Abstract
The objective of this study was to examine the effects of vitamin C on the formation of aflatoxin B1 (AFB1)-DNA adduct and AFB1-induing cellular oxidative damage in rat livers treated with radiation and AFB1. Six-week-old male Sprague-Dawley rats were randomly divided into five groups: the control group, the AFB1-treated group, the group treated with AFB1 and vitamin C, the group treated with X-ray and AFB1, and the group treated with X-ray and AFB1 with vitamin C. On the first day of the experiment, only one dose of X-rays was exposed to the entire liver at 1,500 cGy. Next, vitamin C was injected at 10 mg/kg body weight via intraperitoneal injection, followed an hour later by the administration of 0.4 mg/kg of AFB1 via intraperitoneal injection. These treatments were administered every three days for 15 days. On the 16th day, the animals were sacrificed. The AFB1 contents of the rat sera were determined via indirect competitive ELISA. In the quantitative analysis of AFB1 in the rat sera via ELISA, 5.17±0.34 ng/mL of AFB1 was detected in the AFB1-treated groups, but the amount decreased more significantly to 3.23±0.76 ng/mL in the groups treated with AFB1 and vitamin C (p<0.01) than in the AFB1-treated groups. The effect of vitamin C on AFB1-DNA adduct formation was determined via ELISA. The values of AFB1-DNA adduct formation were 9.38±0.41 ng/ml in the AFB1-treated groups, but the amount decreased more significantly to 5.28±0.32 ng/mL in the groups treated with AFB1 and vitamin C (p<0.01) than in the AFB1-treated groups. Immunohistochemistry revealed that the accumulation of the AFB₁was not observed in the normal liver tissue (G1). The AFB1-positive materials were observed in the central vein and the portal vein of the liver tissue from the AFB1 (G2) treatment or the X-ray and AFB1 (G4) co-treatment, but the AFB1-positive materials were observed weakly in the group treated with vitamin C (G3 and G5). These results indicate that vitamin C had ameliorating effects on the AFB1 accumulation of liver tissue.
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