Body systems affected by acetaldehyde Acetaldehyde binds covalently with proteins, lipids, and nucleic acids. Tao Zeng PhD, Ke-Qin Xie PhD, in Molecular Aspects of Alcohol and Nutrition, 2016. In alcoholics, the oxidation of ethanol is increased by induction of MEOS. Acetaldehyde is an extremely reactive compound and a pure preparation of the chemical boils at room temperature. endstream endobj startxref Acute (short-term) exposure to acetaldehyde results in effects including irritation of the eyes, skin, and respiratory tract. Acetaldehyde is the proximate metabolite generated by ethanol metabolism by liver ADHs, CYP2E1 originally referred to as the microsomal ethanol oxidizing system (MEOS), and catalase pathways. Acetaldehyde is widely used in the production of other industrial chemical substances. By continuing you agree to the use of cookies. At 50 ppm acetaldehyde, no irritation or local tissue damage in the nasal mucosa is observed. The sheer number of enzymes involved in the metabolism and detoxication of acetaldehyde and other aldehyde species is a testament to the impact of its reactivity. The presence of ALDH in most tissues may reduce the toxic effects of acetaldehyde. ScienceDirect ® is a registered trademark of Elsevier B.V. ScienceDirect ® is a registered trademark of Elsevier B.V. URL:, URL:, URL:, URL:, URL:, URL:, URL:, URL:, URL:, URL:, Reference Module in Biomedical Sciences, 2015, Roshanna Rajendram, ... Victor R. Preedy, in, Neuropathology of Drug Addictions and Substance Misuse, Encyclopedia of Toxicology (Third Edition), Ethanol Metabolism and Implications for Disease, Cytochrome P4502E1 Gene Polymorphisms and the Risks of Ethanol-Induced Health Problems in Alcoholics, Molecular Aspects of Alcohol and Nutrition, Alcohol: Absorption, Metabolism, and Physiological Effects, Encyclopedia of Human Nutrition (Third Edition), Fatty Liver, NASH, and Alcoholic Liver Disease, Elizabeth M. Brunt, ... Alastair D. Burt, in, MacSween's Pathology of the Liver (Sixth Edition), Molecular Mechanisms of Alcohol-Associated Carcinogenesis, Helmut K. Seitz MD, PhD, Sebastian Mueller MD, PhD, in, The Effects of Alcohol on The Fetal Brain, Handbook of Developmental Neurotoxicology, Present in all tissues except red blood cells. Hepatic acetaldehyde therefore increases with chronic ethanol consumption. h�bbd``b`Z$�A�6 ��H0g�]�X HI�X �} ��i��b� �:��@b�n&F�% 1Fr���� ��. However, some cigarettes can produce twice as much. This makes acetaldehyde one of the main components of cigarette smoke (after tar, nicotine and carbon monoxide). Analytical results suggest, however, that the normal level of AcH in the blood of rats and humans is very low (<∼0.5 μmol l−1) (Eriksson and Fukunaga 1993; Hobara et al. Source: Reproduced with permission from Kwo PY and Crabb DW (2002) Genetics of ethanol metabolism and alcoholic liver disease. Acetaldehyde causes irritation of the airways, and has been classed as a possible cancer-causing agent by the expert cancer organisation IARC (the International Agency for Research on Cancer). Forty percent of Asians have an ALDH gene, which codes for a low activity ALDH enzyme. However, the capacity of mitochondria to oxidize acetaldehyde is reduced. More toxicological studies and risk assessment on acetaldehyde are required. However, there are many other sources of acetaldehyde, both natural and manufactured. 21 0 obj <> endobj Van Vleet, B.K. Acetaldehyde is very reactive and is known to react with many other substances in the body. Acetaldehyde is highly reactive and toxic. Vinyl acetate is carcinogenic in rats at high concentrations, and a role for AcH in this response has been proposed (Bogdanffy et al. endstream endobj 22 0 obj <> endobj 23 0 obj <>/Border[0 0 0]/Rect[187 523 204 538]/Subtype/Link/Type/Annot>>]/Contents[26 0 R 29 0 R 30 0 R 31 0 R 32 0 R 33 0 R 34 0 R 35 0 R]/CropBox[0 0 612 792]/MediaBox[0 0 612 792]/Parent 19 0 R/Resources<>/Font<>/ProcSet[/PDF/Text]>>/Rotate 0/Type/Page>> endobj 24 0 obj <>stream J.R. Kuykendall, in Comprehensive Toxicology, 2010. The accumulation of acetaldehyde is influenced by the catalytic activities of these enzymes. As ADH is not physiologically active in the brain, the CYP2E1 should play important roles in the conversion of ethanol to acetaldehyde in the rodent brains.35 Therefore, the CYP2E1 gene polymorphisms may influence individual susceptibility to AD by altering the metabolism of ethanol to acetaldehyde in the brain. T.R. Although most of it is converted to acetate some enters the blood stream and reaches a plateau when both the alcohol dehydrogenase and cytochrome P450 systems are saturated. Acetaldehyde has been demonstrated to play important roles in the pathogenesis of AD.33 Acetaldehyde possesses reinforcing properties, a fact that suggests that some of the behavioral pharmacological effects induced by ethanol may be results of the formation of acetaldehyde, and supports the involvement of acetaldehyde in AD.34,35 Ethanol can be metabolized to acetaldehyde through three pathways, that is, the alcohol dehydrogenase (ADH), catalase, and MEOS (mainly CYP2E1). It is important to note that alcoholics achieve significantly higher acetaldehyde plateaus than nonalcoholics, even when the same blood–alcohol level is attained. M. Shimada, ... A. Sanyal, in Pathobiology of Human Disease, 2014. Understanding of the potential adverse effects and the pathogenesis of acetaldehyde is a pressing need. The inactive form of ALDH2 is present in about 50% of Orientals. Substance name: Acetaldehyde CASR number: 75-07-0 Molecular formula: C2H4O Synonyms: Ethanal; ethyl aldehyde; acetic aldehyde; aldehyde; acetylaldehyde; aldehyde acetic aldehyde, NCI-C56326, RCRA waste number U001, UN 1089.

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