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Alcohol Metabolism: Molecular, Physiological, and Behavioral Consequences from Basic Research to Translational Applications

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 25 December 2026 | Viewed by 384

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Guest Editor
Laboratory of Cellular and Molecular Biology, Institute of Biomedical Research (BIOMED), School of Medical Sciences, Pontifical Catholic University of Argentina (UCA), National Scientific and Technical Research Council (CONICET), Buenos Aires, Argentina
Interests: molecular and physiological mechanisms of alcohol metabolism; mitochondrial dysfunction; oxidative/nitrosative stress; synaptic alterations

Special Issue Information

Dear Colleagues,

This Special Issue aims to provide a comprehensive overview of alcohol metabolism and its wide-ranging consequences across molecular, physiological, and behavioral domains. Ethanol metabolism is a key determinant of alcohol-related effects, influencing oxidative stress, inflammation, and neurochemical pathways. Beyond biochemical alterations, alcohol consumption impacts systemic physiology, organ function, and behavioral outcomes, including cognitive and emotional processes. We welcome original research articles and reviews addressing mechanisms of ethanol metabolism, associated molecular and cellular changes, and physiological consequences in different tissues. Studies using animal models, human subjects, and translational approaches are encouraged, as well as investigations into behavioral and neurobiological correlates. By integrating findings from multiple levels of analysis, this Special Issue seeks to advance our understanding of alcohol’s complex impact and identify potential targets for prevention and intervention.

Dr. Analia G. Karadayian
Guest Editor

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Keywords

  • alcohol metabolism
  • acetaldehyde
  • mitochondrial dysfunction
  • oxidative stress
  • behavioral outcomes
  • animal models
  • translational research

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Published Papers (1 paper)

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Research

19 pages, 2566 KB  
Article
Alcohol Metabolism into Acetaldehyde in Developing Cerebral Arteries
by Rika M. Morales, Shiwani Thapa and Anna N. Bukiya
Int. J. Mol. Sci. 2026, 27(14), 6463; https://doi.org/10.3390/ijms27146463 - 21 Jul 2026
Viewed by 131
Abstract
Alcohol exposure during pregnancy leads to fetal alcohol spectrum disorders (FASD), yet the mechanisms through which alcohol disrupts the developing cerebrovasculature remain poorly defined. Acetaldehyde, the first oxidative metabolite of alcohol, can alter vascular function, but whether developing cerebral arteries possess intrinsic capacity [...] Read more.
Alcohol exposure during pregnancy leads to fetal alcohol spectrum disorders (FASD), yet the mechanisms through which alcohol disrupts the developing cerebrovasculature remain poorly defined. Acetaldehyde, the first oxidative metabolite of alcohol, can alter vascular function, but whether developing cerebral arteries possess intrinsic capacity to generate acetaldehyde is unknown. Alcohol is primarily oxidized by alcohol dehydrogenase (ADH), cytochrome P450 2E1 (CYP2E1), and catalase (CAT), and their local metabolic activity may contribute to cerebrovascular vulnerability. In this study, cerebral arteries were isolated from postnatal day (PND) 10 C57BL/6J mouse offspring (third trimester-equivalent to human pregnancy), and incubated ex vivo with physiologically relevant alcohol concentrations (13 or 50 mM). Acetaldehyde generation, transcript expression, protein abundance, and catalase-dependent metabolism were evaluated. Alcohol exposure produced a concentration-dependent increase in acetaldehyde generation within developing cerebral arteries, with comparable responses between males and females. Transcript analysis revealed that Adh1, Cyp2e1, and Cat were expressed across developing tissues; however, Western blotting showed that catalase was the only alcohol-metabolizing enzyme detectable at the protein level within developing cerebral arteries. Accordingly, catalase inhibition by sodium azide altered acetaldehyde production, revealing a significant blocker–sex interaction at the higher inhibitor concentration (0.06 mM). In summary, our ex vivo findings demonstrate that developing cerebral arteries possess intrinsic metabolic capacity to oxidize alcohol to acetaldehyde and that catalase plays an essential role in supporting this process at this developmental stage. These results point to a previously unrecognized metabolic pathway within the developing cerebrovasculature that may potentially contribute to early-life vulnerability to alcohol exposure. Full article
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