Linus Pauling Institute

These studies were conducted to investigate whether ascorbic acid protected guinea pigs from aflatoxin B1 (AFB1) toxicity. Young guinea pigs, fed either 0 (AA) or 25 mg (25 AA) or gavaged 300 mg ascorbic acid (300 AA) per day for 21 days, were gavaged with the LD50 dose of AFB1 on the 22nd day. Seven out of 10 animals in the AA group died within 72 hr of AFB1 administration. The livers of the animals showed regional massive necrosis and multilobular degeneration. There was no mortality in the 25 AA group. Their livers, however, showed changes similar to those seen in AA group. Serum alanine amino transferase (ALAT) and aspartate amino transferase (ASAT) levels were elevated. There was neither mortality nor pathological changes in livers in the 300 AA group. Their ALAT and ASAT levels were unaffected. In vitro production of AFM1 by liver microsomes tended to be higher than that in the other two groups. Three animals saved from the 300 AA group and continued with their supplementation were administered a second, intraperitoneal (ip) LD50 dose of AFB1 1 month after the first AFB1 dose. One animal died. Livers of the animals showed centrilobular degeneration and moderate necrosis in scattered hepatocytes. Liver microsomal cytochrome P450 and cytosolic glutathione S-transferase (GST) levels and AFM1 production were drastically reduced. ALAT and ASAT activities were raised. The results indicated that intake of 300 mg of ascorbic acid almost protected the animals from acute toxicity of AFB1 when given by gavage, but not when administered as a second dose ip.