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Aldehyde dehydrogenase

About: Aldehyde dehydrogenase is a research topic. Over the lifetime, 3365 publications have been published within this topic receiving 107683 citations.


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Journal ArticleDOI
TL;DR: Individuals with the atypical aldehyde dehydrogenase ALDH2 allele, both homozygous and heterozygous status, are alcohol sensitive and have a markedly reduced risk of developing alcoholic diseases.
Abstract: Indiciduals with the atypical aldehyde dehydrogenase ALDH22 allele, both homozygous and heterozygous status, are alcohol sensitive and have a markedly reduced risk of developing alcoholic diseases. Genetic abnormalities of the ALDH1 locus are also associated with alcohol flushing. The ALDH3 and ALDHx , loci are polymorphic and their variations may affect the development of alcoholic diseases. The variations of alcohol dehydrogenase ADH2 and ADH3 loci have no profound effects on alcohol sensitivity. The newly identified ADH6 gene has hormone response elements, and it may cause the gender difference in alcoholic problems.

43 citations

Journal ArticleDOI
Shimon Amir1
TL;DR: It is argued that inherent variation in brain ALDH activity may be a principal biochemical counterpart of the differences in ethanol intake among different strains and sexes of laboratory rats.
Abstract: Voluntary ethanol consumption and brain and liver aldehyde dehydrogenase (ALDH) activity were measured in male and female rats of the Tryon Maze-Bright (S1), Tryon Maze-Dull (S3), and Wistar strains. The levels of brain ALDH measured in the different groups corresponded well to the levels of ethanol consumption, while differences in liver ALDH corresponded well to only the strain differences in ethanol intake. Within individual groups, levels of brain than liver aldehyde-oxidizing capacity. Age affected both voluntary ethanol intake and liver ALDH levels, but there were no systematic relations between the two effects. Age did not significantly affect the cerebral-aldehyde oxidizing capacity. It is argued that inherent variation in brain ALDH activity may be a principal biochemical counterpart of the differences in ethanol intake among different strains and sexes of laboratory rats.

43 citations

Journal ArticleDOI
TL;DR: In contrast to the effects obtained in vivo, disulfiram was found to be an inhibitor in vitro of brain succinate semialdehyde dehydrogenase and liver monoamine oxidase and 1-aminocyclopropanol in vitro.

43 citations

Journal ArticleDOI
TL;DR: Two compounds, 13g and 13h, depleted the CD133+ putative cancer stem cell pool, synergized with cisplatin, and achieved efficacious concentrations in vivo following IP administration, and discovered the first reported modestly selective single isoform 1A2 and 1A3 inhibitors.
Abstract: Aldehyde dehydrogenase (ALDH) activity is commonly used as a marker to identify cancer stem-like cells. The three ALDH1A isoforms have all been individually implicated in cancer stem-like cells and...

43 citations

Journal ArticleDOI
TL;DR: It is hypothesized that ALDH2 ameliorates the proliferation and migration of human pulmonary artery smooth muscle cells (HPASMCs) by inhibiting 4-HNE accumulation and regulating downstream signaling pathways, thereby amaliorating pulmonary vascular remodeling in PAH.
Abstract: The cardioprotective benefits of aldehyde dehydrogenase 2 (ALDH2) are well established, although the regulatory role of ALDH2 in vascular remodeling in pulmonary arterial hypertension (PAH) is largely unknown. ALDH2 potently regulates the metabolism of aldehydes such as 4-hydroxynonenal (4-HNE), the endogenous product of lipid peroxidation. Thus, we hypothesized that ALDH2 ameliorates the proliferation and migration of human pulmonary artery smooth muscle cells (HPASMCs) by inhibiting 4-HNE accumulation and regulating downstream signaling pathways, thereby ameliorating pulmonary vascular remodeling. We found that low concentrations of 4-HNE (0.1 and 1 μM) stimulated cell proliferation by enhancing cyclin D1 and c-Myc expression in primary HPASMCs. Low 4-HNE concentrations also enhanced cell migration by activating the nuclear factor kappa B (NF-κB) signaling pathway, thereby regulating matrix metalloprotein (MMP)-9 and MMP2 expression in vitro. In vivo, Alda-1, an ALDH2 agonist, significantly stimulated ALDH2 activity, reducing elevated 4-HNE and malondialdehyde levels and right ventricular systolic pressure in a monocrotaline-induced PAH animal model to the level of control animals. Our findings indicate that 4-HNE plays an important role in the abnormal proliferation and migration of HPASMCs, and that ALDH2 activation can attenuate 4-HNE-induced PASMC proliferation and migration, possibly by regulating NF-κB activation, in turn ameliorating vascular remodeling in PAH. This mechanism might reflect a new molecular target for treating PAH.

43 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023260
2022192
202170
202081
201980
201895