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Long-term ethanol consumption leads to lung tissue oxidative stress and injury

Publication Type : Journal Article

Publisher : Oxidative Medicine and Cellular Longevity

Source : Oxidative Medicine and Cellular Longevity, Volume 3, Number 6 (2010)

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Keywords : adenosine triphosphatase (potassium sodium), alcohol, Alcohol abuse, alcohol blood level, alcohol consumption, animal, animal tissue, Animalia, Animals, anthropometry, article, Biochemical parameters, Biological organs, Blood, Blood samples, Blood-alcohol concentration, body weight, carbonyl derivative, catalase, chemically induced disorder, Control groups, controlled study, disease severity, drug effect, enzyme activity, Ethanol, Ethanol consumption, glutathione, glutathione disulfide, glutathione peroxidase, glutathione reductase, Glutathiones, Health effects, histopathology, Initial weights, Long-term effects, lung, lung homogenate, Lung injury, lung parenchyma, Lung tissue, male, matrix metalloproteinase, Matrix Metalloproteinases, metabolism, nitrite, Nitrites, nonhuman, oxidative stress, Oxygen, pathology, protein, protein carbonylation, Protein carbonyls, rat, Rats, Rattus, Reactive Oxygen Species, Redox ratio, Reduced glutathione, Relative weights, Sodium, Sodium-Potassium-Exchanging ATPase, superoxide dismutase, Superoxide dismutases, thiobarbituric acid reactive substance, Thiobarbituric Acid Reactive Substances, Tissue, Wistar, Wistar rat

Year : 2010

Abstract : Background: Alcohol abuse is a systemic disorder. The deleterious health effects of alcohol consumption may result in irreversible organ damage. By contrast, there currently is little evidence for the toxicity of chronic alcohol use on lung tissue. Hence, in this study we investigated long-term effects of ethanol in the lung. Results: Though body weight of rats increased significantly with duration of exposure compared to its initial weight, but there was no significant change in relative weight (g/100 g body weight) of lung due to ethanol exposure. The levels of thiobarbituric acid reactive substances (TBARS), nitrite, protein carbonyl, oxidized glutathione (GSS G), redox ratio (GSS G/GSH ) and GST activity elevated; while reduced glutathione (GSH ) level and activities of glutathione reductase (GR), glutathione peroxidase (GPx), catalase, superoxide dismutase (SOD) and Na+K+ATPase reduced significantly with duration of ethanol exposure in the lung homogenate compared to the control group. Total matrix metalloproteinase activity elevated in the lung homogenate with time of ethanol consumption. Histopathologic examination also demonstrated that severity of lung injury enhanced with duration of ethanol exposure. Methods: 16-18 weeks old male albino Wistar strain rats weighing 200-220 g were fed with ethanol (1.6 g/kg body weight/day) up to 36 weeks. At the end of the experimental period, blood samples were collected from reteroorbital plexus to determine blood alcohol concentration and the animals were sacrificed. Various oxidative stress-related biochemical parameters, total matrix metalloproteinase activity and histopathologic examinations of the lung tissues were performed. Conclusions: Results of this study indicate that long-term ethanol administration aggravates systemic and local oxidative stress, which may be associated with lung tissue injury. © 2010 Landes Bioscience.

Cite this Research Publication : S. Ka Das and Mukherjee, Sb, “Long-term ethanol consumption leads to lung tissue oxidative stress and injury”, Oxidative Medicine and Cellular Longevity, vol. 3, 2010.

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