Lipid peroxidation as a possible secondary mechanism of sterigmatocystin toxicity.

Abstract:

: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 alpha-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 b5, cytochrome b5 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.

journal_name

Hum Exp Toxicol

authors

Sivakumar V,Thanislass J,Niranjali S,Devaraj H

doi

10.1191/096032701682692955

subject

Has Abstract

pub_date

2001-08-01 00:00:00

pages

398-403

issue

8

eissn

0960-3271

issn

1477-0903

journal_volume

20

pub_type

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