis; Nutritional Deficiency; Detoxification Pathways; Toxico-Nutritional Spiral; Food
Safety Interventions; Biofortification; Micronutrient Biomarkers; Intestinal Malabsorption; Vulnerable
Populations.
INTRODUCTION
Background on Mycotoxins and Nutritional Vulnerability
Mycotoxins are a diverse group of toxic secondary metabolites produced by fungi such as Aspergillus, Fusarium,
and Penicillium. These toxins commonly contaminate staple crops such as cereals, maize, groundnuts, and other
nuts, especially under warm and humid conditions typical of tropical and subtropical climates. Such regions
often experience both high rates of mycotoxin contamination and widespread nutritional inadequacies, creating
an overlapping public health crisis [3].
Among the most studied mycotoxins are aflatoxin B1 and M1, known for their hepatotoxic, immunosuppressive,
and carcinogenic effects [3]. The risks are further compounded in settings where dietary diversity is limited and
food insecurity is common. Evidence shows that children in rural Tanzania, for example, are frequently exposed
to both aflatoxins and fumonisins through contaminated staple foods, increasing their risk for growth impairment
[4].
Beyond individual-level health effects, mycotoxins impose significant public health and economic burdens.
Interventions such as agricultural control programs and food safety policies have shown varying degrees of cost-
effectiveness in reducing exposure, but their implementation remains limited in low-income settings [5].
Importantly, the overlap between areas of high exposure and high rates of Protein-energy malnutrition has drawn
attention to a synergistic interaction between mycotoxins and undernutrition that magnifies health risks [6,7].
Nutritional Determinants of Host Defense
Adequate nutrition is foundational for the body's defense against environmental toxins [6]. Key nutrients
including protein, vitamins A, C, and E, folate, selenium, and zinc support the immune system and aid in
detoxification processes [7]. Deficiencies in these nutrients, prevalent in under-resourced settings, compromise
host resilience to toxins, including mycotoxins [8].
While the mechanistic roles of these nutrients in hepatic detoxification, immune modulation, and epithelial
protection are acknowledged, detailed discussions are provided in the Results section (3.1–3.2) to avoid
redundancy here.
Bidirectional Interaction between Mycotoxins and Nutrition
The relationship between nutrition and mycotoxins is not unidirectional. While undernutrition increases
susceptibility to mycotoxicosis, mycotoxins themselves can impair nutrient utilization. Experimental and
observational data suggest that aflatoxins and fumonisins disrupt nutrient absorption by damaging the intestinal
epithelium and downregulating key nutrient transporters [4,8]. This can exacerbate existing deficiencies in
essential micronutrients and contribute to the persistence of malnutrition.
Interestingly, not all studies have shown a direct linear relationship between mycotoxin exposure and
anthropometric deficits. In a cohort study of Nepalese children, aflatoxin exposure during the first 36 months of
life was not significantly associated with impaired growth, suggesting that the impact of exposure may depend
on contextual factors such as baseline nutritional status, dietary diversity, or co-existing infections [9].
The concept of the toxico-nutritional spirals a cycle in which malnutrition and mycotoxin exposure reinforce
each other has been proposed as a model to understand these complex interactions. Populations experiencing
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food insecurity, especially children and pregnant women, are particularly vulnerable to this spiral due to their
higher metabolic demands and limited access to nutrient-dense foods.
Rationale and Objectives of the Review
Mycotoxins continue to pose a significant challenge to food safety and public health, particularly in nutritionally
vulnerable populations. With climate change projected to exacerbate fungal proliferation and extend the growing
seasons for mycotoxin-producing crops, the global risk of dietary exposure is expected to increase [10]. At the
same time, genomic advances offer promising tools for predicting and mitigating contamination risks at the
source [10].
This review aims to systematically evaluate the interplay between nutritional status and susceptibility to
mycotoxicosis, with the following specific objectives:
To explore how malnutrition or nutrient deficiencies increase host vulnerability to mycotoxins;
To examine how mycotoxins, impair nutrient absorption and utilization;
To identify high-risk groups and discuss nutritional strategies for mitigation.
By highlighting this bidirectional relationship, the review seeks to support integrated approaches to food safety,
nutrition, and public health policy that can reduce the burden of mycotoxin-related diseases in vulnerable
communities.
MATERIALS AND METHODS
Overview
This section details the methodology employed to conduct a systematic review on the relationship between
nutritional status and susceptibility to mycotoxicosis. A rigorous and structured approach was applied following
internationally recognized standards for systematic review conduct and reporting. The process included
comprehensive literature searching, transparent inclusion criteria, and critical appraisal using validated tools to
ensure methodological integrity. The approach integrates evidence from both randomized and non-randomized
studies, ensuring a robust assessment of the interaction between nutrition and dietary mycotoxins.
Search Strategy
A comprehensive search was conducted in PubMed, Scopus, and Web of Science for peer-reviewed studies
published between January 2020 and March 2025 [11]. This timeframe was selected to align with the release of
the PRISMA 2020 guidelines, as well as to capture emerging data related to mycotoxin exposure in the context
of climate variability and recent nutritional surveillance updates [12].
Inclusion and Exclusion Criteria
Eligible studies were selected based on predefined inclusion and exclusion criteria. To be included, studies had
to:
- Be published in peer-reviewed journals between 2020 and 2025,
- Be written in English,
- Investigate the relationship between nutritional status and dietary mycotoxins, and
- Report defined endpoints involving nutrient status, absorption, or physiological responses to mycotoxin
exposure.
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Studies were excluded if they were editorials, preprints, conference abstracts, animal-only studies without
translational relevance, or lacked clear nutritional or toxicological endpoints. These criteria helped streamline
the review process and ensure that only studies relevant to the toxico-nutritional interface were analyzed [13].
Data Management and Risk of Bias Assessment
Screening and data extraction were conducted using Rayyan QCRI, a web-based software specifically designed
for systematic reviews [14]. The initial screening was done independently by two reviewers based on titles and
abstracts, followed by full-text assessment for eligibility. Conflicts were resolved by consensus.
To assess the methodological quality of included studies, multiple tools were applied based on study design. For
randomized controlled trials, the RoB 2 tool was used to evaluate the risk of bias across five domains [13]. For
scoping and observational studies, the PRISMA-ScR checklist was applied [15], and guidance from the Cochrane
Handbook version 6.3 was followed [16]. Literature database combinations were optimized using evidence-
based recommendations [17], and academic platform selection followed findings on the retrieval quality of
search systems [18]. Reporting fidelity of search methods was ensured using PRISMA-S guidelines [19]. Non-
randomized case series were appraised using the JBI tool [20].
Table 1 tabulates the validated tools, guidelines, and software used during literature searching, screening, bias
assessment, and reporting for this systematic review. It links each review component (e.g., reporting standard,
bias tool, screening software) to the specific instrument applied and its citation, providing transparency for the
methods described in Section 2.
Table 1: Tools Used in Literature Screening and Review
Component Tool/Guideline Applied Citation
Review Reporting Standard PRISMA 2020 [11]
Search String Validation PRESS 2021 Checklist [12]
Bias Assessment in RCTs RoB 2 Tool [13]
Screening Software Rayyan QCRI [14]
Observational Study
Evaluation
PRISMA-ScR Checklist [15]
Eligibility and Method
Guidance
Cochrane Handbook v6.3 [16]
Database Search Optimization Bramer Method for translating and
Optimizing Search Strategies
[17]
Academic Search Platform
Suitability
Gusenbauer & Haddaway, 2020 [18]
Search Method Reporting PRISMA-S Statement [19]
Case Series Appraisal JBI Critical Appraisal Tool [20]
Table of components used in the review process with columns showing the review component, the specific tool
or guideline applied, and the citation for that tool. Entries include reporting standards (PRISMA 2020), search
validation (PRESS 2021), bias tools (RoB 2), and screening software (Rayyan QCRI). Abbreviations: PRISMA
= Preferred Reporting Items for Systematic Reviews and Meta-Analyses; PRESS = Peer Review of Electronic
Search Strategies; RoB 2 = Risk of Bias 2; JBI = Joanna Briggs Institute; PRISMA-ScR = PRISMA Extension
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for Scoping Reviews; PRISMA-S = PRISMA for Search Reporting; QCRI = Qatar Computing Research
Institute.
Study Selection Flowchart
Figure 1 presents the PRISMA 2020 flow diagram summarizing the study selection process detailed in Section
2. It illustrates the sequential stages of Identification, Screening, Eligibility, and Inclusion, showing how records
were identified, filtered, and included for final synthesis to ensure transparency and reproducibility.
Figure 1: PRISMA 2020 Flow Diagram of Study Selection for the Systematic Review [11-20].
