Chapter 30 - Role of selenium, iron, copper, and zinc in parkinsonism

Abstract

A number of essential trace elements play a major role in various metabolic pathways. Selenium (Se), copper (Cu), zinc (Zn), and iron (Fe) are essential trace elements that have been studied in many diseases, including autoimmune, neurological, and psychiatric disorders. The observations from these studies suggest that alterations in essential trace elements Se, Cu, Zn, and Fe may play a role in the pathogenesis of Parkinson's disease (PD) patients. However, the findings from plasma levels of the trace elements show a variety of results that are difficult to interpret. The extracellular concentrations of transition metals such as Cu and Fe are substantially elevated during aging and in some neurodegenerative disorders. Increases in the extracellular redox capacity can potentially generate neurotoxic free radicals from reduction of Cu(II) or Fe(III), thereby resulting in neuronal cell death. Although observations support the role of iron as a neurotoxin, it remains to be established whether accumulation of iron in PD is primary or secondary to other known events such as glutathione (GSH) depletion and the mitochondrial transport chain complex I inhibition. Cu and Zn have significant antiatherogenic effects influencing the activity of antioxidant enzymes (glutathione-peroxidase and superoxide-dismutase), mechanism of apoptosis, and other mechanisms. In addition to the alterations in the homeostasis, redox activity, and localization of transition metals, it is also important to realize that the alterations in specific zinc-, copper-, and iron-containing metalloenzymes appear to play a crucial role in the neurodegenerative process.