EFFECT OF RETINOL ON OCHRATOXIN-PRODUCED GENOTOXICITY IN MICE

Ochratoxin (1 mu g/kg body weight/day), when administered orally daily to albino Swiss mice for 14 continuous days, increased the incidence of abnormalities in mitotic and meiotic metaphase chromosomes, and the gross morphology of the sperm head; the sperm count per unit volume of caput epididymal suspension also decreased. These genotoxic effects were substantially reduced by concurrent oral administration of retinol at double the clinically therapeutic dose. It is possible that the electrophilic metabolites of ochratoxin form adducts with DNA or produce replacement-type mutations. Retinol may achieve its antigenotoxic effect by means of blocks and shunts in the ochratoxin metabolic pathway. Vitamin A-mediated cellular repair and scavenging of the mutagenic radicals can also take place. The vitamin itself has some genotoxic potential.