PRISMA 2020 flow diagram showing records identified (n=1,200) from databases and additional sources
(n=55), screened (n=1,255), excluded (n=1,100), assessed for eligibility (n=155), excluded with reasons
(n=105), and included in the final synthesis (n=50). Color codes: blue = Identification, yellow = Screening, red
= Eligibility, green = Inclusion. Abbreviations: PRISMA = Preferred Reporting Items for Systematic Reviews
and Meta-Analyses; n = number.
RESULTS AND DISCUSSION
Overview
This section presents the key findings from the literature and offers an integrative discussion on the interactions
between nutritional status and mycotoxicosis susceptibility. The discussion is structured around thematic sub-
sections reflecting core mechanisms by which nutrient availability modulates host responses to dietary
mycotoxins. These include impaired detoxification capacity, immune dysfunction, intestinal malabsorption, and
the perpetuation of a toxico-nutritional spiral. Interventions and future research directions are also considered.
Malnutrition and Impaired Host Detoxification
Nutrient deficiencies particularly of protein, folate, vitamins A, C, E, selenium, iron, and zinc have been
consistently shown to impair the liver’s capacity to detoxify mycotoxins. The detoxification of xenobiotics,
including aflatoxins, primarily involves two critical hepatic enzyme systems: Phase I (cytochrome P450 family)
responsible for oxidation, and Phase II (conjugation enzymes like glutathione-S-transferases or GSTs) that
facilitate the conversion of toxic intermediates into water-soluble compounds for excretion.
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Protein-energy malnutrition directly compromises hepatic enzyme synthesis. Experimental models show that
diets deficient in protein significantly reduce hepatic CYP3A4 activity, a key enzyme in aflatoxin B1
biotransformation [21]. This reduction impairs the oxidation of aflatoxin B1, leading to prolonged circulation of
the parent toxin and increased cellular damage.
Selenium, a cofactor of glutathione peroxidases (GPX), plays a crucial antioxidant role in detoxification.
Selenium-deficient hepatocytes exposed to fumonisins exhibit heightened oxidative stress and mitochondrial
damage, indicating impaired hepatic resilience to mycotoxin insult [22]. Similarly, zinc deficiency has been
shown to suppress GST expression, weakening Phase II conjugation and thereby compromising toxin
elimination [23].
In populations with vitamin E deficiency, particularly malnourished children, studies report exacerbated
aflatoxin-induced damage to CYP450 enzymes, further disrupting Phase I detoxification [24]. These findings
align with broader evidence that low-protein diets not only limit enzyme synthesis but also diminish the
availability of essential amino acids required for glutathione production and conjugation reactions [25].
Micronutrient imbalances extend beyond selenium and zinc. Deficiencies in multiple trace elements collectively
disrupt conjugation pathways, lowering enzymatic defense against multiple mycotoxins [26]. Folate deficiency,
for instance, leads to increased DNA adduct formation in the liver when exposed to aflatoxin B1, highlighting
the mutagenic risk posed by micronutrient insufficiency [27].
Iron status also modulates detoxification. Iron deficiency anemia has been linked to the downregulation of flavin-
containing monooxygenase 3 (FMO3), a lesser-known but critical detoxification enzyme, resulting in slower
clearance of mycotoxins from circulation [28]. Meanwhile, vitamin C, through epigenetic modulation of
CYP2D6, can influence the metabolism of ochratoxin A, with deficiency reducing enzymatic turnover and
increasing toxin burden [29].
Recent studies have added further mechanistic insights. Selenium-dependent suppression of GPX1 during
malnutrition was shown to heighten deoxynivalenol toxicity in hepatic cells, pointing to the importance of redox
regulation in modulating toxin-induced injury [30].
Figure 2 schematizes how deficiencies in protein and key micronutrients impair Phase I and Phase II hepatic
detoxification enzymes.
It highlights the downstream effects (reduced CYP activity, lower GST/GPX function) that increase mycotoxin
bioaccumulation and oxidative stress.
The figure links biochemical mechanisms to the subsection’s discussion of nutrient-dependent detoxification
vulnerability.
Figure 2. Biochemical Pathway of Hepatic Detoxification Impairment Under Nutrient Deficiency [21-30].
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Schematic of hepatic Phase I (oxidation) and Phase II (conjugation) detoxification illustrating how protein and
micronutrient deficiencies reduce enzyme activity and increase toxin persistence. Key labeled enzymes and
pathways are shown with inhibitory arrows from nutrient deficits to enzyme groups and resulting increase in
oxidative stress. Abbreviations: CYP = Cytochrome P450; GST = Glutathione-S-Transferase; GPX =
Glutathione Peroxidase.
Nutrient Deficiencies and Immune Dysfunction in Mycotoxicosis
Nutrient Deficiencies and Immune Dysfunction in Mycotoxicosis
Nutritional deficiencies compromise the immune system’s ability to manage mycotoxin exposure. Table 2
summarizes the immunological consequences of deficiencies in vitamins A, C, D, E, folate, selenium, zinc, and
iron.
Rather than repeating individual pathways, this section focuses on synthesizing how these micronutrients
collectively disrupt mucosal immunity, cytokine regulation, and barrier integrity factors that heighten
vulnerability to dietary mycotoxins. Vitamin A plays a pivotal role in mucosal integrity and secretory IgA
responses. Its deficiency weakens gut-associated lymphoid tissue (GALT) and increases intestinal permeability,
facilitating greater aflatoxin B1 translocation and reducing local immune responses [31]. Zinc deficiency further
exacerbates intestinal damage, promoting T-cell apoptosis and reducing lymphocyte viability under fumonisin
exposure [32].
Selenium, a trace element vital to glutathione peroxidase activity, also influences immune surveillance. In
malnourished children exposed to ochratoxin A, selenium supplementation was found to restore natural killer
(NK) cell activity, suggesting its relevance in innate immune defense [33]. Vitamin D3, though not classically
associated with antioxidant protection, was shown to modulate T-helper cell differentiation, and its deficiency
skewed immune responses toward a pro-inflammatory Th17 phenotype in mycotoxin-exposed individuals [34].
Vitamin E, a lipid-soluble antioxidant, mitigates oxidative damage in immune cells. Its deficiency disrupts
macrophage function, suppresses phagocytic activity, and impairs nuclear factor erythroid 2–related factor 2
(Nrf2) signaling, leading to exaggerated responses to aflatoxin B1 [35]. Zinc's role extends beyond T-cell
survival to include the regulation of epithelial transporters. Specifically, ZIP1 and ZIP8 downregulation under
mycotoxin challenge compromises barrier repair and facilitates antigen penetration into submucosal layers [36].
Iron, essential for neutrophil extracellular trap (NET) formation, also influences innate immunity under toxic
stress. Deoxynivalenol (DON) exposure under iron-deficient conditions results in diminished NET release,
impairing the host’s first-line defense against pathogen-mycotoxin co-exposure [37]. Concurrently, vitamin C
deficiency intensifies fumonisin B1 (FB1)-induced pulmonary inflammation by overactivating the NLRP3
inflammasome, suggesting a link between antioxidant balance and inflammasome regulation [38].
Folate, often depleted in malnourished individuals, plays an immunomodulatory role through methylation and
nucleotide biosynthesis. Its deficiency has been shown to worsen trichothecene-induced cytokine dysregulation,
particularly enhancing pro-inflammatory cytokine release [39]. Lastly, the combined deficiency of vitamin A
and zinc was found to exacerbate aflatoxin-associated gut dysbiosis, indicating synergistic nutrient-toxin
interactions that disturb microbial homeostasis and immune equilibrium [40].
Table 2 summarizes key nutrients, their primary immune or protective functions, and the major consequences
when each is deficient, as discussed in Section 3.2. This table supports the subsection by condensing mechanistic
and functional evidence that connects specific micronutrient deficits to increased mycotoxin susceptibility.
