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Mitochondrial Complex I - Regulated alteration of carbohydrate oxidation and energy metabolites reduces ischemia-reperfusion injury in hearts from mice exposed to moderate ethanol intake
Summary: The authors state that moderate alcohol consumption is cardioprotective in large part through mechanisms that converge on mitochondria. As a primary entry point for reducing equivalents into the respiratory chain, the state of complex I activation has important consequences for overall mitochondrial function and cell homeostasis. Complex I is a key control point in regulation of carbohydrate oxidation and energy production that influence the extent of cardiac injury in hearts from ethanol-fed animals subjected to ischemia-reperfusion (I/R). In this study, isolated hearts from C57BL/6 mice that had been fed 10% ethanol (vol/vol) as drinking water for 16 weeks (E) and age-matched controls were subjected to 30 min global ischemia and 30 min reperfusion.

Hemodynamic results showed E hearts had better contractile recovery (left ventricular developed pressure 62±6 vs. 24±5 mmHg) and less cell damage (creatine kinase release 0.32±0.1 vs. 0.65±0.1 U/min/g) than controls after reperfusion. Mitochondrial NADH-Oxidase (1.2±0.2 vs.0.58±0.1 _g/m/mg), NADH-ubiquinone reductase (complex I, 1.04±0.2 vs. 0.48±0.1 _g/m/mg), state 3 oxygen consumption rates (266±28 vs. 152 ± 18 ngAtomO/m/mg), respiratory control ratios (5.2±0.4 vs. 3.1±0.2), aconitase activity (0.73±0.2 vs. 0.48±0.1 _mol/m/mg), and lipid peroxidation (MDA 216±22 vs. 348±14 nmol/g ) were significantly improved in E hearts after I/R compared to control hearts (all P<0.05, n=3-12). EM showed that the severity of mitochondrial ultrastructure deformation in E hearts was attenuated. In addition, high resolution 1H NMR spectroscopy revealed that the myocardial metabolites alanine, glycine, creatine/phosphocreatine, NAD, total adenosine nucleotide, and ATP were better preserved, whereas lactate and succinate were reduced in E heart tissue extracts relative to control hearts. The authors conclude that (1) moderate alcohol consumption reduces myocardial I/R injury; (2) the mechanism of the cardioprotection in part depends on mitochondria -mediated survival pathways; (3) within the mitochondria, preservation of complex I activity is critical for maintaining overall respiratory function and cardiac energy generation.

Comments: A large number of experiments have shown that animals that are preconditioned by giving them alcohol before creating a myocardial infarction (MI) in the laboratory tend to have less damage to the heart and better survival. This study confirms such protection, showing several changes in the mitochondria that are associated with reduced injury (as well as less increase in cardiac enzymes and better ventricular function after a MI) and less oxidation of lipids. The dose of alcohol each animal received cannot be easily determined, as the only water furnished to the experimental animals for 16 weeks prior to the MI contained 10% alcohol (essentially the equivalent of drinking no water but only light wine, such as a Riesling, for four months!), and blood alcohol levels in the animals were not reported. This is another study of biologic mechanisms that describes an important process by which moderate alcohol may protect against cardiovascular disease.

Mitochondrial Complex I - Regulated alteration of carbohydrate oxidation and energy metabolites reduces ischemia-reperfusion injury in hearts from mice exposed to moderate ethanol intake. Zhou H-Z, Ma X, Cecchini G, Simonis U,Gray MO. Abstracts related to alcohol consumption from the scientific sessions of the American Heart Association, October 4-7, 2007 reviewed by R Curtis Ellison, Abst 511

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