Lipid peroxidation as a possible secondary mechanism of sterigmatocystin toxicity

Sterigmatocystin (Stg), a major secondary metabolite of Aspergillus versico lor and A. nidulans, is the precursor of aflatoxin B-1. In this study, male albino rats were treated with Stg-contaminated diet for 30 days, resulting in reduced levels of glutathione, ascorbic acid, and alpha -tocopherol. Th e activity of catalase in liver was reduced, whereas an increase in the act ivities of superoxide dismutase and glutathione peroxidase was observed. Th e levels of cytochrome P-450, cytochrome b(5), cyto-chrome b(5) reductase, cytochrome c reductase, hydroxyl radical, and hydrogen peroxide formation s ignificantly increased in the Stg-treated rat liver microsomes. Hepatic par enchymal cell injury, necrosis, and Kupffer cells proliferation were notice d in histological sections of liver from animals treated with Stg. Overall results suggest that generation of free radicals imposes depletion of antio xidants. This led to enhanced lipid peroxidation. The observed elevation of hepatic thiobarbituric acid reactive substances appears to originate mainl y from the damaged Kupffer cells. As a result, elevated levels of serum mar ker enzymes were also observed.