الفهرس 
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Abstract
Aflatoxins are group of closely related mycotoxins that are widely distributed in nature. The most important of the group is aflatoxin (AFB1). AFB1 is a fungal toxin that has been implicated as a causative
agent in human hepatic and extrahepatic carcinogenesis.
Since the complete elimination of exposure to environmental carcinogens is not possible, chemoprotective interventions could be targeted for specific human population identified as at particularly high
risk for neoplasia.
Vitamins C and A are well known antioxidants, substantially minimize apoptosis, DNA damage and carcinogenic effects of many
toxins.
Hence, the present study aimed to explore the different adverse effects of aflatoxin B1 in experimental albino rats and clarify the protective effect of vitamins C and A which used as antioxidant agents in
ameliorating AFB1 toxicity.
This study was carried on three hundreds and eighty adult albino rats. All rats were subjected to the following:
1-Biochemical assay which included liver and kidney function and complete blood picture;
2-Histopathological changes in the liver, kidneys, and lungs.
3-Molecular study which was detected by DNA fragmentation, laddering pattern, on gel electrophoresis.
ear 203 we
Summary
Our results showed that AFB1 induced hepatotoxic, nephrotoxic and haematotoxic effects. where there was very highly significant increase (P < 0.0005) in ALT, AST, T. Bil., BUN and serum creatinine levels. It also shows a very highly significant decrease (P < 0.0005) in Hb concentration and RBCs, and WBCs counts in intoxicated rats as compared with control groups and rats pretreated with antioxidants. These biochemical parameters of hepatotoxic and nephrotoxic effects were confirmed by the histopathological results. Also, AFB1 induced apoptosis confirmed by the appearance of DNA fragmentation on gel electrophoresis. Antioxidant vitamins C and A largely prevented these
effects.
Therefore the present study suggests that antioxidants may provide a good protective effects against the induction of apoptosis and other
toxic effects caused by AFB1.