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Table 2. Key Nutrients Influencing Susceptibility to Mycotoxins
Nutrient Primary Immune Function Deficiency Consequence Citation
Vitamin A Maintains mucosal surfaces and
IgA production
Increases intestinal
permeability and aflatoxin
uptake
[31]
Zinc Supports epithelial repair and
T-cell function
Promotes barrier breakdown
and lymphocyte apoptosis
[32], [36]
Selenium Cofactor for GPX, enhances
NK cell activity
Reduces oxidative defense and
innate immunity
[33]
Vitamin D3 Modulates T-helper cell balance Favors pro-inflammatory Th17
polarization
[34]
Vitamin E Protects immune cells via Nrf2-
regulated antioxidant signaling
Disrupts macrophage function
and increases oxidative stress
[35]
Iron Enables NET formation Impairs pathogen defense
during DON exposure
[37]
Vitamin C Neutralizes ROS, regulates
inflammasome activation
Exacerbates FB1-induced
inflammation via NLRP3
activation
[38]
Folate Essential for methylation, DNA
synthesis, cytokine regulation
Aggravates trichothecene-
related cytokine dysregulation
[39]
Vitamin A +
Zinc
Maintains gut microbiota
balance and mucosal immunity
Amplifies gut dysbiosis under
aflatoxin exposure
[40]
Table summarizing selected nutrients, the immune/physiological functions they support, and the observed
consequences of deficiency relevant to mycotoxin susceptibility. Each row pairs a nutrient with its principal
protective role and the deficit-related outcome (e.g., barrier loss, immune dysregulation, impaired
detoxification). Abbreviations: IgA = Immunoglobulin A; NK = Natural Killer (cell); Nrf2 = Nuclear factor
erythroid 2–related factor 2.
Mycotoxin-Induced Malabsorption and Nutrient Loss
Despite sufficient dietary intake, nutrient bioavailability can be severely compromised due to the deleterious
effects of mycotoxins on the gastrointestinal tract. Several mycotoxins, including aflatoxins, fumonisins,
trichothecenes, ochratoxins, and zearalenone, disrupt epithelial integrity, blunt intestinal villi, and impair the
function of nutrient transporters. These intestinal insults lead to malabsorption syndromes, resulting in secondary
malnutrition and growth impairment, particularly in children and immunocompromised individuals.
Aflatoxin B1 has been shown to impair fatty acid absorption by downregulating intestinal fatty acid-binding
protein 2 (FABP2), a key mediator in the uptake and intracellular transport of dietary lipids [41]. In parallel,
trichothecene mycotoxins such as deoxynivalenol (DON) inhibit glucose transporters SGLT1 and GLUT2,
reducing intestinal glucose absorption and energy availability [42].
Fumonisin B1 (FB1), commonly found in maize-based diets, decreases folate absorption by suppressing the
reduced folate carrier (RFC1) in enterocytes. This disrupts one-carbon metabolism and increases the risk of
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neural tube defects and anemia [43]. Zearalenone, another estrogenic mycotoxin, impairs bile acid reabsorption
through the farnesoid X receptor (FXR) pathway, further compromising lipid-soluble vitamin uptake [44].
Ochratoxin A disrupts intestinal zinc homeostasis by altering the expression of metallothioneins and zinc
transporters in epithelial cells, as demonstrated in Caco-2 cell models [45]. These changes not only impair zinc
absorption but also weaken epithelial repair and immune resilience.
Trichothecenes also damage the physical architecture of the intestinal lining. Specifically, they induce villus
atrophy and crypt hyperplasia through inhibition of the Wnt/β-catenin signaling pathway, which is essential for
intestinal regeneration and nutrient assimilation [46]. This structural disruption translates into impaired
absorptive surface area and compromised brush border function.
FB1 has additionally been reported to inhibit vitamin D absorption by disrupting the heterodimerization of
vitamin D receptor (VDR) with retinoid X receptor (RXR), a necessary step for genomic activation of calcium
and phosphorus uptake mechanisms [47]. In lactose intolerance models, aflatoxin M1 has been observed to
reduce lactase enzyme activity, exacerbating gastrointestinal distress and further limiting nutrient availability
[48].
T-2 toxin, a potent trichothecene, has been shown to increase hepcidin expression, a hormone that blocks
intestinal iron transporters, thereby impairing iron absorption and predisposing to anemia despite adequate intake
[49]. Moreover, combinations of mycotoxins have a cumulative effect, with co-exposure shown to impair amino
acid transporters such as LAT1, restricting the uptake of essential amino acids required for protein synthesis and
immune function [50].
Figure 3 depicts how common mycotoxins target intestinal transporters and signaling (villus blunting, transporter
downregulation) to reduce nutrient uptake. It identifies affected transporters (e.g., SGLT1, GLUT2, RFC1,
FABP2, LAT1) and signaling nodes (FXR, VDR–RXR) that mediate malabsorption. This visual links directly
to the subsection’s evidence that mycotoxins produce measurable transporter and structural damage that cause
secondary malnutrition.
Figure 3. Mycotoxin-Induced Disruption of Intestinal Absorption and Transporter Function [41-50].
Diagram of intestinal epithelial disruption showing villus blunting and downregulation of specific nutrient
transporters and nuclear receptors that mediate absorption. Transporters and signaling nodes are annotated where
mycotoxins exert inhibitory effects on uptake of glucose, folate, lipids, amino acids, and vitamins.
Abbreviations: FABP2 = Fatty Acid-Binding Protein 2; SGLT1 = Sodium-Glucose Co-Transporter 1; GLUT2
= Glucose Transporter 2; RFC1 = Reduced Folate Carrier 1; FXR = Farnesoid X Receptor; VDR = Vitamin D
Receptor; RXR = Retinoid X Receptor; LAT1 = L-Type Amino Acid Transporter 1.
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The Toxico-Nutritional Spiral in Undernourished Populations
While many studies documenting the toxico-nutritional spiral originate from sub-Saharan Africa, similar patterns
have been observed globally. For example, research in Nepal has linked aflatoxin exposure with stunting among
children, while Guatemalan studies show co-occurrence of maize contamination and growth impairment. These
findings affirm the global relevance of the interplay between Micronutrient deficiency and mycotoxins,
especially in regions dependent on cereal-based diets.
In undernourished children, co-exposure to aflatoxins and stunting has been shown to synergistically impair
neurodevelopment, indicating that the nutritional and toxic burdens are not merely additive but multiply
detrimental [51]. Chronic aflatoxin exposure has also been implicated in worsening kwashiorkor, an edematous
form of Protein-energy malnutrition, through increased albumin oxidation and systemic oxidative stress [52].
A longitudinal study among Tanzanian children highlighted how maize-based diets chronically contaminated
with mycotoxins set off a nutritional spiral initiating with malabsorption and ending in growth faltering and
stunting [53]. This nutrient depletion can extend to fat-soluble vitamins, such as vitamin A. For example,
aflatoxin exposure in Nigerian children was shown to directly deplete vitamin A levels, increasing susceptibility
to infection and epithelial damage [54].
Prenatal exposure is equally concerning. Infants exposed to mycotoxins in utero are at elevated risk of postnatal
growth faltering, highlighting the multi-generational implications of toxico-nutritional synergy [55]. In Kenyan
households that rely on groundnut-based diets a food frequently contaminated with aflatoxins the cycle is
magnified, as persistent intake leads to a compounding effect on malnutrition [56].
In pregnant women, exposure to dietary mycotoxins like fumonisins and aflatoxins has been linked to iron
metabolism disruption and anemia, which not only affects maternal health but also compromises fetal
development [57]. Animal studies have similarly shown that Fusarium toxins reduce dietary energy efficiency,
a mechanism translatable to human populations experiencing food insecurity and marginal diets [58].
Moreover, in adults living with HIV, enteric mycotoxin absorption can aggravate wasting syndromes. In such
cases, poor mucosal immunity and existing nutritional deficiencies accelerate the downward spiral, undermining
both therapeutic and nutritional interventions [59]. Perhaps most alarmingly, fumonisin-induced folate depletion
has been implicated in the increased risk of neural tube defects, providing molecular evidence for the
transgenerational consequences of the toxico-nutritional cycle [60].
Figure 4 presents a cyclical model showing how malnutrition impairs detoxification and immunity, increasing
toxin uptake, which in turn worsens nutritional status. Arrows trace feedback loops (impaired detox → increased
absorption → nutrient loss → immune compromise) and identify high-risk groups (children, pregnant women).
The model visualizes the subsection’s argument that these processes form a self-reinforcing spiral across
generations and vulnerable populations.
Figure 4. The Toxico-Nutritional Spiral in Undernourished Populations [51-60].
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Conceptual cyclical model showing interactions between undernutrition, impaired detoxification/immune
function, increased mycotoxin absorption, and progressive nutrient loss. Feedback loops are emphasized to show
how each node (e.g., gut damage, oxidative stress, immune suppression) amplifies subsequent risk and sustains
the spiral.
Nutritional Biomarkers as Predictors of Mycotoxin Risk
Recent advances in nutritional biochemistry and toxicology have highlighted the predictive value of
micronutrient biomarkers in identifying populations at risk for mycotoxicosis. These biomarkers, measurable in
serum, plasma, or urine, can provide early warning signals of exposure and help guide dietary or clinical
interventions. Unlike traditional exposure markers that detect mycotoxins directly, nutritional biomarkers reflect
the host’s physiological vulnerability and capacity to detoxify these xenobiotics.
