Alcohol and Alcoholism Advance Access originally published online on August 10, 2004
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Alcohol & Alcoholism Vol. 39, No. 5, pp. 450-454, 2004
Alcohol & Alcoholism Vol. 39, No. 5 © Medical Council on Alcohol 2004; all rights reserved
ACETALDEHYDE-INDUCED CARDIAC CONTRACTILE DYSFUNCTION MAY BE ALLEVIATED BY VITAMIN B1 BUT NOT BY VITAMINS B6 OR B12
Department of Pharmacology, Physiology and Therapeutics and 1 North Dakota Fetal Alcohol Syndrome Center, University of North Dakota School of Medicine and Health Science, Grand Forks, ND 58203, USA
* Author to whom correspondence should be addressed at: Center for Cardiovascular Research and Alternative Medicine, Division of Pharmaceutical Sciences, University of Wyoming, Laramie, WY 82071, USA. Fax: +307 766 2953; E-mail: jren{at}uwyo.edu
(Received 24 March 2004; first review notified 23 April 2004; in revised form 12 May 2004; accepted 25 June 2004)
Aims: Chronic alcohol exposure leads to a deficiency of group B vitamins and increased risk of alcoholic cardiomyopathy characterized by impaired ventricular contractility. This study was designed to examine the effect of group B vitamin supplementation on short-term exposure of the main alcohol metabolite acetaldehyde (ACA)-induced cardiac contractile dysfunction in rat ventricular myocytes. Methods: Mechanical contractile properties were evaluated by an IonOptix SoftEdge® system. Protein damage and apoptosis were determined by protein carbonyl and caspase-3 assays, respectively. Results: Short-term (4–6 h) culture of myocytes with ACA (10 µM) depressed peak shortening amplitude, maximal velocity of shortening/relengthening, shortened duration of shortening but not the duration of relengthening. ACA exposure also enhanced protein carbonyl formation and apoptosis in ventricular myocytes. The toxin-induced mechanical defects, protein damage and apoptosis were ablated by vitamin B1 (10 µM), an essential vitamin required for DNA synthesis and repair. Vitamin B6 (10 µM) attenuated ACA-induced impairment of shortening duration. Vitamin B12 (1 mM) attenuated ACA-induced reduction in maximal velocity of shortening/relengthening. Unlike vitamin B1, none of the other ACA-elicited alterations in myocyte mechanical function were affected by vitamin B6 or vitamin B12. Vitamin B6 and vitamin B12 partially, but significantly, attenuated the ACA-induced carbonyl formation without affecting ACA-induced apoptosis. Conclusions: These data provide evidence that vitamin B1 supplementation may be protective for ACA-induced cytotoxicity through protection against protein damage and apoptotic cell death in ventricular myocytes.
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