โ Scribed by Kimiko Hirayama; Akira Yasutake
No coin nor oath required. For personal study only.
The โ OH generated in the reaction of Fe 2 or Cu + with H 2 O 2 initiates lipid peroxidation, which results in oxidative damage of tissues. This oxidative stress may play an important role in the pathological processes triggered by iron or copper overload. Iron overload in the liver was produced by various iron compounds such as Fe-dextran, Fe-NTA, carbonyl iron, etc. These studies suggested that the occurrence of lipid peroxidation following iron overload seemed to require both uptake of iron by hepatocytes and a concentration of the metal in excess of the threshold. Carcinogenic effects of iron overload or iron conjugation with a chlorinated environmental chemical have been shown in vivo. Moreover, iron-induced oxidative stress has been reported to participate in the pathology of Parkinson's disease and various heart disease. Copper also showed carcinogenic effects in vitro and in vivo.
The oxidative damages seem to participate in toxic effects of various kinds of heavy metals. MeHg treatment altered glutathione metabolism in the kidney of rats or female mice. Heavy metal-induced elevation of GSH levels have been reported in other organs and cultured cells. As one of the protective functions of glutathione, free radicals produced by the action of the heavy metals would be scavenged directly by the SH group or indirectly through the action of GSH-Px. Additionally, glutathione could participate in repair of SH proteins damaged by reactive oxygen species. Thus, the alteration of glutathione metabolism caused by heavy metals seems to relate to the oxidative stress.
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