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

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

Comparison of Erythrocytes for Individual Indications of Metabolism Changes in Parkinson’s and Alzheimer’s Diseases

Alzheimer’s and Parkinson’s diseases are neurodegenerative diseases where several biomarkers have suggested that a single measurement is not a sufficient biomarker. The observation of increased concentration of cadmium (Cd), lead (Pb), and silver (Ag) in erythrocytes by inductively coupled plasma mass spectrometry (ICP-MS) shows a need to look for new approaches to understand the complex synchronistic effects of the cell metabolism. We have used a simplified scheme to follow some of the effects by following a hierarchy of reactions simplified to monitor elements in peripheral blood cells, e.g., erythrocytes. Erythrocytes carry oxygen to cells and carbon dioxide and waste to the lungs and back when passing from different organs including the brain. Erythrocytes also have the capacity to carry metal ions, which may be transferred to other organs, e.g., brain, despite the blood-brain barrier (BBB) and choroid plexus filter. If transfer of Cd, Pb, and Ag is continued too long, the repair systems may not be sufficient, and epigenetic effects on DNA and RNA may begin. Peripheral blood cells, e.g., erythrocytes, may help get earlier individual indications of changes at the cell level by using ICP-MS