| First Author | Ishii T | Year | 2005 |
| Journal | Free Radic Res | Volume | 39 |
| Issue | 7 | Pages | 697-705 |
| PubMed ID | 16036348 | Mgi Jnum | J:114348 |
| Mgi Id | MGI:3688805 | Doi | 10.1080/10715760500130517 |
| Citation | Ishii T, et al. (2005) Accelerated impairment of spermatogenic cells in SOD1-knockout mice under heat stress. Free Radic Res 39(7):697-705 |
| abstractText | For normal spermatogenesis, the temperature of the scrotum is lower than that of the body. The mechanism by which mammalian testes undergoes cell death as the result of exposure to heat continues to be a matter of debate. Since generation of reactive oxygen species (ROS) during heat stress and involvement in spermatogenic cell damage are postulated, we induced experimental cryptorchidism in the testes of SOD1-knockout mice and examined effects of the gene deficiency. The cleavage of DNA in testicular cells, as judged by TUNEL staining, were elevated in SOD1-knockout mice at an earlier stage than in the wild-type mice. To confirm responsiveness of SOD1 for this high susceptibility to heat stress, spermatogenic cells were isolated from SOD1-knockout and wild-type mice and cultured at 32.5 and 37 degrees C. The cells isolated from SOD1-knockout were more vulnerable at both temperatures than those from wild-type mice. The exposure of cultured rat spermatogenic cells to ROS induced the release of cytochrome c from mitochondria, while Sertoli cells were more resistant under the same conditions. Tiron, a superoxide scavenger, suppressed the heat-induced release of cytochrome c from mitochondria. Collectively, these data suggest that ROS are generated during heat stress and cause spermatogenic cell death. Alternatively, since even a short exposure triggers harmful damage to spermatogenic cells, generated ROS may function as a type of signal for cell death rather than directly causing oxidative damage to cells. |
