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THE EFFECTS OF HYPERTHERMIA ON SPERMATOGENESIS, APOPTOSIS, GENE EXPRESSION AND FERTILITY IN ADULT MALE MICE
Citation:
Rockett, J C., F. L. Mapp, J B. Garges, J. C. Luft, C. Mori, AND D J. Dix. THE EFFECTS OF HYPERTHERMIA ON SPERMATOGENESIS, APOPTOSIS, GENE EXPRESSION AND FERTILITY IN ADULT MALE MICE. BIOLOGY OF REPRODUCTION 65(1):229-239, (2001).
Description:
The effects of hyperthermia on spermatogenesis, apoptosis, gene expression and fertility in adult male mice
John C. Rockett1, Faye L. Mapp1, J. Brian Garges1, J. Christopher Luft1, Chisato Mori2 and David J. Dix1.
1Reproductive Toxicology Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711
2 Department of Anatomy, School of Medicine, Chiba University, Chiba 260-8670, Japan, and Core Research for Evolutional Science and Technology, Kawaguchi City, Saitama 332-0012, Japan.
Abstract
A well-characterized mouse model of temporary infertility, testicular heat shock, was used to further characterize the cellular and molecular mechanisms that may be involved in male infertility. This model is pertinent because heat shock proteins (HSPs), induced by heat shock, are required both in spermatogenesis and in protecting cells from the cytotoxic effects of environmental hazards such as heat, radiation and chemicals. Thus, perturbation of temporal or spatial HSP expression in the testis by exposure to such hazards may negatively impact sperm production. Cellular and molecular methods were used to characterize the effects of a single testicular heat shock (43?C for 20 minutes) at different times following treatment. A 10-week mating study following heat shock reaffirmed previous studies reporting that spermatocytes are the most susceptible subpopulation. Hyperthermia transiently disrupted spermatogenesis, resulting in spermatocytes with pyknotic nuclei and apoptotic bodies. Apoptosis in spermatocytes and spermatids was identified by TUNEL as soon as 8h after treatment, and correlated with the expression of inducible HSP70-1/-3 proteins. Use of DNA arrays facilitated the identification of changes in gene expression which supported cellular observations, e.g. apoptosis, and suggested different mechanisms for heat shock-induced infertility involving as many as six different families of HSPs and chaperonins.