Recent Advances in Alcohol‐Induced Adduct Formation
Abstract
This article presents the proceedings of a symposium presented at the ISBRA 12th World Congress on Biomedical Alcohol Research, held in Heidelberg/Mannheim, Germany, September 29 through October 2, 2004. The organizers of the symposium were Simon Worrall and Victor Preedy, and the symposium was chaired by Onni Niemelä and Geoffrey Thiele. The presentations scheduled for this symposium were (1) Adduct chemistry and mechanisms of adduct formation, by Thomas L. Freeman; (2) Malondialdehyde‐acetaldehyde adducts: the 2004 update, by Geoffrey Thiele; (3) Adduct formation in the liver, by Simon Worrall; (4) Protein adducts in alcoholic cardiomyopathy, by Onni Niemelä; and (5) Alcoholic skeletal muscle myopathy: a role for protein adducts, by Victor R. Preedy.
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Treatment with an antioxidant can halt AA-AGE adduct formation, supporting that AA-AGE adducts can be generated from a Schiff base product similar to AA adducts and AGEs.
“However, treatment with an antioxidant can halt AA-AGE adduct formation, supporting the idea that AA-AGE adducts can be generated from a Schiff base product similar to AA adducts and AGEs.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [168]
AA-AGE adducts are observed after chronic alcohol exposure, exhibit similar properties to AGE adducts cross-linked with sugar molecules, and are different from MAA adducts formed by AA and MDA interactions.
“The formation of AA-AGE adducts can be observed after chronic alcohol exposure.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [168]
Ethanol and its reactive metabolites generated by CYP2E1 are likely involved in AGE synthesis pathways to produce final acetaldehyde and AGE (AA-AGE) adducts.
“Ethanol and its reactive metabolites generated by CYP2E1 are also likely involved in the AGE synthesis pathways to produce the final acetaldehyde and AGE (AA-AGE) adducts.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [168]
Under conditions that include increased lipid peroxidation, such as exposure to alcohol and/or high n-6 fat diets or intake of high fructose drinks, different AGEs are produced by Schiff base formation.
“Under conditions that include increased lipid peroxidation, such as exposure to alcohol and/or high n-6 fat diets or intake of high fructose drinks, different AGEs are produced by Schiff base formation (Fig. 1).”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [168]
AA adducts are produced in two separate pathways: the first forms AA adducts with specific amino acids and N-ethyl amino acid groups under reducing conditions; the second is AA adduct synthesis under nonreducing conditions, with initial Schiff base formation followed by rearrangements to yield diverse AA adducts.
“AA adducts are produced in two separate pathways that yield two different types of adducts, depending on the existing conditions.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [168]
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References 47 · Cited by 48
- Authors
- Freeman, T. L., Tuma, D. J., Thiele, G. M., Klassen, L. W., Worrall, S., Niemelä, O., Parkkila, S., Emery, P. W., & Preedy, V. R.
- Affiliations
- The University of Queensland (AU)
- Corresponding author
- Niemelä, Onni
- Venue
- Alcoholism: Clinical and Experimental Research
- Publisher
- Wiley
- Published
- 2005-07
- Volume
- 29
- Issue
- 7
- Pages
- 1310-1316
- ISSN
- 0145-6008 (ISSN-L)
- 1530-0277
- OpenAlex
- W2116898590
- Cited by
- 48
- References
- 47
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 4 · 2023: 4 · 2022: 1 · 2021: 2 · 2020: 3 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 2 · 2015: 1 · 2014: 3 · 2013: 1 · 2012: 2
- FWCI
- 2.23
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Alcoholism Clinical and Experimental Research (publishedVersion)
- PubMed (publishedVersion)
- Research Portal (King's College London) (submittedVersion)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Health Sciences › Medicine › Neurology › Alcoholism and Thiamine Deficiency
- Keywords
- protein adducts, malondialdehyde, acetaldehyde, alcoholic cardiomyopathy, alcohol metabolism, oxidative stress
- MeSH terms
- Acetaldehyde, Ethanol, Alcoholism, Animals, Cardiomyopathy, Alcoholic, Humans, Liver, Liver Diseases, Alcoholic, Malondialdehyde, Muscular Diseases, Myocardium, Lipid Peroxidation, Muscle, Skeletal, DNA Adducts, Alcohol-Related Disorders
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