Mutation induction by rodent liver microsomal metabolites of aflatoxins B 1 and G 1 in Neurospora crassa

Abstract

The mutagenic activities of aflatoxins B 1 and G 1 were studied in the ad-3 test system of Neurospora crassa by treatment of conidia with aflatoxin and liver homogenate for 2 h. No significant increase in the ad-3 mutation frequency over the spontaneous frequency was observed when either aflatoxin or mammalian liver homogenate was omitted from the test system. The ad-3 mutation frequencies increased to between 29 and 87/10 6 survivors, which is a 73- to 217-fold increase over the average spontaneous ad-3 mutation frequency (0.4/10 6 survivors), after conidia of N. crassa were treated with 0.67 mM aflatoxin B 1, hamster liver homogenate, and a NADPH generating system. A 9- to 15-fold increase int eh mutation frequency over the spontaneous mutation frequency was found when 0.67 mM of aflatoxin G 1 instead of aflatoxin B 1 was used in the test system. Treatment of conidia with 0.44 mM aflatoxin B 1 mice liver homogenate and a NADPH generating system caused a small, but significant increase in the ad-3 mutation frequencies. No significant increase in the mutation frequency was found when a single sample of human liver homogenate was used in the test system. These studies show that metabolic activation is necessary for the expression of the mutagenic activity of aflatoxins B 1 and G 1 in N. crassa.