Reactive Oxygen Species and Selenium in Epilepsy and in Other Neurological Disorders

Abstract

Oxidative stress has been implicated in epilepsy and various neurodegenerative disorders. In this review, we elaborate oxidative stress-mediated neuronal loss and assess the role of selenium in some neurological disorders including epilepsy. Selenium as an essential trace element has attracted the attention of many researchers because of its potentialities in human health. It has an important role in the brain, immune response, defense against tissue damage, and thyroid function. Selenium forms part of the active site of the peroxide-destroying enzyme glutathione peroxidase (GSHPx), and it also has other functions, for example in biotransformation and detoxification. Functional and clinical consequences of selenium deficiency states in neurological diseases have been described, and the selenium requirement, which is influenced by various processes, has been discussed. Wide variations have been found in selenium status in different parts of the world, and populations or groups of patients exposed to marginal deficiency are more numerous than was previously thought. Chronic diseases, such as neurological disorders, heart disease, diabetes, cancer, aging, and others, are reported to associate with markers of oxidative damage. It is, therefore, not unreasonable to suggest that antioxidants would alleviate the oxidative damage, resulting in health improvements. In recent years, accumulated evidence in nutrigenomics, laboratory experiments, clinical trials, and epidemiological data have established the role of selenium in a number of conditions. Most of these effects are related to the function of selenium in the antioxidant enzyme systems. Current research activities in the field of human medicine and nutrition are devoted to the possibilities of using selenium as an adjuvant for the treatment of degenerative or free radical diseases such as neurological disorders, inflammatory diseases, and cancer.