Selenium and Reproduction

Selenium deficiency has long been known to be associated with decrease male and female fertility in live stock. The underlying mechanisms may be numerous. The male reproductive system is drastically affected by selenium deficiency. Characteristically sperm motility is substantially reduced and, depending on the degree of deficiency, structural alterations up to breakages in the midpiece of spermatozoa are seen in several mammalian species. In rat spermatozoa selenium is almost restricted to the midpiece of spermatozoa containing the mitochondria, i.e., exactly the part where breakages are observed in selenium deficiency. The molecular basis for the well established dependency of mammalian reproduction on satisfactory selenium supply is far from being understood. In fact, little is known about the precise role of selenium in female fertility. A likely candidate to account for selenium dependency of male fertility is PHGPx. It is abundantly espressed in round spermatids under direct control of testosterone and becomes an enzymatically inactive component of the mitochondrial capsule during the final stages of sperm maturation. It thus may play a dual role in spermatogenesis: prevention of mutagenic events due to its enzymatic activity in early spermatogenesis and organizing the matrix embedding mitochondria in mature spermatozoa.