Study of oxidative-stress in isoniazid-rifampicin induced hepatic injury in young rats.

Abstract:

:The role of oxidative-stress as a mechanism of hepatotoxicity caused by combination of isoniazid (INH) and Rifampicin (RMP) was investigated in young growing rats. A successful model of hepatotoxicity was produced by giving 50 mg/kg/day each of INH and RMP in two weeks. Liver showed type II hepatocellular changes (microvesicular fat deposition) with mild portal triaditis. The glutathione and related thiols were significantly decreased in both blood and liver tissues with combination of INH and RMP treatment. Superoxide dismutase, glutathione peroxidase, catalase and glutathione-S-transferases with CDNB and DCNB as substrates were decreased in the combination treated group. Glutathione reductase, glutathione-S-transferase with ethacrynic acid as substrate and lipid peroxidation exhibited a significant increase with treatment. The altered profile of antioxidant enzymes with increased lipid peroxidation indicated the enhanced oxidative-stress in combination of INH and RMP treatment. All the findings are faithfully reflected in the blood tissue except superoxide dismutase which showed significant enhancement in this tissue. INH and RMP hepatotoxicity is thus appeared to be mediated through oxidative-stress.

journal_name

Drug Chem Toxicol

authors

Sodhi CP,Rana SV,Mehta SK,Vaiphei K,Attari S,Mehta S

doi

10.3109/01480549709003881

subject

Has Abstract

pub_date

1997-08-01 00:00:00

pages

255-69

issue

3

eissn

0148-0545

issn

1525-6014

journal_volume

20

pub_type

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