Alcohol‐induced oxidative stress and cell responses

Abstract

Epidemiological and animal studies have demonstrated that alcohol abuse is directly associated with the increase of multiple organ diseases, such as liver injury, cardiovascular diseases, and neurological disorders. While the mechanisms of alcohol-induced cell injury and disease remain to be investigated, recent studies indicate that reactive oxygen species (ROS) may play an important role. Reactive oxygen species are able to cause various cellular injuries, such as DNA damage, lipid peroxidation and protein modification. Cellular systems are protected from ROS-induced cell injuries by an array of defenses composed of various anti-oxidants with different functions. When the ROS present in the cellular system overpower the defense systems, they will cause oxidative stress or cell injury, leading to the development of diseases. This article reviews recent literature on alcohol-induced ROS production, oxidative stress, signal transduction, and cellular responses. The implication of these processes in alcohol-related diseases is also discussed.

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“…This idea of investigating the interactions between environmental exposures and MMR polymorphisms is strengthened by findings of increased oxidative stress and DNA damage resulting from tobacco smoking as well as from a Western diet, alcohol and obesity. [23][24][25][26] However, for a better explanation of these phenomena further research is warranted.…”

Updates on Glucose 6-Phosphate Dehydrogenase (G6PD): From Prokaryotes to Human

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Effect of <i>Capsosiphon fulvescens</i> on Ethanol-induced Liver Damage in HepG2 Cells over Expressing CYP2E1

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