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.
Aberle
Nicholas S
NS
Deparment of Pharmacology, Physiology and Therapeutics, Univeresity of North Dakota School of Medicine and Health Science, Grand Forks, ND 58203, USA.
Burd
Larry
L
Zhao
Bonnie H
BH
Ren
Jun
J
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