One of the most well-established associations is between serum retinol (vitamin A) and aflatoxin-albumin adduct
levels. In Gambian children, lower levels of retinol were strongly correlated with higher aflatoxin biomarker
concentrations, suggesting that vitamin A status may influence toxin absorption or systemic persistence [61].
Similarly, reduced glutathione peroxidase activity dependent on adequate selenium intake was found to be a
reliable indicator of fumonisin-induced oxidative stress, especially in regions where maize is a dietary staple
[62].
Plasma folate levels have also been inversely associated with fumonisin B1 (FB1) excretion in pregnant women.
This inverse relationship underscores folate’s protective role in maintaining methylation balance and preventing
teratogenic outcomes linked to fumonisin exposure [63]. Zinc status has emerged as another critical marker;
individuals with low serum zinc levels tend to exhibit increased aflatoxin-DNA adduct formation, implicating
zinc in the maintenance of epithelial barrier function and DNA repair pathways [64].
Selenium-dependent glutathione peroxidase 3 (GPX3) activity was also validated as a biomarker of ochratoxin
A susceptibility in a cohort exposed to high environmental levels of the toxin. Lower GPX3 activity was
associated with increased oxidative DNA damage and reduced detoxification capacity [65]. Beyond classical
antioxidants, newer markers are emerging. For example, deoxynivalenol (DON) has been shown to form adducts
with vitamin D-binding protein, suggesting its potential utility in monitoring DON exposure via proteomic
assays [66].
Iron-related biomarkers, such as transferrin saturation, have also demonstrated promise. In aflatoxicosis-endemic
settings, altered transferrin saturation reflects disruptions in iron metabolism due to chronic toxin exposure and
inflammatory cytokine activity [67]. Similarly, low serum carotenoid levels, particularly β-carotene, have been
inversely associated with urinary DON levels, linking oxidative micronutrient depletion to mycotoxin burden
[68].
Prealbumin, a marker of protein-energy nutritional status, was found to be significantly reduced in individuals
with high zearalenone exposure, indicating its dual utility as both a marker of Micronutrient deficiencies and
exposure severity [69]. Finally, urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG), a marker of oxidative DNA
damage, has shown consistent elevations in mycotoxin-exposed individuals, providing insight into the genotoxic
potential of chronic exposure [70].
Table 3 lists nutritional and protein biomarkers, their biological functions, associated mycotoxins, and the
implications of altered biomarker levels for exposure and risk assessment. It links measurable host indicators
(e.g., serum retinol, GPX activity, urinary 8-OHdG) to specific mycotoxin associations discussed in Section 3.5,
supporting biomarker-based risk stratification.
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Textual Table: Nutritional Biomarkers Linked to Mycotoxin Exposure
Biomarker Function Mycotoxin
Association
Implication Citation
Serum Retinol Regulates epithelial
integrity, immune
defense
Aflatoxin B1 Low levels increase
aflatoxin uptake and
DNA damage
[61]
GPX Activity
(Selenium)
Detoxification via
antioxidant defense
Fumonisin B1,
Ochratoxin A
Reduced activity
linked to poor
oxidative clearance
[62], [65]
Plasma Folate DNA synthesis and
methylation
Fumonisin B1 Inverse correlation
with urinary FB1;
risk of neural tube
defects
[63]
Serum Zinc Supports mucosal
barrier, antioxidant
systems
Aflatoxin B1 Low levels enhance
toxin-induced
genotoxicity
[64]
Vitamin D-Binding
Protein
Carrier protein with
detox potential
Deoxynivalenol Potential biomarker
for DON-protein
adduct formation
[66]
Transferrin
Saturation
Iron status indicator Aflatoxin B1 Disrupted iron
metabolism and
immune function
[67]
Serum Carotenoids Antioxidant reserve DON Low levels signal
increased oxidative
stress and exposure
[68]
Prealbumin Protein-energy
malnutrition marker
Zearalenone Depletion reflects
both nutritional status
and toxin burden
[69]
Urinary 8-OHdG Oxidative DNA
damage indicator
Multiple
mycotoxins
Marker of cumulative
genotoxic impact
[70]
Table of nutritional and protein biomarkers showing function, the mycotoxin(s) with which they have been
associated, and the practical implication of altered biomarker levels. Biomarkers include serum retinol, GPX
activity (selenium-dependent), plasma folate, serum zinc, vitamin D–binding protein, transferrin saturation,
serum carotenoids, prealbumin, and urinary 8-OHdG. Abbreviations: GPX = Glutathione Peroxidase; 8-OHdG
(8-OHdG / 8-OhdG) = 8-hydroxy-2'-deoxyguanosine (marker of oxidative DNA damage); VDBP = Vitamin D–
Binding Protein; FB1 = Fumonisin B1.
Intervention Strategies for Nutritionally Vulnerable Populations
Nutritionally vulnerable populations, particularly those in regions heavily dependent on mycotoxin-prone staples
like maize and groundnuts, require integrated strategies that address both toxin exposure and nutritional
inadequacy. A multi-sectoral framework combining food safety, nutritional support, and public health education
is vital to reduce the cumulative burden of mycotoxicosis.
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Biofortification has shown promising outcomes in reducing mycotoxin susceptibility. In Zambia, the
consumption of biofortified maize not only improved nutritional status but also significantly lowered biomarkers
of aflatoxin exposure in children, demonstrating the dual benefits of nutrient enrichment and toxin mitigation
[71]. This approach can be complemented with micronutrient supplementation. Ayalew and colleagues showed
that combined vitamin A and zinc supplementation reduced aflatoxin-albumin adduct formation, indicating
improved detoxification capacity and barrier integrity [72].
Additionally, probiotic interventions are gaining traction. Lactobacilli-based probiotics have been shown to
mitigate fumonisin-induced intestinal damage, enhancing gut resilience and potentially restoring absorption
capacity [73]. Similarly, food fortification programs in Ghana demonstrated a reduction in mycotoxin
biomarkers following the consumption of nutrient-enhanced foods, highlighting the importance of population-
scale interventions [74].
From an agricultural perspective, Aflasafe®, a biocontrol product that outcompetes aflatoxin-producing fungi,
has proven effective not only in lowering aflatoxin contamination but also in improving dietary diversity due to
improved food safety confidence [75]. Moreover, nutrition education programs targeting school-aged children
have successfully reduced risk behaviors associated with mycotoxin exposure. A study in Kenya showed that
school-based learning improved awareness and dietary practices, demonstrating the value of early-life education
in long-term exposure reduction [76].
Traditional food processing techniques also offer significant benefits. Fermentation, widely practiced in many
African and Asian communities, has been shown to degrade various mycotoxins while enhancing nutrient
bioavailability, presenting a culturally acceptable, low-cost detoxification method [77].
On a micronutrient-specific level, zinc supplementation has been shown to protect renal function against
ochratoxin A nephrotoxicity, further reinforcing the importance of trace mineral adequacy in toxin resistance
[78]. Community-level interventions are equally important improved grain storage practices, such as hermetic
bagging and elevated platforms, reduce post-harvest contamination and long-term aflatoxin accumulation [79].
Finally, dietary diversification, particularly the inclusion of low-mycotoxin cereals such as millet, has been
shown to lower fumonisin exposure while improving micronutrient intake, making it a scalable, sustainable
dietary intervention [80].
Figure 5 shows a multi-layered intervention model integrating food-safety, nutritional, agricultural, and
community strategies to reduce mycotoxin burden. Layers include pre-harvest biocontrol (e.g., Aflasafe®), post-
harvest storage, biofortification/supplementation, probiotics, and education/behavior change. It connects these
intervention tiers to the subsection’s recommended combined approaches for nutritionally vulnerable
communities.
Figure 5. Layered Framework for Mycotoxin Mitigation in Nutritionally Vulnerable Populations [71-80].
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Layered mitigation schematic illustrating integrated interventions at pre-harvest, post-harvest, nutritional, gut-
health, and community/education levels to reduce mycotoxin risk. Each layer includes representative tools and
programs (e.g., biocontrol, biofortification, supplementation, probiotics, storage improvements). Abbreviations:
Aflasafe® = commercial biocontrol product to reduce aflatoxin contamination (Aflasafe® is a registered trade
name).
In addition to modern interventions, traditional food processing techniques also play a pivotal role in mycotoxin
mitigation. Nixtamalization, a process involving the cooking and soaking of maize in an alkaline lime solution,
significantly reduces aflatoxin and fumonisin levels. However, this method may also alter mineral
bioavailability, such as reducing zinc and calcium absorption, highlighting the need to balance detoxification
with nutrient retention. This approach, widely used in Latin America, offers a culturally adapted, scalable
intervention in maize-dependent populations [71-80]
Future Research Directions
The complexity of interactions between nutritional status and mycotoxin exposure underscores the need for a
robust, multidisciplinary research agenda. While recent advances have improved our understanding of these
interactions, significant gaps remain in identifying effective, scalable interventions tailored to vulnerable
populations. Future research must move beyond observational associations to uncover mechanistic pathways
and translate these into actionable public health strategies.
