Alcohol-induced deterioration in primary antioxidant and glutathione family enzymes reversed by exercise training in the liver of old rats

Document Type

Article

Publication Date

9-1-2010

Abstract

Chronic alcohol consumption causes severe hepatic oxidative damage, particularly to old subjects by decreasing various antioxidant enzymes. In this study, we test the hypothesis that exercise training can protect the aging liver against alcohol-induced oxidative damage. Two different age groups of Wistar albino rats (3 months young, n=24; 18 months old, n=24) were evenly divided into four groups: control (Con), exercise trained (Tr, 23. m/min 30. min/day, 5 days/week for 2 months), ethanol drinking/treated (Et, 2.0g/kg b.w. orally), and exercise training plus ethanol drinking/treated (Tr + Et). We found significantly (P<001) lowered hepatic antioxidant enzymes including superoxide dismutase, catalase, selenium (Se)-dependent glutathione peroxidase (Se-GSH-Px), Se-non-dependent glutathione peroxidase (non-Se-GSH-Px), glutathione reductase, and glutathione S-transferase activities in aged rats compared with young. Age-related decrease in antioxidant enzyme status was further exacerbated with ethanol drinking, which indicates liver in aged rats is more susceptible to oxidative damage because of decreased free radical scavenging system in aged/old ethanol-drinking rats. However, the decrease in liver antioxidant enzymes status with ethanol consumption was ameliorated by 2 months exercise training in old and young rats. These results demonstrate that age-associated decrease in hepatic free radical scavenging system exacerbated by ethanol drinking. For the first time, we found that this deterioration was significantly reversed by exercise training in aging liver, thus protects against alcohol-induced oxidative damage. © 2010 Elsevier Inc.

Identifier

77956649283 (Scopus)

Publication Title

Alcohol

External Full Text Location

https://doi.org/10.1016/j.alcohol.2010.07.004

ISSN

07418329

PubMed ID

20705416

First Page

523

Last Page

529

Issue

6

Volume

44

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