Aflatoxin B1 and ethanol co-exposure induces hepatic oxidative damage in mice

Abstract

The present study investigated the effects of aflatoxin B1 (AFB1) and ethanol co-exposure on biomarkers of hepatic damage in mice. Four groups of adult male mice were treated for 7 consecutive days. Control mice received corn oil alone at a dose of 2 mL/kg bw. One group was treated with ethanol at a dose of 500 µL/kg bw and another group administered 9 mg/kg bw of AFB1 dissolved in corn oil. The fourth group was co-administered with ethanol and AFB 1. The body and liver weights of treated mice decreased significantly when compared with corresponding control. Alone, ethanol and AFB1 treatment separately increased serum activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyl transferase (GGT) and alkaline phosphatase (ALP). Alcohol dehydrogenase (ALD) activity was markedly elevated in ethanol-treated mice but was unaffected by AFB1 treatment. Co-exposure of AFB1 and ethanol escalated the activities of these serum enzymes. Administration of ethanol and AFB1 separately resulted in significant decrease in both non-enzymatic antioxidant glutathione (GSH) level and enzymatic antioxidant catalase (CAT) and glutathione-S-transferase (GST) activities, whereas lipid peroxidation was markedly elevated. Superoxide dismutase activity and vitamin C level remained unaffected in all treatment groups. Co-exposure of animals to ethanol and AFB1 showed additive effects on the activities of GST and CAT as well as on the GSH level. Histopathological study revealed that these compounds interact together to exacerbate their individual effects on the liver. In summary, the data presented showed that AFB1 and ethanol co-exposure induced severe oxidative damage to the liver of mice and as such humans consuming excessive amount of ethanol and diets contaminated with AFB1 simultaneously may be at greater risk of the hepatotoxic effects of these compounds.