Publication Type:

Journal Article


Life Sciences, Volume 81, Number 3, p.177-187 (2007)



alcohol, alcohol consumption, alcohol metabolism, aldehyde dehydrogenase, Animals, antioxidant activity, Antioxidants, biological marker, cell proliferation, cell viability, Central Nervous System Depressants, chemokine, Cytochrome P-450 CYP2E1, cytochrome P450 2E1, cytokine, electron transport, Ethanol, FAS ligand, Free Radicals, glutathione, human, human cell, Humans, hydroxyethyl radical, hydroxynonenal, I kappa B, immunoglobulin enhancer binding protein, interleukin 1, interleukin 6, Kupffer cell, Kupffer Cells, lipid metabolism, malonaldehyde, microsome, Mitochondria, mitochondrial membrane, mitogen activated protein kinase, mitogen activated protein kinase 1, mitogen activated protein kinase 3, mitogen activated protein kinase p38, Myc protein, nitric oxide, nonhuman, Oxidants, oxidative stress, protein c fos, protein c jun, protein p53, protein protein interaction, Proteins, radical, reactive nitrogen species, reactive oxygen metabolite


Alcohol-induced oxidative stress is linked to the metabolism of ethanol involving both microsomal and mitochondrial systems. Ethanol metabolism is directly involved in the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS). These form an environment favourable to oxidative stress. Ethanol treatment results in the depletion of GSH levels and decreases antioxidant activity. It elevates malondialdehyde (MDA), hydroxyethyl radical (HER), and hydroxynonenal (HNE) protein adducts. These cause the modification of all biological structures and consequently result in serious malfunction of cells and tissues. © 2007 Elsevier Inc. All rights reserved.


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Cite this Research Publication

D. M. Vasudevan and Das, S. K., “Alcohol-induced oxidative stress”, Life Sciences, vol. 81, pp. 177-187, 2007.