Key result
Acute ethanol exposure induced myocardial injury and oxidative stress in mice, which was significantly inhibited by pretreatment with N-acetyl-L-cysteine.
Why the study?
Does acute ethanol exposure induce myocardial injury through oxidative stress in a mouse model?
Does acute ethanol exposure induce myocardial injury through oxidative stress in a mouse model?
Acute ethanol exposure induces myocardial injury via oxidative stress, which can be mitigated by the antioxidant NAC in a mouse model, providing mechanistic insight into alcoholic cardiomyopathy.
Supports oxidative stress mechanisms in ethanol cardiotoxicity; leaves open translation of NAC effects to human alcoholic cardiomyopathy.
Alcoholic cardiomyopathy has been known for a long time, but there is little mechanistic insight into this important clinical problem. The present study was undertaken using a mouse model to test the hypothesis that alcohol exposure induces cardiac injury through induction of oxidative stress. Adult female Friend Virius B-type (FVB) mice were treated with ethanol by gavage at a dose of 5 g/kg. Six hours after the treatment, ethanol-induced myocardial injury was observed, as indicated by a significant increase in serum creatine phosphokinase activity, a common biomarker of myocardial injury, and myocardial ultrastructural alterations, predominantly mitochondrial swelling and cristae disarray and reduction in numbers. The myocardial injury was associated with a significant increase in the myocardial lipid peroxidation, determined by measuring thiobarbituric acid reactive substances (TBARS), and a significant increase in protein oxidation as measured by a protein carbonyl content assay. Acute alcohol exposure decreased glutathione (GSH) content in the heart, more so in the mitochondria than in the cytosol. These alcohol-induced myocardial injuries and oxidative stresses were all significantly inhibited by supplementation with N-acetyl-L-cysteine (NAC) prior to alcohol exposure. However, NAC did not affect the rise in blood alcohol concentrations following alcohol exposure. This study thus demonstrates that acute alcohol administration causes myocardial injury through, at least in part, the induction of oxidative stress. A rapid decrease in mitochondrial GSH content may be partially responsible for the observed mitochondrial damage.
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Kannan et al. (2004) studied Alcoholic cardiomyopathy. Ethanol was evaluated on Myocardial injury and oxidative stress (serum creatine phosphokinase, lipid peroxidation, protein oxidation, GSH content). Acute ethanol exposure induced myocardial injury and oxidative stress in mice, which was significantly inhibited by pretreatment with N-acetyl-L-cysteine.
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