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Review
. 2019 Jan;76(2):231-244.
doi: 10.1007/s00018-018-2931-8. Epub 2018 Oct 10.

Stem cells under the influence of alcohol: effects of ethanol consumption on stem/progenitor cells

Affiliations
Review

Stem cells under the influence of alcohol: effects of ethanol consumption on stem/progenitor cells

Giuliana Di Rocco et al. Cell Mol Life Sci. 2019 Jan.

Abstract

Stem cells drive embryonic and fetal development. In several adult tissues, they retain the ability to self-renew and differentiate into a variety of specialized cells, thus contributing to tissue homeostasis and repair throughout life span. Alcohol consumption is associated with an increased risk for several diseases and conditions. Growing and developing tissues are particularly vulnerable to alcohol's influence, suggesting that stem- and progenitor-cell function could be affected. Accordingly, recent studies have revealed the possible relevance of alcohol exposure in impairing stem-cell properties, consequently affecting organ development and injury response in different tissues. Here, we review the main studies describing the effects of alcohol on different types of progenitor/stem cells including neuronal, hepatic, intestinal and adventitial progenitor cells, bone-marrow-derived stromal cell, dental pulp, embryonic and hematopoietic stem cells, and tumor-initiating cells. A better understanding of the nature of the cellular damage induced by chronic and episodic heavy (binge) drinking is critical for the improvement of current therapeutic strategies designed to treat patients suffering from alcohol-related disorders.

Keywords: Acetaldehyde; Alcohol dehydrogenase; Alcohol-related disorders; Alcoholic beverages; Fetal alcohol spectrum disorders; Mesenchymal stromal cells.

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Fig. 1
Fig. 1
Main pathways of alcohol oxidative metabolism. Ethanol is converted into acetaldehyde by the cytosolic enzyme alcohol dehydrogenase and by the microsomal cytochrome P450 2E1 (CYP2E1); acetaldehyde is then oxidized into acetate by the mitochondrial enzyme aldehyde dehydrogenase 2. Alcohol metabolism increases the ratio of the reduced nicotinamide adenine dinucleotide (NADH) to the oxidized nicotinamide adenine dinucleotide (NAD+) and promotes reactive oxygen species (ROS) production
Fig. 2
Fig. 2
Possible mechanisms of alcohol toxicity on stem cell biology

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