Effects of Acute Acetaldehyde, Chronic Ethanol, and Pargyline Treatment on Agonist Responses of the Rat Aorta

Brown, Ronald C.; Savage, Adedapo O.

doi:10.1006/taap.1996.0021

Cited by 21 publications

(8 citation statements)

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“…Aldh3 belongs to a family of NAD(P) + ‐dependent enzymes that catalyze the oxidation of various toxic aldehydes to carboxylic acids. Chronic acetaldehyde exposure of endothelium–denuded preparations results in depressed responsiveness to membrane depolarization (Brown and Savage, 1996).…”

Section: Discussionmentioning

confidence: 99%

Differential gene expression in skeletal muscle cells after membrane depolarization

Juretić

Urzúa

Munroe

et al. 2006

Journal Cellular Physiology

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Skeletal muscle is a highly plastic tissue with a remarkable capacity to adapt itself to challenges imposed by contractile activity. Adaptive response, that include hypertrophy and activation of oxidative mechanisms have been associated with transient changes in transcriptional activity of specific genes. To define the set of genes regulated by a depolarizing stimulus, we used 22 K mouse oligonucleotide microarrays. Total RNA from C2C12 myotubes was obtained at 2, 4, 18, and 24 h after high K+ stimulation. cDNA from control and depolarized samples was labeled with cyanine 3 or 5 dyes prior to microarray hybridization. Loess normalization followed by statistical analysis resulted in 423 differentially expressed genes using an unadjusted P-value < or = 0.01 as cut off. Depolarization affects transcriptional activity of a limited number of genes, mainly associated with metabolism, cell communication and response to stress. A number of genes related to Ca2+ signaling pathways are induced at 4 h, reinforcing the potential role of Ca2+ in early steps of signal transduction that leads to gene expression. Significant changes in the expression of molecules involved in muscle cell structure were observed; K+-depolarization increased Tnni1 and Acta1 mRNA levels in both differentiated C2C12 and rat skeletal muscle cells in primary culture. Of these two, depolarization induced slow Ca2+ transients appear to have a role only in the regulation of Tnni1 transcriptional activity. We suggest that depolarization induced expression of a small set of genes may underlie Ca2+ dependent plasticity of skeletal muscle cells.

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Section: Discussionmentioning

confidence: 99%

Differential gene expression in skeletal muscle cells after membrane depolarization

Juretić

Urzúa

Munroe

et al. 2006

Journal Cellular Physiology

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“…Acetaldehyde is the principal metabolic by‐product of ethanol metabolism causing cytotoxicity, and may be limited by administering vitamin C [ 10]. In an animal study, chronic acetaldehyde exposure impaired the inotropic response to membrane depolarization in endothelium‐denuded preparations of rat aorta, resulting in depressed responsiveness; acute acetaldehyde exposure significantly reduced both noradrenaline‐ and KCl‐induced contractile responses [ 11], but low concentrations of acetaldehyde enhanced the spontaneous phasic contractile activity [ 12]. Under normal circumstances, the acetaldehyde produced as a result of ethanol metabolism is rapidly oxidised to acetate by aldehyde dehydrogenase, and other microsomal enzymes [ 13].…”

Section: Discussionmentioning

confidence: 99%

Effects of ethanol and its metabolite acetaldehyde on responses of the rat bladder

Kim

Moon²,

Sohng³

et al. 1999

BJU International

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“…Acetaldehyde may trigger cardiac hypertrophy or dilated cardiomyopathy associated with a significant increase in the hypertrophic marker skeletal actin and ANF (Li & Ren, 2008; Liang et al, 1999). Direct effects of acute (5 to 10 min) acetaldehyde exposure on cardiovascular function have been extensively studied (Aberle & Ren, 2003; Aistrup et al, 2006; Brown et al, 1999, 2001; Brown & Savage 1996; Ren et al, 1997; Savage et al, 1995). Acetaldehyde produces vasoconstriction and positive inotropic and chronotropic responses at concentrations of 3 mM or below.…”

Section: Acetaldehyde and The Heartmentioning

confidence: 99%

ALDH2 in alcoholic heart diseases: Molecular mechanism and clinical implications

Zhang

Ren

2011

Pharmacology & Therapeutics

134

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Alcoholic cardiomyopathy is manifested as cardiac hypertrophy, disrupted contractile function and myofibrillary architecture. An ample amount of clinical and experimental evidence has depicted a pivotal role for alcohol metabolism especially the main alcohol metabolic product acetaldehyde, in the pathogenesis of this myopathic state. Findings from our group and others have revealed that the mitochondrial isoform of aldehyde dehydrogenase (ALDH2), which metabolizes acetaldehyde, governs the detoxification of acetaldehyde formed following alcohol consumption and the ultimate elimination of alcohol from the body. The ALDH2 enzymatic cascade may evolve as a unique detoxification mechanism for environmental alcohols and aldehydes to alleviate the undesired cardiac anomalies in ischemia-reperfusion and alcoholism. Polymorphic variants of the ALDH2 gene encode enzymes with altered pharmacokinetic properties and a significantly higher prevalence of cardiovascular diseases associated with alcoholism. The pathophysiological effects of ALDH2 polymorphism may be mediated by accumulation of acetaldehyde and other reactive aldehydes. Inheritance of the inactive ALDH2*2 gene product is associated with a decreased risk of alcoholism but an increased risk of alcoholic complications. This association is influenced by gene-environment interactions such as those associated with religion and national origin. The purpose of this review is to recapitulate the pathogenesis of alcoholic cardiomyopathy with a special focus on ALDH2 enzymatic metabolism. It will be important to dissect the links between ALDH2 polymorphism and prevalence of alcoholic cardiomyopathy, in order to determine the mechanisms underlying such associations. The therapeutic value of ALDH2 as both target and tool in the management of alcoholic tissue damage will be discussed.

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Effects of Acute Acetaldehyde, Chronic Ethanol, and Pargyline Treatment on Agonist Responses of the Rat Aorta

Cited by 21 publications

References 0 publications

Differential gene expression in skeletal muscle cells after membrane depolarization

Differential gene expression in skeletal muscle cells after membrane depolarization

Effects of ethanol and its metabolite acetaldehyde on responses of the rat bladder

ALDH2 in alcoholic heart diseases: Molecular mechanism and clinical implications

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