The effect of modulation of glutathione levels on markers for Aflatoxin B1-induced cell damage

Abstract

The modulatory effect of glutathione levels on markers for aflatoxin B1 (AFB1) -induced cell damage has been investigated in the rat (susceptible specie) and the (mouse resistant specie). The concentration of GSH was depleted and increased by administering paracetamol (PAM) and cysteine respectively and activities of glutathione S-transferase (GST) and ϒ-glutamyl transpeptidase (ϒ-GT) were determined. The effect of AFB1 on hepatic lipid peroxidation in both species was also investigated. Treatment of rats with 2 mg/kg.bwt AFB1 intraperitoneal caused a depletion of GSH in the liver to a minimum at 6 h (80% of the control value) and the level returned to normal after 24 h. GST was similarly increased to a maximum at 6 h and the level also returned to normal after 24 h. GSH and GST activities were not significantly affected in AFB, -treated mice. Orally administered PAM (400 mg/ kg.bwt) caused a depletion of GSH with a minimum at 6 h (59% and 36% of the control rats and mice respectively). Pretreatment of AFB1 with PAM produced a serious depletion at 6 h (34% and 35% of the control rats and mice respectively). GST activities were also marginally increased in both animals. AFB1 pretreatment mediated (P>0.05) when cysteine was pretreated alone with AFB1. Combined treatment of AFB1 and PAM induced 177% increase in ϒ-GT activity. Overall, our results suggest that the metabolism of aflatoxin B by GSH docs not lead to the formation of toxic products but rather GSH plays a protective role in AFB1-induced cell damage and GSH pathway is less utilised in mice.