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.
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Genomic analyses took place at UF, the Stanford Genome Technology Center and Washington University in St. Louis. Overall data analysis was based at Massachusetts General Hospital at Harvard Medical School.
Specially trained clinical personnel sampled whole blood and other available tissues from more than 200 severely traumatized or burned patients and 23 healthy individuals in an effort to correlate molecular markers with white blood cell behavior, and ultimately, with patient outcome. Studies in healthy patients were conducted at UF, Washington University in St. Louis, the University of Rochester School of Medicine and the University of Medicine and Dentistry of New Jersey. Patients with severe traumatic injuries were studied at the University of Washington at Seattle and the University of Rochester.
In the end, scientists could see dramatic changes in genes turning on and off in trauma victims compared with healthy people. Among the trauma patients, researchers say "analytical noise" - differences attributable to the testing method - was not significant, suggesting that profiling gene reactions may provide meaningful information to doctors.
The next step is for scientists to continue the experimental procedures in larger multicenter trials, following hundreds of patients over time to describe the molecular profile of healing in response to burns and traumatic injury, researchers say.
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