Effect of Antioxidant Trace Elements on the Response of Cardiac Tissue to Oxidative Stress^a

Abstract

It is now well established that several trace elements, because of their involvement in the catalytic activity and spatial conformation of antioxidant enzymes, may contribute to the prevention of oxidative stress such as occurs upon reperfusion of ischemic tissue. The aim of this paper is (1) to review the role of these trace elements (Cu, Mn, Se, and Zn) in antioxidant cellular defenses in the course of post-ischemic reperfusion of cardiac tissue, (2) to provide experimental data suggesting that variations in trace element dietary intake may modulate the vulnerability of cardiac tissue to ischemia-reperfusion, and (3) to discuss in more detail the effect of Mn ions, which seem to play a special protective role against reperfusion injury. Some results obtained from experiments in animal models of myocardial reperfusion have shown that the dietary intake of such trace elements can modulate cardiac activity of antioxidant enzymes and, consequently, the degree of reperfusion damage. In addition, experimental data on the protective effects of an acute treatment with Mn are presented. Finally, experimental evidence on the protective role of salen-Mn complexes, which exhibit catalytic SOD- and CAT-like activities against reperfusion injury, are described. These complexes should be of considerable interest in clinical conditions.

Dietary Mineral Sources Altered Lipid and Antioxidant Profiles in Broiler Breeders and Posthatch Growth of Their Offsprings

“…Cu, Zn, Mn, and Se were found to be important for apolipoprotein (apo), the major structural protein of lipoprotein, so as to participate in lipid metabolism [7][8][9][10][11]. Cu, Zn, Mn, and Se are also essential for catalytic activity and proper spatial conformation of antioxidant enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH-Px) and thereby play important roles in the antioxidant defense and lipid peroxidation [12]. In accordance with mechanism above, Se was observed to exhibit protective roles on risks of oxidative damage by lowering lipid concentrations and increasing antioxidant enzyme activities when animals were challenged with cigarette smoke and enflurane anesthetized [13,14].…”

The Effect of Different Doses of Oral Salinomycin on Oxidative Stress Biomarkers in Sheep

“…In contrast, vitamin C may indicate a significant role to protect the cells from the invasion of free radicals. It can be proposed that despite cellular protective action of vitamins against oxidative stress as a result of salinomycin toxicity, the increased level of vitamins A and E in our work may be attributed to the occurrence of an equilibrium between the levels of vitamin uptake and their levels in the serum and body tissues, particularly the liver storage which probably has a role in enhancing the decreased serum level of these vitamins in salinomycin intoxicated sheep [29], also as vitamin A and E are fat-soluble, these increases might be due to lipid peroxidation in salinomycin toxicity. Although the status of antioxidant vitamins has not been clearly investigated in salinomycin toxicity in sheep, a number of previous studies demonstrated the decreased blood levels of such vitamins in the serum of the affected animals and suggest that this phenomenon was a consequence of elevation in the level of oxidative damages [14,30,31].…”

Improved Hepatic Regeneration With Reduced Injury by Redox Factor-1 in a Rat Small-Sized Liver Transplant Model

“…Accumulated data from many studies currently suggest that intracellular as well as extracellular oxidative stress may play an important role in inducing postischemic tissue injury (4)(5)(6)(7). At a very early phase of reperfusion, production of reactive oxygen species (ROS) associated with Rac1 has recently been reported to mediate intracellular oxidative stress (8), which consequently activates redox-dependent pathologic signals including NF-jB (9)(10)(11).…”