Effects of elevated ambient temperature and local testicular heating on the expressions of heat shock protein 70 and androgen receptor in boar testes.

Heat stress damaged spermatogenesis and semen quality, however, the exact molecular mechanism is not clear. The objective of this study was to determine the effects of elevated ambient temperature and local testicular heating on the expressions of heat shock protein 70 and androgen receptor in boar testes. A growing body of evidence demonstrated that germ cell apoptosis can be aggravated by heat stress and androgen deprivation, and at normal temperature, withdrawal of androgen led to germ cell apoptosis. There were no reports that heat stress damaged spermatogenesis has relationship with androgen. In this study, adult boars (Landrace, n = 9) were used and randomly divided into: control group (CON), 20-27 °C; environmental hyperthermia group (EH), 37-40 °C, 3 h/d 42 d; and local testicular heating group (LTH), 42 °C 1 h. After heat treatments, all boars were castrated and the testes were harvested. qRT-PCR and Western Blot results showed that the mRNA and protein levels of heat shock protein 70 and androgen receptor were significantly increased after heat treatments. Immunohistochemistry results showed that heat stress caused a redistribution of heat shock protein 70 from the cytoplasm to the nucleus, and androgen receptor was mainly expressed in Sertoli cells. These results indicated that heat stress promoted the inhibition of heat shock protein 70 on the androgen receptor, suggesting that the possible mechanism of heat stress damaged spermatogenesis and semen quality was that heat stress reduced the sensitivity of testicular cells to androgen by up-regulating heat shock proteins.