Abstract
Antioxidants such as butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) are known to inhibit AFB1-DNA binding thereby protecting liver against the chronic effects of the carcinogen. It is believed that they inhibit liver mixed function oxidases while including GSH S-transferases. Both BHA and BHT are poor inducers of pulmonary GSH S-transferases. BHA pretreatment, but not BHT reduced the pulmonary microsome-mediated AFB1 binding to DNA in vitro. Therefore the influence of these antioxidants on GSH - conjugation of AFB1 is limited to liver. Inhibition of AFB1-DNA binding mediated by BHT-treated microsomes is probably due to alterations in microsomal enzymes.