Hepatoprotective role of captopril on paraquat induced hepatotoxicity.

Abstract:

:Paraquat (PQ) is a highly toxic herbicide that is used in most of the countries without restriction. The cytotoxic effect of PQ is mediated by radicals, which are the products of PQ reduction in cells. The anti-oxidative action of captopril, an angiotensin-converting enzyme inhibitor, appears to be through its ability to scavenge reactive oxygen species. In this study, the heptoprotective effect of captopril against PQ-induced hepatotoxicity was evaluated using primary cultured rat hepatocytes. Hepatocytes were isolated from male Wistar rats using a two-step collagenase perfusion, following incubation in the presence of captopril at 0.1, 0.2, 0.4 and 0.8 mM with or without PQ (5 mM). Hepatoprotective effects of captopril were studied indicating glutathione level intensity, thiobarbituric acid reactive substances (TBARs) formation, lactate dehydrogenase (LDH) leakage and cell viability every 70 min for 210 min. Captopril at 0.2 mM concentration maintained the LDH leakage, glutathione level and cell viability in the presence of 5 mM PQ. In spite of a significant elevation in TBARs formation in the PQ group, captopril did not show any significant protection. In conclusion, our data reveals that incubation of freshly isolated rat hepa-tocytes with captopril (0.2 mM) significantly protected the hepatocytes against the cytotoxicity of PQ (P < 0.05).

journal_name

Hum Exp Toxicol

authors

Elmi A,Sadeghi Zh,Elmi S,Daraei B,Ghazi-Khansari M

doi

10.1177/0960327107084533

subject

Has Abstract

pub_date

2007-10-01 00:00:00

pages

789-94

issue

10

eissn

0960-3271

issn

1477-0903

pii

26/10/789

journal_volume

26

pub_type

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