ACETALDEHYDE-INDUCED CARDIAC CONTRACTILE DYSFUNCTION MAY BE ALLEVIATED BY VITAMIN B1 BUT NOT BY VITAMINS B6 OR B12

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 met...

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Bibliographic Details
Published in:Alcohol and alcoholism (Oxford) 2004-09, Vol.39 (5), p.450-454
Main Authors: Aberle, Nicholas S., Burd, Larry, Zhao, Bonnie H., Ren, Jun
Format: Article
Language:English
Subjects:
Acetaldehyde - adverse effects
Animals
Cardiomyopathies - chemically induced
Cardiomyopathies - drug therapy
Cardiomyopathies - physiopathology
Caspase 3
Caspases - metabolism
Comparative studies
Ethyl alcohol
Exposure
Laboratory research
Myocardial Contraction - drug effects
Myocardium - metabolism
Myocytes, Cardiac - metabolism
Rats
Rats, Sprague-Dawley
Risk factors
Sulfur Oxides - metabolism
Thiamine - therapeutic use
Treatment
Ventricular dysfunction
Vitamin B 12 - therapeutic use
Vitamin B 6 - therapeutic use
Vitamin B deficiency
Vitamin B1
Vitamin B12
Vitamin B6
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Summary: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.
ISSN:0735-0414
1464-3502
DOI:10.1093/alcalc/agh085