Lipid peroxidation as a possible secondary mechanism of sterigmatocystin toxicity

Human and Experimental Toxicology - Tập 20 Số 8 - Trang 398-403 - 2001
Sivakumar Vijayaraghavalu1, J. Thanislass2, S Niranjali, Halagowder Devaraj3
1Unit of Biochemistry, Department of Zoology, University of Madras, Chennai, India
2Unit of Biochemistry, Department of Zoology , University of Madras, Guindy Campus, Chennai, 600 025, India
3Department of Biochemistry and Molecular Biology, University of Madras, Guindy Campus, Chennai 600 025, India

Tóm tắt

Sterigmatocystin (Stg), a major secondary metabolite of Aspergillus versicolor and A. nidulans, is the precursor of aflatoxin B1 In this study, male albino rats were treated with Stg-contaminated diet for 30 days, resulting in reduced levels of glutathione, ascorbic acid, and tocopherol. The activity of catalase in liver was reduced, whereas an increase in the activities of superoxide dismutase and glutathione peroxidase was observed. The levels of cytochrome P450, cytochrome b 5, cyto-chrome b 5 reductase, cytochrome c reductase, hydroxyl radical, and hydrogen peroxide formation significantly increased in the Stg-treated rat liver microsomes. Hepatic parenchymal cell injury, necrosis, and Kupffer cells proliferation were noticed in histological sections of liver from animals treated with Stg. Overall results suggest that generation of free radicals imposes depletion of antioxidants. This led to enhanced lipid peroxidation. The observed elevation of hepatic thiobarbituric acid reactive substances appears to originate mainly from the damaged Kupffer cells. As a result, elevated levels of serum marker enzymes were also observed.

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Human and Experimental Toxicology

Tập 20 Số 8

398-403

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