Aflatoxin 6, has been fed for 6 months t o young rats in low o r high protein diets. In agreement with previous research, it was found that the high protein diet was associated with hyperplastic activity i n the liver, of a type similar t o that usually found i n rats developing aflatoxin 6,-induced hepatoma. During the same period, negligible precancerous-like changes were seen i n the ratsfed the low protein diet with aflatoxin B,. This model has been used t o test the sensitivity of various liver function tests t o the dietary-induced difference i n liver reaction t o atlatoxin 6, feeding. The serum enzymes lactic dehydrogenase and alkaline phosphatase were considerably elevated in rats with precancerous-like lesions, but the former was the most sensitive enzyme. Serum glutamate-oxalate transaminase and serum glutamate-pyruvate transaminase were both raised in the rats with precancerous-like lesions, but much less so than lactic dehydrogenase and alkaline phosphatase. Urinary aflatoxin metabolites were also measured. Aflatoxin M, and atlatoxin P, were both found after feeding aflatoxin 6,. During the feeding period, aflatoxin P, excretion steadily increased, while aflatoxin M, increased between the second and fourth months and then fell.
In the first 4 months, rats fed a low protein diet tended to produce a lower ratio of atlatoxin M, t o atlatoxin P, compared t o the rats fed a high protein diet. A t 6 months, the ratio decreased markedly, especially in the rats with the precancerous-like lesions. It was concluded that lactic dehydrogenase, alkaline phosphatase, and the ratio of urinary excretion of aflatoxin M, t o aflatoxin P, could be useful tests for inclusion in a diagnostic procedure for aflatoxin 6,-induced precancerous liver changes that might be expected i n human studies. P-450 found in the livers of these same rats. Tilak et al. (1975) argued that microsomal drug-metabolizing enzymes are required to detoxify AFB, to AFM, but they also produce the carcinogenic metabolite, i.e. 2,3-oxide. Therefore, low protein diets apparently protect the animal from the carcinogenic action of AFBl by allowing lower production of 2,3-oxide, as well as AFMI.