Assessment of Lipid Peroxidation in Liver and Heart Of D-Galagctose Induced Chick Embryo

Oxidative stress is a critical mediator of cellular injury, leading to lipid peroxidation and organ dysfunction. The present study evaluates D-galactose-induced oxidative damage in the liver and heart of 8-day-old chick embryos by quantifying lipid peroxidation through thiobarbituric acid reactive substances (TBARS) assay. Fertilized hen eggs were incubated and divided into control and experimental groups, with the latter receiving 50 µg D-galactose/egg via the air sac. After 48 h, liver and heart tissues were analyzed for malondialdehyde (MDA), an indicator of lipid peroxidation. D-galactose administration significantly elevated (p < 0.001) MDA levels in both tissues, suggesting enhanced oxidative stress. The heart showed slightly higher peroxidation, possibly due to its post-mitotic nature. Histopathological interpretations (literature-based) support that oxidative injury could manifest as hepatocellular vacuolization and cardiomyocyte disruption. This study reinforces the chick embryo as a promising model for developmental oxidative stress and aging research, highlighting the pathophysiological impact of glycation-induced oxidative injury in early organogenesis.

oxidative stress, lipid peroxidation, D-galactose, chick embryo, MDA, aging, advanced glycation

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