One promising area is the application of omics technologies, which offer systems-level insights into nutrient–
toxin interactions. Integrative omics spanning metabolomics, transcriptomics, and proteomics has been proposed
as a novel approach to decode how dietary components influence the metabolic fate of mycotoxins and host
susceptibility to toxicity [81]. Building on this, multi-omics platforms are being explored for biomarker
discovery, enabling earlier and more precise detection of mycotoxin effects at subclinical stages [82].
Clinical trials validating the protective effects of micronutrients such as selenium, zinc, and folate are also
needed. A framework for testing selenium supplementation against aflatoxin-induced liver damage has already
been proposed and offers a template for future nutrient-toxin intervention trials [83]. Moreover, growing interest
in the gut microbiome
as a mediator between nutrition and toxicant response has opened a new avenue of inquiry. Microbiome shifts
modulate toxin absorption, metabolism, and immune response, suggesting that probiotics or microbiome-
targeted diets could modulate risk [84].
Economic feasibility must also guide future strategies. Research has shown that biofortification remains a cost-
effective intervention in mitigating mycotoxin exposure, particularly in resource-limited settings [85]. To
optimize implementation, machine learning models have been proposed to predict regional mycotoxin burdens
based on climatic, dietary, and socioeconomic factors, offering a precision-nutrition framework for at-risk
communities [86].
Biotechnological innovations, such as CRISPR-edited crops, hold the potential to reduce fungal contamination
at the source by introducing genetic resistance traits in staple crops. These advances may prove transformative
in reducing mycotoxin load in the food supply chain [87]. Complementing field-level solutions, in vitro 3D gut
models are providing physiologically relevant platforms to study toxin absorption, epithelial disruption, and
nutrient competition under controlled conditions [88].
Furthermore, metabolomic studies have begun to identify metabolic signatures of nutrient depletion due to
chronic mycotoxin exposure, which may serve as future diagnostic tools or monitoring endpoints in field studies
[89]. Finally, climate-resilient agricultural strategies, such as drought-resistant crop varieties and predictive
modeling for mycotoxin outbreaks, must be integrated into nutrition and food safety policies to ensure long-term
sustainability [90].
Figure 6 is a funnel-style roadmap mapping mechanistic discovery (omics, CRISPR) → biomarker/clinical
validation → field deployment (ML, climate-smart agriculture). It identifies priority methodologies (multi-
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omics, microbiome models, clinical trials) and translational stages toward scalable mitigation. The figure links
to the subsection’s call for interdisciplinary, evidence-driven research to translate mechanistic insights into
policy and practice.
Figure 6. Strategic Research Roadmap for the Toxico-Nutritional Interface [81-90]
Funnel roadmap from mechanistic discovery (omics, gene editing) through biomarker/clinical validation to field
implementation using predictive tools and climate-smart strategies. Stages are annotated with representative
methods (multi-omics, CRISPR/biotech, clinical trials, machine learning for regional prediction). Abbreviations:
OMICS = Integrated omics technologies (e.g., genomics, transcriptomics, metabolomics); CRISPR = Clustered
Regularly Interspaced Short Palindromic Repeats (gene-editing technology); ML = Machine Learning.
Although the review integrates mechanistic and observational findings, a meta-analysis was not feasible due to
heterogeneity in study designs, endpoints, and exposure measures. Future research should aim to produce
standardized effect sizes to enable quantitative synthesis and pooled risk estimation, particularly for associations
like aflatoxin exposure and childhood stunting.
CONCLUSION
In conclusion, this review demonstrates that mycotoxin exposure and poor nutrition form a mutually reinforcing
cycle that substantially increases health risks for children, pregnant women, and other vulnerable groups. As
synthesized here, nutritional deficits impair hepatic detoxification and antioxidant defenses while mycotoxins
damage intestinal integrity and reduce nutrient absorption, together driving stunting, anemia, and adverse birth
outcomes. Validated biomarkers such as serum retinol, selenium dependent glutathione peroxidase activity, and
urinary oxidative damage markers offer practical tools to identify high risk individuals and monitor
interventions. Effective mitigation requires coordinated, multisectoral action that links agricultural practices,
post-harvest storage, biofortification, targeted supplementation, and gut focused strategies within culturally
appropriate delivery models. We recommend prioritizing context specific trials, biomarker validation, and
integrated policy initiatives to translate these findings into scalable programs that break the toxico nutritional
spiral and strengthen food system resilience.
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Significant Statement
This review reveals how mycotoxin exposure and poor nutrition form a self-reinforcing cycle that magnifies
health risks in children, pregnant women, and other vulnerable groups. It synthesizes mechanistic and
epidemiological evidence and highlights actionable biomarkers to identify high risk individuals and measure
intervention impact. The findings support integrated, context specific strategies linking crop management,
nutrition programs, and targeted clinical research to break the cycle and protect food system resilience.
ACKNOWLEDGEMENT
None
Abbreviations
GPX - Glutathione Peroxidase
CYP - Cytochrome P450
GST - Glutathione-S-Transferase
FABP2 - Fatty Acid-Binding Protein 2
SGLT1 - Sodium-Glucose Co-Transporter 1
GLUT2 - Glucose Transporter 2
RFC1 - Reduced Folate Carrier 1
FXR - Farnesoid X Receptor
VDR - Vitamin D Receptor
RXR - Retinoid X Receptor
T-2 - T-2 Toxin
DMT1 - Divalent Metal Transporter 1
LAT1 - L-Type Amino Acid Transporter 1
NET - Neutrophil Extracellular Trap
NLRP3 - NOD-like Receptor Pyrin Domain Containing 3
PRISMA - Preferred Reporting Items for Systematic Reviews and Meta-Analyses
RoB 2 - Risk of Bias 2 Tool
JBI - Joanna Briggs Institute
SARS-CoV-2 - Severe Acute Respiratory Syndrome Coronavirus 2
WHO - World Health Organization
NCDs - Non-Communicable Diseases
RCT - Randomized Controlled Trials
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OMICS - Integrated Omics Technologies
PRISMA-S - PRISMA Search Strategy
FMO3 - Flavin-Containing Monooxygenase 3
8-OHdG - 8-Hydroxy-2'-Deoxyguanosine
SNP - Single Nucleotide Polymorphism
PRISMA-ScR - PRISMA Extension for Scoping Reviews
AI - Artificial Intelligence
Aflasafe® - Biocontrol Product for Aflatoxin Mitigation
Competing Interests
Authors have declared that they have no known competing financial interests or non-financial interests or
personal relationships that could have appeared to influence the work reported in this paper.
FUNDING
The research did not receive any specific grant from funding agencies in the public, commercial or non-profit
sectors.
REFERENCES
1. Al-Jaal BA, Jaganjac M, Barcaru A, Horvatovich P, Latiff A. Aflatoxin, fumonisin, ochratoxin,
zearalenone and deoxynivalenol biomarkers in human biological fluids: A systematic literature review,
2001–2018. Food Chem Toxicol. 2019;129:211–228. https://doi.org/10.1016/j.fct.2019.04.047
2. Smith LE, Prendergast AJ, Turner PC, Humphrey JH, Stoltzfus RJ. Aflatoxin exposure during pregnancy,
maternal anemia, and adverse birth outcomes. Am J Trop Med Hyg. 2017;96(4):770–776.
https://doi.org/10.4269/ajtmh.16-0730
1. Marchese S, Polo A, Ariano A, Velotto S, Costantini S, Severino L. Aflatoxin B1 and M1: Biological
properties and their involvement in cancer development. Toxins (Basel). 2018;10(6):214.
https://doi.org/10.3390/toxins10060214
2. Chen C, Mitchell NJ, Gratz J, Houpt ER, Gong YY, Egner PA, et al. Exposure to aflatoxin and fumonisin
in children at risk for growth impairment in rural Tanzania. Environ Int. 2018;115:29–37.
https://doi.org/10.1016/j.envint.2018.03.001
3. Sipos P, Peles F, Brassó DL, Béri B, Pusztahelyi T, Pócsi I, Győri Z. Physical and chemical methods for
reduction in aflatoxin content of feed and food. Toxins (Basel). 2021;13(3):204.
