Acetaldehyde-induced cardiac contractile dysfunction may be alleviated by vitamin B1 but not by vitamins B6 or B12.
OBJECTIVE
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 microM) 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 microM), an essential vitamin required for DNA synthesis and repair. Vitamin B6 (10 microM) 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.
Deparment of Pharmacology, Physiology and Therapeutics, Univeresity of North Dakota School of Medicine and Health Science, Grand Forks, ND 58203, USA.
Nicholas S
NS
Aberle
Larry
L
Burd
Bonnie H
BH
Zhao
Jun
J
Ren
D000079:Acetaldehyde / Q000009:adverse effects*; D000818:Animals; D009202:Cardiomyopathies / Q000139:chemically induced / Q000188:drug therapy / Q000503:physiopathology; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D009200:Myocardial Contraction / Q000187:drug effects*; D009206:Myocardium / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013461:Sulfur Oxides / Q000378:metabolism; D013831:Thiamine / Q000627:therapeutic use*; D014805:Vitamin B 12 / Q000627:therapeutic use; D025101:Vitamin B 6 / Q000627:therapeutic use
D013461:Sulfur Oxides; D025101:Vitamin B 6; C010063:carbonyl sulfide; C505410:Casp3 protein, rat; D053148:Caspase 3; D020169:Caspases; D000079:Acetaldehyde; D014805:Vitamin B 12; D013831:Thiamine