Selenium deficiency and brain functions: The significance for methylmercury toxicity

Abstract

Selenium has been long recognized as one of the essential trace elements. Although many selenoproteins have been identified in the last decade, the physiological roles of Se and selenoproteins remain to be elucidated. Since iodothyronine deiodinases (DIs), which regulate the tissue levels of thyroid hormone, are (likely to be) selenoproteins, Se might have specific roles for developing brain. In fact, when rodents are depleted of Se perinatally, the thyroid hormone economy of the fetus is disturbed, which may lead to the abnormal development of the brain and to the abnormal postnatal behavior observed in Se-deficient animals. When the animals were depleted of Se after weaning, when the role of thyroid hormone on brain development is minimal, neurochemical and neurophysiological alterations were found in the dopaminergic system. These postnatally-depleted rodents also showed abnormal open-field behavior, which was distinct from that observed with perinatally-depleted animals. The molecular events that convert Se-deficient status to these neurochemical, neurophysiological, and behavioral functions are largely unknown, and need to be further examined. The interaction between Se and mercury compounds has also been the focus of many research, but there have been few reports on the interaction between the physiological (nutritional) level of Se and the toxicity of prenatal methylmercury (MeHg). Experimental findings showed that Se-deficient rodents are more susceptible to the prenatal toxicity of MeHg. It is noteworthy that MeHg specifically altered the metabolism of Se in fetal/neonatal brain. Significance of the alteration of the activities of selenoenzymes such as glutathione peroxidase and Dis in animals by prenatal MeHg exposure are discussed in relation to the neurobehavioral toxicity of MeHg.