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

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 gr...

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Published in:Alcohol (Fayetteville, N.Y.) Vol. 44; no. 6; pp. 523 - 529
Main Authors: Mallikarjuna, K, Shanmugam, K.R, Nishanth, K, Wu, Ming-Chieh, Hou, Chien-Wen, Kuo, Chia-Hua, Reddy, K. Sathyavelu
Format: Journal Article
Language:English
Published: United States Elsevier Inc 01-09-2010
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Abstract 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, 2.0 g/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.
AbstractList 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, 2.0 g/kg b.w. orally), and exercise training plus ethanol drinking/treated (Tr+Et). We found significantly (P&lt;.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.
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, 2.0 g/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.
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, 2.0 g/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.
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, 23m/min 30min/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.
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, 2.0 g/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.
Author Hou, Chien-Wen
Shanmugam, K.R
Wu, Ming-Chieh
Reddy, K. Sathyavelu
Kuo, Chia-Hua
Mallikarjuna, K
Nishanth, K
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  fullname: Kuo, Chia-Hua
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  fullname: Reddy, K. Sathyavelu
BackLink https://www.ncbi.nlm.nih.gov/pubmed/20705416$$D View this record in MEDLINE/PubMed
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Issue 6
Keywords Oxidative stress
Aging liver
Exercise
Free radical scavenging enzymes
Ethanol
ROS
Language English
License Copyright © 2010 Elsevier Inc. All rights reserved.
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Snippet Abstract Chronic alcohol consumption causes severe hepatic oxidative damage, particularly to old subjects by decreasing various antioxidant enzymes. In this...
Chronic alcohol consumption causes severe hepatic oxidative damage, particularly to old subjects by decreasing various antioxidant enzymes. In this study, we...
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StartPage 523
SubjectTerms Aging
Aging liver
Animals
Antioxidants
Catalase - analysis
Enzymes
Ethanol
Ethanol - administration & dosage
Ethanol - adverse effects
Exercise
Free radical scavenging enzymes
Glutathione Peroxidase - analysis
Glutathione Reductase - analysis
Glutathione Transferase - analysis
Liver - enzymology
Liver Diseases, Alcoholic - prevention & control
Male
Oxidative Stress
Physical Conditioning, Animal
Psychiatry
Rats
Rats, Wistar
Rodents
ROS
Superoxide Dismutase - analysis
Title Alcohol-induced deterioration in primary antioxidant and glutathione family enzymes reversed by exercise training in the liver of old rats
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https://dx.doi.org/10.1016/j.alcohol.2010.07.004
https://www.ncbi.nlm.nih.gov/pubmed/20705416
https://www.proquest.com/docview/1027214639
https://search.proquest.com/docview/755190020
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