The present study examined the apoptosis and the oxidative stress induced by the food Preservative, butylated hydroxytoluene (BHT) in liver of albino rats and the protective role might be played by vitamin E was assessed. Apoptosis was evaluated via determination of cytochrome C release and the oxidative stress was assessed by determination of lipid peroxidation and the total antioxidant status in liver homogenate. It was found that feeding the animals 1% BHT supplemented food for 4 weeks resulted in a significant increase of cytochrome C release in medium containing liver mitochondria. This may provide evidence that apoptosis is a possible mechanism of cell death in liver tissues. Meanwhile, lipid peroxides levels measured as malondialdehyde (MDA) in liver tissue homogenates and antioxidant power significantly increased and decreased, respectively in the 1% BHT fed animal group. Feeding the animals 0.4% vitamin E acetate added to the 1% BHT supplemented food for 4 weeks resulted in a significant reduction in the level of cytochrome C release concomitant with an improvement of the antioxidant power and a reduction in the MDA induced by BHT alone. These findings may further suggest that BHT-induced apoptosis in liver is mediated, at least in part, by oxidative stress. Therefore, the protective effect of vitamin E acetate against BHT-induced hepatocyte apoptosis raised a great concern of adding vitamin E acetate to food and their preparations containing BHT.
Key words: Butylated Hydroxytoluene (BHT), apoptosis, antioxidant power.
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