Myocardial lipid peroxidation in rats after chronic alcohol ingestion and the effects of different antioxidants

Abstract

The effects of chronic intake of dietary alcohol on myocardial peroxidation (measured as formation of diene conjugates), reduced glutathione content, and morphology and the protective actions of different antioxidant compounds (vitamin E and (+)-cyanidanol-3) were studied in rats. Alcohol, comprising more than 30% of the dietary calorie content, was administered to rats for six weeks. Compared with the controls, the left ventricle of the alcoholic animals had an increased diene conjugate content (5.4(0.5) vs 4.3(0.6) optical density X g wet weight-1) and a slightly, but not significantly, decreased glutathione content (1.62(0.05) vs 1.66(0.07) mumol X g wet weight-1). Simultaneous administration of antioxidants (vitamin E or (+)-cyanidanol-3) prevented the pathological changes in diene conjugates and significantly increased the glutathione content compared with the alcoholic rats. Electron microscopy showed remarkably few ultrastructural abnormalities in the myocardium of alcoholic animals fixed by vascular perfusion. The data are consistent with the hypothesis that reactive oxygen radicals are involved in the ethanol induced biochemical changes and that the antioxidants could prevent the increased formation of peroxides in the myocardium.

The profound effects of microcystin on cardiac antioxidant enzymes, mitochondrial function and cardiac toxicity in rat

“…Myocardium possesses several features such as abundant mitochondria and rich polyunsaturated fatty acids in the mitochondrial and plasma membranes, all of which make the myocardium vulnerability to free radical attack (Kowaltowski and Vercesi, 1999). Oxidative stress is associated with the pathophysiology of many cardiomyopathies, such as anthracycline-mediated cardiomyopathy (Singal et al, 1997;Xu et al, 2001) and alcoholic cardiomyopathy (Edes et al, 1986). Nowadays, accumulating evidences imply that MC-dependent damage is accompanied by oxidative stress in liver, kidney and intestinal mucosa in mammals (Botha et al, 2004;Ding et al, 1998Ding et al, , 2001Moreno et al, 2003Moreno et al, , 2005.…”

Kidneys of Chronic Alcoholic Rats Are More Vulnerable to Ischemic Insult

“…The activity of phospholipase A2 was shown to increase [19], This pheno menon may play a role, because this enzyme directly attacks the membrane phospholipids. After chronic alco hol ingestion, oxygen free-radicals were reported to in crease [20][21], These radicals may also damage the renal membranes in the event of ischemia. It is interesting to note that the kidneys of alcoholic rats were also more susceptible to mercuric chloride poisoning [22].…”

Cardioprotection by Regular Ethanol Consumption: Potential Mechanisms and Clinical Application

“…Ethanol has been shown to increase antioxidant enzymes such as superoxide dismutase and catalase in myocytes [86]. A recent in vivo mouse study revealed that activation of ALDH2 by acute ethanol exposure is involved in the detoxification of toxic 13 aldehyde such as 4-HNE which mediates oxidative damage through activated ε-PKC translocated to mitochondria [78].…”