https://doi.org/10.3390/toxins13030204
4. Liu S, Jiang S, Yao Z, Liu M. Aflatoxin detection technologies: recent advances and future prospects.
Environ Sci Pollut Res Int. 2023;30(66):79627–79653. https://doi.org/10.1007/s11356-023-28110-x
5. Casu A, Camardo Leggieri M, Toscano P, Battilani P. Changing climate, shifting mycotoxins: a
comprehensive review of climate change impact on mycotoxin contamination. Compr Rev Food Sci
Food Saf. 2024;23(2):e13323. https://doi.org/10.1111/1541-4337.13323
6. Kos J, Radić B, Lešić T, Anić M, Jovanov P, Šarić B, Pleadin J. Climate change and mycotoxins trends
in Serbia and Croatia: a 15‑year review. Foods. 2024;13(9):1391. https://doi.org/10.3390/foods13091391
7. Wang X, You SH, Lien KW, Ling MP. Using disease‑burden methods to evaluate strategies for reduction
of aflatoxin exposure in peanuts. Toxicol Lett. 2019;314:75–81.
https://doi.org/10.1016/j.toxlet.2019.07.006
8. Kos J, Anić M, Radić B, Zadravec M, Hajnal EJ, Pleadin J. Climate change—A global threat resulting
in increasing mycotoxin occurrence. Foods. 2023;12(14):2704. https://doi.org/10.3390/foods12142704
INTERNATIONAL JOURNAL OF RESEARCH AND SCIENTIFIC INNOVATION (IJRSI)
ISSN No. 2321-2705 | DOI: 10.51244/IJRSI |Volume XII Issue X October 2025
Page 2821
9. Ge L, Agrawal R, Singer M, Xie W, Yu Z, Fan J, et al. Leveraging artificial intelligence to enhance
systematic reviews in health research: advanced tools and challenges. Syst Rev. 2024;13:269.
https://doi.org/10.1186/s13643-024-02682-2
10. Sandner E, Gütl C, Jakovljevic I, Wagner A. Screening automation in systematic reviews: analysis of
tools and methods using machine learning support. Stud Health Technol Inform. 2024;340:123–8.
https://doi.org/10.3233/SHTI240034
11. Yuan H, Yu K, Xie F, Liu M, Sun S. Automated machine learning with interpretation: a systematic
review of methodologies and applications in healthcare. Med Adv. 2024;2(3):205–37.
https://doi.org/10.1002/med4.75
12. Ofori-Boateng R, Aceves-Martins M, Wiratunga N, Zargaran E, Han X, Benitez-Pena CE, et al. Towards
the automation of systematic reviews using natural language processing, machine learning, and deep
learning: a comprehensive review. Artif Intell Rev. 2024;57:200. https://doi.org/10.1007/s10462-024-
10844-w
13. Page MJ, McKenzie JE, Bossuyt PM, Boutron I, Hoffmann TC, Mulrow CD, et al. The PRISMA 2020
statement: an updated guideline for reporting systematic reviews. J Clin Epidemiol. 2021;134:178–89.
https://doi.org/10.1016/j.jclinepi.2021.03.001
14. Page MJ, Moher D, Bossuyt PM, Boutron I, Hoffmann TC, Mulrow CD, et al. PRISMA 2020 explanation
and elaboration: updated guidance and exemplars for reporting systematic reviews. BMJ. 2021;372:n160.
https://doi.org/10.1136/bmj.n160
15. Heinen L, Goossen K, Lunny C, Hirt J, Puljak L, Pieper D. The optimal approach for retrieving
systematic reviews was achieved when searching MEDLINE and Epistemonikos in addition to reference
checking: a methodological validation study. BMC Med Res Methodol. 2024;24:271.
https://doi.org/10.1186/s12874-024-02384-2
16. Khalid S, Almutairi S, Namoun A, Khan J, Khattak HA, Shah H. Comprehensive review of academic
search systems: evolution, analysis, and future research directions. Soc Netw Anal Min. 2025;15:66.
https://doi.org/10.1007/s13278-025-01476-1
17. Rethlefsen ML, Page MJ. PRISMA 2020 and PRISMA-S: common questions on tracking records and
the flow diagram. J Med Libr Assoc. 2022;110(2):253–7. https://doi.org/10.5195/jmla.2022.1449
18. Moher D, Beller EM, Barrowman NJ, Campbell L, Clark J, Devereaux PJ, et al. Preferred Reporting
Items for Systematic Review and Meta-Analysis Protocols (PRISMA-P) 2015 statement. Syst Rev.
2015;4(1):1. https://doi.org/10.1186/2046-4053-4-1
19. Yao HD, Du Q, Yao LL, Zhang ZW, Xu SW. Roles of oxidative stress and endoplasmic reticulum stress
in selenium deficiency-induced apoptosis in chicken liver. Biometals. 2015;28(2):255–65.
https://doi.org/10.1007/s10534-014-9819-3
20. Lee JG, Lee SE, Lee SH, Kim JH, Kim DJ, Kim JY, et al. Selenium as an antioxidant: roles and clinical
applications in critically ill and trauma patients. Antioxidants (Basel). 2025;14(3):294.
https://doi.org/10.3390/antiox14030294
21. Akbari G. Role of zinc supplementation on ischemia/reperfusion injury in various organs. Biol Trace
Elem Res. 2020;196:1–9. https://doi.org/10.1007/s12011-019-01892-3
22. Yılmaz S, Kaya E, Karaca A, Kaya Y. Vitamin E attenuates toxicity and oxidative stress induced by
aflatoxin in rats. Adv Clin Exp Med. 2017;26(6):907–17. https://doi.org/10.17219/acem/66347
23. Ampong I, Boateng M, Osei-Tutu L, Laar A, Asare GA, Steiner-Asiedu M. Dietary protein insufficiency:
an important consideration in fatty liver disease. Br J Nutr. 2020;123(6):601–9.
https://doi.org/10.1017/S0007114519003064
24. Mshanga N, Moore S, Kassim N, Martin HD, Auma CI, Gong YY. Association between aflatoxin
exposure and haemoglobin, zinc, and vitamin A, C, and E levels/status: a systematic review. Nutrients.
2025;17(5):855. https://doi.org/10.3390/nu17050855
25. Faccioli J, Vancan L, Orlandi FS, da Rocha MD, Bordin D, Marchioro TL, et al. Nutrition assessment
and management in patients with cirrhosis and cognitive impairment: a comprehensive review. J Clin
Med. 2022;11(10):2842. https://doi.org/10.3390/jcm11102842
26. Toriyama K. Pathophysiology of hepatic encephalopathy: therapeutic interventions and strategies. J
Hepatol Gastroint Dis. 2024;10(2):297. https://doi.org/10.35248/2475-3181.24.10.297
27. Khoi CS, Chen JH, Lin TY, Chiang CK, Hung KY. Ochratoxin A-induced nephrotoxicity: up-to-date
evidence. Int J Mol Sci. 2021;22(20):11237. https://doi.org/10.3390/ijms222011237
INTERNATIONAL JOURNAL OF RESEARCH AND SCIENTIFIC INNOVATION (IJRSI)
ISSN No. 2321-2705 | DOI: 10.51244/IJRSI |Volume XII Issue X October 2025
Page 2822
28. Huang Z, Zhong H, Li T, Wang Z, Chen X, Zou T, et al. Selenomethionine alleviates deoxynivalenol-
induced oxidative injury in porcine intestinal epithelial cells independent of MAPK pathway regulation.
