Previously, the function of this protein, selenoprotein P, was unknown, although it was believed to play a role as an antioxidant and to transport selenium throughout the body.
Dietary selenium is essential for normal sperm development and male fertility. Selenoprotein P, or SEPP1, carries about 60 percent of the selenium in blood plasma.
To understand the physiological function of SEPP1 in the testes and epididymis of mammals, a team of scientists at Vanderbilt University in Nashville studied male mice that lack the gene to produce SEPP1. These genetically altered males have levels of selenium in the testis that are less than 10 percent of those in control mice, and they are generally infertile.
The research team, headed by Dr. Gary E. Olson, found that the mutant male mice lacking SEPP1 develop sperm with defective tails, similar to the sperm produced by unaltered male mice fed a low-selenium diet.
Furthermore, the mutant mice do not recover normal sperm production after prolonged feeding on a diet supplemented with high levels of selenium, and they remain infertile. Thus, even selenium supplements could not overcome the need for SEPP1 to facilitate normal sperm development.
These findings, according to Olson and colleagues, strongly indicate that SEPP1 is the source of the selenium needed for development of normal sperm and for male mice to maintain their fertility.
Biology of Reproduction, published by the Society for the Study of Reproduction, is the top-rated peer-reviewed journal in the field of reproductive biology.