Pharmacology of acetaldehyde

Brien, James F.; Loomis, Christopher W.

doi:10.1139/y83-001

Cited by 102 publications

(39 citation statements)

References 29 publications

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“…The ALDH1A1 gene is expressed in various tissues throughout the body, including the central nervous system (Stewart et al, 1996), and is known to be involved in two important biochemical functions: ethanol metabolism and cell differentiation. ALDH1A1 eliminates acetaldehyde, a potentially pharmacological and neurotoxic agent, from the nervous system (Brien and Loomis, 1983). ALDH1A1 has also been implicated in the synthesis of retinoic acid, an important agent in many developmental processes and an essential precursor in vitamin A production (Crabb et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Aldehyde Dehydrogenase 1 Promoter Polymorphisms Identified in Human Populations

Spence¹,

Liang²,

Eriksson³

et al. 2003

Alcoholism Clin & Exp Res

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Background-Cytosolic aldehyde dehydrogenase, or ALDH1A1, functions in ethanol detoxification, metabolism of neurotransmitters, and synthesis of retinoic acid. Because the promoter region of a gene can influence gene expression, the ALDH1A1 promoter regions were studied to identify polymorphism, to assess their functional significance, and to determine whether they were associated with a risk for developing alcoholism.

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Section: Discussionmentioning

confidence: 99%

Evaluation of Aldehyde Dehydrogenase 1 Promoter Polymorphisms Identified in Human Populations

Spence¹,

Liang²,

Eriksson³

et al. 2003

Alcoholism Clin & Exp Res

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“…For a 70 kg person, this is equal to the concurrent uptake of the mainstream smoke of 700 cigarettes (167). During smoking the gas phase mainstream smoke component, acetaldehyde, is absorbed to 45-70% in the mouth and the upper airways (168) and rapidly metabolized to acetate by aldehyde dehydrogenase (169). Due to the very short half-life of a few seconds in biological environments no increase of acetaldehyde levels was observed in the blood of smokers (170).…”

Section: Tobacco Additives That Are Alleged To Increase Nicotine Addimentioning

confidence: 99%

Influence of Additives on Cigarette Related Health Risks

Klus¹,

Scherer²,

Müller

2012

Beiträge Zur Tabakforschung International/Contributions to Tobacco Research

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Tobacco additives play an important role in the manufacturing and for the quality of tobacco products, particularly cigarettes and roll-your-own tobaccos. Attention is increasingly given to the potential effects of additives on consumer behavior and health. This review is intended to compile, collate and - to some degree - evaluate the wealth of pertinent scientific information available from the published literature and other special sources. At first, the reasons are set forth for the use of additives in cigarette manufacturing. In response to the growing controversy over the attractiveness and addictiveness of smoking, the clarification of terms and concepts is followed by a detailed discussion of two kinds of substances with particular relevance: Additives like ammonium compounds that are claimed to increase nicotine availability, and additives that are claimed to increase nicotine addictiveness.The composition and toxicity of mainstream smoke of cigarettes with and without additives are assessed in several respects. The potentials of pyrolysis studies are explored by looking at a number of key studies and some basic considerations regarding in vitro and in vivo toxicity testing are addressed. Five major literature reviews on additives published between 1994 and 2004, and the results of several comprehensive experimental studies covering a large range of additives, released between 2002 and 2012, are dealt with in detail. Single tobacco additives of particular importance (menthol, glycerol, 1,2-propylene glycol, sorbitol, sugars, cocoa, licorice, citric acid, triacetin, and ammonium compounds) are discussed in dedicated chapters, which are generally subdivided into special sections: Use and toxicological assessment; inclusion level in cigarettes, transfer and pyrolysis; attractiveness and addictiveness; effect on cigarette mainstream smoke composition; effect on cigarette mainstream smoke toxicity. Epidemiological findings and data obtained by the biomonitoring of smokers consuming cigarettes with and without additives are compiled and interpreted specifically for American blend cigarettes, Virginia cigarettes, “French” (dark) cigarettes and menthol cigarettes whereby the focus is on the effects of additives on smoking topography and potential health risks.Opinionated reviews were published in recent years that are compromised by arbitrary selection of sources and unbalanced views. Leaving those unconsidered, the aggregated scientific knowledge shows that tobacco additives have only occasional and limited effects on cigarette mainstream smoke composition, which are almost never reflected in the results of toxicological in vitro assays or in vivo studies. This supports the conclusion that tobacco additives are not likely to increase the known health risks of smoking. There is also no evidence for sustaining claims that certain additives increase nicotine availability or nicotine addictiveness.

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“…Acetaldehyde is rapidly metabolized to acetic acid by aldehyde dehydrogenase (ALDH; Brein and Loomis, 1983). ALDH is better known as one of the enzymes involved in the ethanol metabolizing process.…”

Section: Introductionmentioning

confidence: 99%

Paired Acute Inhalation Test Reveals That Acetaldehyde Toxicity Is Higher in Aldehyde Dehydrogenase 2 Knockout Mice Than in Wild-Type Mice

et al. 2005

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-Aldehyde dehydrogenase 2 (ALDH2) is an important enzyme that oxidizes acetaldehyde.Approximately 45% of Chinese and Japanese individuals have the inactive ALDH2 genotypes (ALDH2*2/ *2 and ALDH2*1/*2); acute inhalation toxicity of acetaldehyde has not been evaluated in these populations. We compared the toxicity between wild-type (Aldh2+/+) and Aldh2-inactive transgenic (Aldh2−/−) mice by using the paired acute inhalation test modified from the acute toxic class method (OECD TG433). Blood acetaldehyde level was measured 4 hr after the inhalation. A pair of Aldh2+/+ and Aldh2−/− mice was put into a chamber and was exposed to 5000 ppm of acetaldehyde. At the start of the inhalation, the mice exhibited hypoactivity and closing of the eyes. Subsequently, symptoms such as crouching, bradypnea, and piloerection were observed. Flushing was observed only in the Aldh2+/+ mice. Symptoms such as tears, straggling gait, prone position, pale skin, abnormal deep respiration, dyspnea, and one case of death were observed only in the Aldh2−/− mice. The symptoms did not change 1 hr after inhalation in the Aldh2+/+ mice. In contrast, in the Aldh2−/− mice, the symptoms became more severe until the end of the inhalation. The blood acetaldehyde level in the Aldh2−/− mice was approximately twice that in the Aldh2+/+ mice 4 hr after inhalation. The Aldh2−/− mice evidently showed more severe toxicity as compared with the Aldh2+/+ mice due to acute inhalation of acetaldehyde at a concentration of 5000 ppm. Acetaldehyde toxicity in Aldh2+/+ and Aldh2−/− mice was estimated and classified one class different. Based on this study, acetaldehyde inhalations were inferred to pose a higher risk to ALDH2-inactive human individuals.

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Pharmacology of acetaldehyde

Cited by 102 publications

References 29 publications

Evaluation of Aldehyde Dehydrogenase 1 Promoter Polymorphisms Identified in Human Populations

Evaluation of Aldehyde Dehydrogenase 1 Promoter Polymorphisms Identified in Human Populations

Influence of Additives on Cigarette Related Health Risks

Paired Acute Inhalation Test Reveals That Acetaldehyde Toxicity Is Higher in Aldehyde Dehydrogenase 2 Knockout Mice Than in Wild-Type Mice

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