Antioxidants (Basel). 2024;13(3):356. https://doi.org/10.3390/antiox13030356
29. Mshanga N, Kassim N, Martin HD, Auma CI, Gong YY. A cross-sectional association between serum
aflatoxin and micronutrient status among children aged 6–24 months in rural Tanzania. Matern Child
Nutr. 2025;21(1):e70068. https://doi.org/10.1111/mcn.70068
30. Wong CP, Ho E, Zinc R. Effects of zinc status on age-related T cell dysfunction and chronic
inflammation. Biometals. 2021;34(2):291–301. https://doi.org/10.1007/s10534-020-00279-5
31. Sun Y, Zhou J, Zhang X, Wang Y, Wang Q. Review on the health-promoting effect of adequate selenium
status. Front Nutr. 2023;10:1136458. https://doi.org/10.3389/fnut.2023.1136458
32. Li Q, Chan H. Vitamin D and skin disorders: bridging molecular insights to clinical innovations. Mol
Med. 2025;31:259. https://doi.org/10.1186/s10020-025-01311-5
33. Yan H, Ge J, Gao H, Pan Y, Hao Y, Li J. Melatonin attenuates AFB1-induced cardiotoxicity via the
NLRP3 signalling pathway. J Int Med Res. 2020;48(10):300060520952656.
https://doi.org/10.1177/0300060520952656
34. Jobe MC, Rajendran R, Bhunia RK, Ghanta R, Ramesh D, Anand T, et al. Pathological role of oxidative
stress in aflatoxin-induced toxicity in different experimental models and protective effect of
phytochemicals: a review. Molecules. 2023;28(14):5369. https://doi.org/10.3390/molecules28145369
35. Schulz MT, Rink L. Zinc deficiency as possible link between immunosenescence and age-related
diseases. Immun Ageing. 2025;22(1):19. https://doi.org/10.1186/s12979-025-00511-1
36. Jaff S, Zeraattalab-Motlagh S, Khosroshahi RA, Gubari M, Mohammadi H, Djafarian K. The effect of
selenium therapy in critically ill patients: an umbrella review of systematic reviews and meta-analysis of
randomized controlled trials. Eur J Med Res. 2023;28:104. https://doi.org/10.1186/s40001-023-01075-w
37. Bishop EL, Ismailova A, White JH. Vitamin D and immune regulation: antibacterial, antiviral, anti-
inflammatory. JBMR Plus. 2021;5(1):e10405. https://doi.org/10.1002/jbm4.10405
38. Mehdi Y, Hornick JL, Istasse L, Dufrasne I. Selenium in the environment, metabolism and involvement
in body functions. Molecules. 2013;18(3):3292–311. https://doi.org/10.3390/molecules18033292
39. Zhou J, Tang L, Wang JS. Aflatoxin B1 disrupts gut microbial metabolism of fatty acids and bile acids
in rats. Toxicol Sci. 2018;164(2):453–64. https://doi.org/10.1093/toxsci/kfy102 ;
40. Tang X, Zeng Y, Xiong K, Li M. Deoxynivalenol induces inflammatory injury and impairs glucose
absorption via SGLT1 and GLUT2 downregulation in porcine intestinal epithelial cells. J Anim Sci.
2024;102(4):skae107. https://doi.org/10.1093/jas/skae107
41. Wang Y, Xie J, Zhang H, Li X, Chen Y, Liu Z. Fumonisin B1 disrupts folate metabolism and induces
DNA damage in human intestinal epithelial cells. Toxicol Lett. 2021;343:1–9.
https://doi.org/10.1016/j.toxlet.2021.02.005
42. Yuan P, Li H, Wang Q, Zhu S, Zhao X. Zearalenone decreases food intake by disrupting
gut‑liver‑hypothalamus axis signaling via bile acids and FXR. J Agric Food Chem. 2024;72(14):8200–
13. https://doi.org/10.1021/acs.jafc.4c00421
43. Yang X, Gao Y, Huang S, Li J, Wang L, Zhao G. Ochratoxin A compromises intestinal tight junction
proteins through Wnt/Ca²⁺ signaling pathway in mice and Caco‑2 cells. Ecotoxicol Environ Saf.
2021;224:112637. https://doi.org/10.1016/j.ecoenv.2021.112637
44. Zhou JY, Huang DG, Gao CQ, Chen YL, Li XY, Tang JH. Heat‑stable enterotoxin inhibits intestinal
stem cell expansion and disrupts epithelial integrity via Wnt/β-catenin downregulation. Stem Cells.
2021;39(4):482–96. https://doi.org/10.1002/stem.3324
45. Mao J, Li Z, Wang H, Chen F, Zhang X, Xia L, et al. Gut microbiota‑mediated bile acid transformations
regulate aflatoxin B1 transport via FXR and CYP8B1 signaling. J Anim Sci Biotechnol. 2025;16:38.
https://doi.org/10.1186/s40104-025-01169-x
46. Rotimi OA, Adeyemi OS, Adebayo ET, Ojo AA, Olalekan AO. Aflatoxin M1 exposure alters
mitochondrial lipids and oxidative stress in rat liver. Front Pharmacol. 2019;10:467.
https://doi.org/10.3389/fphar.2019.00467
47. Ahmad S, Single S, Liu Y, Khaliq A, Huang W, Liu G, et al. Heavy metal exposure dysregulates
sphingolipid metabolism and impairs iron homeostasis in human lung tissues. Antioxidants.
2024;13(8):978. https://doi.org/10.3390/antiox13080978
INTERNATIONAL JOURNAL OF RESEARCH AND SCIENTIFIC INNOVATION (IJRSI)
ISSN No. 2321-2705 | DOI: 10.51244/IJRSI |Volume XII Issue X October 2025
Page 2823
48. Su D, Lu J, Nie C, Wang L, Li X, Zhang Y, et al. Combined effects of acrylamide and ochratoxin A on
intestinal barrier function in Caco‑2 cells. Foods. 2023;12(6):1318.
https://doi.org/10.3390/foods12061318
49. Ghorbani Nejad B, Mostafaei Z, Balouchi Rezaabad A, Mehravar F, Zarei M, Dehghani A, Raeisi
Estabragh MA, Karami‑Mohajeri S, Alizadeh H.
50. Aflatoxin B1 exposure and growth impairment in infants and children: a systematic review and
meta‑analysis. BMC Pediatr. 2023;23:614. https://doi.org/10.1186/s12887-023-04275-9
51. McMillan A, Renaud JB, Burgess KMN, Orimadegun AE, Akinyinka OO, Allen SJ, Miller JD, Reid G,
Sumarah MW. Aflatoxin exposure in Nigerian children with severe acute malnutrition. Food Chem
Toxicol. 2018;111:356–362. https://doi.org/10.1016/j.fct.2017.11.030
52. Stafstrom W, Walker S, Komba E, Kinyua M, Hird H. Modeling maize aflatoxins and fumonisins in a
Tanzanian smallholder system: accounting for diverse risk factors improves mycotoxin models. PLoS
One. 2025;20(1):e0316457. https://doi.org/10.1371/journal.pone.0316457
53. Gichohi-Wainaina WN, Kimanya M, Muzanila YC, Kumwenda NC, Msere H, Rashidi M, et al.
Aflatoxin contamination, exposure among rural smallholder farming Tanzanian mothers and associations
with growth among their children. Toxins (Basel). 2023;15(4):257.
https://doi.org/10.3390/toxins15040257
54. Rivera‑Núñez Z, Smarr MM, Barr DB, Wolfe CD, Waidyanatha S, Olshan AF. Mycoestrogen exposure
during pregnancy: impact of the ABCG2 Q141K variant on birth and placental outcomes. Environ Health
Perspect. 2025;133(5):057001. https://doi.org/10.1289/EHP14478
55. Kyei NNA, Boakye D, Awuah RT, Agbenyega T, Moya B. Maternal mycotoxin exposure and adverse
pregnancy outcomes: a systematic review. Mycotoxin Res. 2020;36:243–255.
https://doi.org/10.1007/s12550-019-00384-6
56. Hassen JY, Debella A, Eyeberu A, Mussa I. Level of exposure to aflatoxins during pregnancy and its
association with adverse birth outcomes in Africa: a meta-analysis. Int Health. 2024;16(6):577–591.
https://doi.org/10.1093/inthealth/ihae015
57. Tan T, Li L, Zhang J, Chen Y, Fang H, Li Y, et al. Maternal deoxynivalenol exposure and birth outcomes:
a prospective cohort study in China. BMC Med. 2023;21:328. https://doi.org/10.1186/s12916-023-
03011-5
58. Bastos‑Moreira Y, Argaw A, Di Palma G, Dailey‑Chwalibóg T, El‑Hafi J, Ouédraogo LO, Coulibaly M,
Savadogo G, Nikièma L. Ochratoxin A status at birth is associated with reduced birth weight and
ponderal index in rural Burkina Faso. J Nutr. 2025;155(1):260–9.
https://doi.org/10.1016/j.tjnut.2024.10.015
59. Watson S, Chen G, Sylla A, Routledge MN, Gong YY. Dietary exposure to aflatoxin and micronutrient
status among young children from Guinea. Mol Nutr Food Res. 2016;60(3):511–518.
https://doi.org/10.1002/mnfr.201500382
60. Caudill MA, Gregory JF, Hutson AD, Bailey LB. Folate catabolism in pregnant and nonpregnant women
with controlled folate intakes. J Nutr. 1998;128(2):204–208. https://doi.org/10.1093/jn/128.2.204
61. Yayeh T, Jeong HR, Park YS, Moon S, Sur B, Yoo HS, Oh S. Fumonisin B1-induced toxicity was not
exacerbated in glutathione peroxidase-1/catalase double knockout mice. Biomol Ther (Seoul).
