Abstract
Immature spermatozoa are vulnerable to oxidative stress after their release from the
testes, due in part to an innate deficiency in antioxidant enzymes. The male
reproductive tract compensates for this deficiency by secreting antioxidant enzymes
such as glutathione peroxidase 5 (Gpx5) into the epididymal lumen. In this issue of
the JCI, Chabory et al. examined the phenotype of
Gpx5–/– mice and found that
while deletion of this gene did not seem to affect fertility per se, it did influence
the incidence of miscarriage and embryonic defects in mated wild-type female mice
(see the related article beginning on page 2074). Importantly, the appearance of
these problems was age dependent and associated with signs of oxidative stress in the
spermatozoa. These results demonstrate the key importance of Gpx5 as an extracellular
antioxidant designed to protect maturing mammalian spermatozoa from oxidative stress.
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