Zinc deficiency, ethanol, and myocardial ischemia affect lipoperoxidation in rats

Abstract

The production of oxygen free radicals can be stimulated by excess iron, cadmium, nickel, and the like. Inversely, copper, zinc, and selenium inhibit production, either via their own action or via antiradical metalloenzymes. The study involved determining the effect of zinc deficiency combined with chronic ethanol administration on the status of blood and tissue free radicals, as well as on cardiac function in isolated, perfused rats' hearts. Animals were fed a basic diet containing residual zinc at 0.2-0.3 ppm. Following a zinc deficiency lasting 5 wk, which during the last 4 wk was accompanied by chronic ethanol administration, hearts were submitted to ischemia for 30 min in vitro, followed by reperfusion. Biochemical analyses (zinc, superoxide dismutase, malondialdehyde, conjugated dienes, and so on) were performed in the blood and in the homogenates of different organs. The experimental zinc deficiency caused a slight decrease of superoxide dismutase activity, accompanied by increased production of peroxidated lipids. Ethanol administration appeared to increase the levels of peroxidated lipids in the heart. Finally, the combination of zinc deficiency and ethanol administration had very harmful effects, especially on lipid peroxidation and contractile function of the isolated, perfused heart in preischemic conditions.

Oxidants antioxidants and alcohol implications for skeletal and cardiac muscle

“…Animal studies have shown more compelling evidence of ROS-induced damage whereby chronic alcohol consumption causes an increase in cardiac lipid peroxidation, the effects of which are more severe in animals with concomitant zinc deficiency (53,54). Evidence to support some element of a free-radical mediated event in the cause of AHMD has been obtained in studies showing that, in alcohol-treated rats, the shift in fatty acid profile was inhibited by dietary alpha-tocopherol (55).…”

Oxidant injury in coronary heart disease [Part-1]

“…[7][8][9] Excess metals like iron, nickel and cadmium stimulate the production of free radicals. 10 Among all factors, cigarette smoking is a major source of oxidant stress, which alters antioxidant ability and antioxidant resistance. 11 It should be noted that plasma peroxide, free radical, and antioxidant levels may vary with age.…”

Ethanol, Wine, and Experimental Cardioprotection in Ischemia/Reperfusion: Role of the Prooxidant/Antioxidant Balance

“…It has been suggested that the pathogenic mechanisms responsible for these alterations involve ROS-induced cell injury (49). In fact, ROS and free radicals are generated during ethanol metabolism, causing oxidative stress and lipid peroxidation in cardiac tissue (10), as well as in many other organs, such as liver, brain, and skeletal muscle (36,49). Furthermore, ethanol metabolism-induced oxidative stress also causes oxidative degradation of the mitochondrial genome (36).…”