2021;29(1):52–57. https://doi.org/10.4062/biomolther.2020.062
62. Zhou YB, Si KY, Li HT, Li XC, Meng Y, Liu JM. Trends and influencing factors of plasma folate levels
in Chinese women at mid-pregnancy, late pregnancy and lactation periods. Br J Nutr. 2021;126(6):885–
891. https://doi.org/10.1017/S0007114520004821
63. Fasullo M. Cellular responses to aflatoxin-associated DNA adducts. In: DNA Repair [Internet].
IntechOpen; 2018. Chapter 64225. https://doi.org/10.5772/intechopen.81763
64. Tam E, Keats EC, Rind F, Das JK, Bhutta ZA. Micronutrient supplementation and fortification
interventions on health and development outcomes among children under five in low- and middle-income
countries: a systematic review and meta-analysis. Nutrients. 2020;12(2):289.
https://doi.org/10.3390/nu12020289
65. Macé K, Aguilar F, Wang JS, Vautravers P, Gómez-Lechón M, Gonzalez FJ, Groopman JD, Harris CC,
Wild CP. Aflatoxin B1-induced DNA adduct formation and p53 mutations in CYP450-expressing human
liver cell lines. Carcinogenesis. 1997;18(7):1291–1297. https://doi.org/10.1093/carcin/18.7.1291
INTERNATIONAL JOURNAL OF RESEARCH AND SCIENTIFIC INNOVATION (IJRSI)
ISSN No. 2321-2705 | DOI: 10.51244/IJRSI |Volume XII Issue X October 2025
Page 2824
66. Xu Y, Gong YY, Routledge MN. Aflatoxin exposure assessed by aflatoxin albumin adduct biomarker in
populations from six African countries. World Mycotoxin J. 2018;11(3):411–426.
https://doi.org/10.3920/WMJ2017.2271
67. Niesser M, Demmelmair H, Weith T, Moretti D, Rauh-Pfeiffer A, van Lipzig M, Rist MJ, Saur M, Fürst
P, Koletzko B. Folate catabolites in spot urine as non-invasive biomarkers of folate status during habitual
intake and folic acid supplementation. PLoS One. 2013;8(2):e56194.
https://doi.org/10.1371/journal.pone.0056194
68. Kövesi B, Kulcsár S, Zándoki E, Szabó-Fodor J, Mézes M, Balogh K, Erdélyi M, Tuboly T, Tóth S,
Szabó A. Short-term effects of deoxynivalenol, T-2 toxin, fumonisin B1 or ochratoxin on lipid
peroxidation and glutathione redox system and its regulatory genes in common carp liver. Fish Physiol
Biochem. 2020;46(6):1921–1932. https://doi.org/10.1007/s10695-020-00845-1
69. Sarıkaya E, Doğan S. Glutathione peroxidase in health and diseases. In: Bagatini MD, editor. Glutathione
System and Oxidative Stress in Health and Disease. London: IntechOpen; 2020.
https://doi.org/10.5772/intechopen.91009
70. Kachapulula PW, Akello J, Bandyopadhyay R, Cotty PJ. Aflatoxin contamination of groundnut and
maize in Zambia: observed and potential concentrations. J Appl Microbiol. 2017;122(6):1471–1482.
https://doi.org/10.1111/jam.13448
71. Xia L, Wu H, Saleem AF, Mupere E, Lancioni C, Diallo H, et al. Aflatoxin exposure and mortality in
acutely ill children: results from the CHAIN network cohort. BMJ Glob Health. 2025;10(7):e017375.
https://doi.org/10.1136/bmjgh-2024-017375
72. Deepthi BV, Somashekaraiah R, Rao KP, Deepa N, Dharanesha NK, Girish KS, Agrawal R, Sreenivasa
MY. Lactobacillus plantarum MYS6 ameliorates fumonisin B1-induced hepatorenal damage in broilers.
Front Microbiol. 2017;8:2317. https://doi.org/10.3389/fmicb.2017.02317
73. Agriopoulou S, Stamatelopoulou E, Varzakas T. Advances in occurrence, importance, and mycotoxin
control strategies: prevention and detoxification in foods. Foods. 2020;9(2):137.
https://doi.org/10.3390/foods9020137
74. Konlan AB, Assumang I, Abe-Inge V. Crop biofortification—a key determinant towards fighting
micronutrient malnutrition in Northern Ghana. In: Malnutrition [Internet]. IntechOpen; 2022.
https://doi.org/10.5772/intechopen.104460
75. Tola M, Kebede B. Occurrence, importance and control of mycotoxins: a review. Cogent Food Agric.
2016;2(1):1191103. https://doi.org/10.1080/23311932.2016.1191103
76. Fovo FP, Maeda DG, Kaale LD. Microbiological approaches for mycotoxin decontamination in foods
and feeds to enhance food security: a review. Mycotoxin Res. 2025;41:385–404.
77. Li J, Shi M, Wang Y, Liu J, Liu S, Kang W, Zhang X, Li C, Wang Q, Wu Q. Probiotic-derived
extracellular vesicles alleviate AFB1-induced intestinal injury by modulating the gut microbiota and
AHR activation. J Nanobiotechnol. 2024;22:697. https://doi.org/10.1186/s12951-024-02979-3
78. Nyumuah RO, Hoang TC, Amoaful EF, Agble R, Meyer M, Wirth JP, Rohner F, Panagides D, Kupka
R. Implementing large-scale food fortification in Ghana: lessons learned. Food Nutr Bull. 2012;33(4
Suppl):S293–S303. https://doi.org/10.1177/15648265120334s305
79. Zhao T, Wang H, Liu Z, Liu Y, Ji D, Li B, Zhang H, Sun W, Li Y, Sun Z. Recent perspective of
Lactobacillus in reducing oxidative stress to prevent disease. Antioxidants. 2023;12(3):769.
https://doi.org/10.3390/antiox12030769
80. Samarajeewa U. Gene recognition and role of foodomics in mycotoxin control: a review. J Toxicol Stud.
2025;3(1):1857. https://doi.org/10.59400/jts1857
81. Owolabi IO, Leng G, MacIntosh DL, Hoet P, Leoni C, van Engelen JGM, et al. Applications of
mycotoxin biomarkers in human biomonitoring for exposome-health studies: past, present, and future.
Expo Health. 2024;16:837–859. https://doi.org/10.1007/s12403-023-00595-4
82. Sun LH, Zhang NY, Zhu MK, Zhao L, Zhou JC, Qi DS. Prevention of aflatoxin B1 hepatoxicity by
dietary selenium is associated with inhibition of cytochrome P450 isozymes and up-regulation of
selenoprotein genes in chick liver. J Nutr. 2016;146(4):655–661. https://doi.org/10.3945/jn.115.224626
83. Valencia S, Casillas-Figueroa F, Mejía-Cabrera A, Figueroa-Salcido OG, Rodríguez-Hernández AI,
Guerrero-Analco JA, et al. Human gut microbiome: a connecting organ between nutrition, metabolism,
and health. Int J Mol Sci. 2025;26(9):4112. https://doi.org/10.3390/ijms26094112
INTERNATIONAL JOURNAL OF RESEARCH AND SCIENTIFIC INNOVATION (IJRSI)
ISSN No. 2321-2705 | DOI: 10.51244/IJRSI |Volume XII Issue X October 2025
Page 2825
84. Birol E, Bouis H, Saltzman A. Biofortification: the evidence. HarvestPlus White Paper. 2021. Available
from: https://www.harvestplus.org/wp-content/uploads/2021/12/BiofortificationThe-Evidence.pdf
85. Lapris M, Dubois M, Debontridder F, Schneider R, Scippo ML. The potential of multi-screening methods
and omics technologies to detect both regulated and emerging mycotoxins in different matrices. Foods.
2024;13(11):1746. https://doi.org/10.3390/foods13111746
86. Guerre P. Mycotoxin and gut microbiota interactions. Toxins (Basel). 2020;12(12):769.
https://doi.org/10.3390/toxins12120769
87. González-López NM, Lozano MV, Gutiérrez S, Vázquez C, Llorens JV, Marín S, et al. Omics in the
detection and identification of biosynthetic pathways related to mycotoxin synthesis. Anal Methods.
2021;13(36):4287–4302. https://doi.org/10.1039/D1AY01017D
88. Vidal A, Marín S, Ramos AJ, Cano-Sancho G, Sanchis V.
89. Mycotoxin biomarkers of exposure: a comprehensive review. Compr Rev Food Sci Food Saf.
2018;17(5):1127–1155. https://doi.org/10.1111/1541-4337.12367
90. Wu Y, Zhou X, Li X, Yang Y, Wang Z, Liu Y, et al. nSelenium: 48-year journey of global clinical trials.
Mol Cell Biochem. 2025;480:3253–3265. https://doi.org/10.1007/s11010-024-05202-x