Researchers have identified a protein that helps protect immature mouse sperm from oxidative stress. When male mice over one year old lacking this protein were mated with normal female mice, an increased incidence of miscarriages and fetal developmental defects were observed.
These data have clinical relevance, as age-related DNA damage to human sperm is associated with decreased fertility and increased rates of miscarriage and childhood disease.
Joel Drevet and colleagues, at Clermont Université, France, have identified a protein that helps protect immature mouse sperm after they have been released into a region of the testis known as the epididymis, which is where they undergo maturation.
Although male mice lacking this protein, Gpx5, had normal looking sperm and were equally as efficient as normal male mice at fertilizing female mice, an increased incidence of miscarriages and fetal developmental defects were observed when normal female mice were mated with Gpx5-deficient males over 1 year old compared with normal male mice of the same age.
Further analysis indicated that Gpx5 acts as an antioxidant in the epididymis, protecting the sperm from oxidative stress. As discussed by the authors, and, in an accompanying commentary, John Aitken, at the University of Newcastle, Australia, these data have immense clinical relevance as age-related DNA damage to human sperm has been associated with a range of adverse outcomes including decreased fertility, and increased rates of miscarriage and childhood disease.
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