| With the development of nuclear power and nuclear technology, the effect of ionizing radiation on human health, especially genetic effect problems caused by low dose radiation (LDR) have become a research hotspot in radiomedical domain. In recent years, we have obtained some considerable results on the adaptive response induced by LDR in cell genetics. The adaptive response not only reduces the chromosome damage to subsequent larger dose irradiation, showing a better filial generation genetic effect, but also has significant regularity in cell types. Namely LDR can reduce the damage effect of spermatogonia and spermatocytes and not that of spermatids and spermatozoa. However, it was confirmed that there is a kind of spontaneous spermatogenic cell apoptotic phenomena in normal rat and mouse testis, and it can vary with ages, cell types and different cycles of seminiferous epithelium. The spontaneous apoptosis of spermatogonia and spermatocytes were taken as the main during mitosis prophase in mouse testis. We have known many important biological events taken place in mitosis prophase, so this kind of spontaneous apoptosis had an important significance in eliminating abnormal cells during DNA synthesis and homologous chromosome exchanging genetic materials, controling the quality and quantity of spermatogenic cells and maintaining the homeostasis. Moreover, spermatogenic cell apoptosis is very sensitive to ionizing radiation and very low dose irradiation can induce it to increase. The main mechanisms of rays as a kind of genetic toxicity factor causing cell death was regarded as apoptosis, which not only had dose-dependent characters, but it also depended on cell types and cell cycle. Therefore, it is very important to further explore the effect of LDR on mouse spermatogenic cell apoptosis and its molecular mechanisms. In this dissertation through analyzing the apoptosis and its related gene mRNA and protein expressions, we studied the effect of LDR on mouse spermatogenic cell apoptosis and its molecular mechanisms and the apoptotic adaptive response induced by LDR and its rudiment mechanisms. Effects of LDR on mouse spermatogenic cell apoptosisThe Kunming mice were sacrified and testis was got 0, 6, 12, 18 and 24 h after 0.025～0.2 Gy irradiation. The apoptotic dose and time course effect relationships during the different stages of seminous epithelium cycles were observed using hematoxylin- eosin (HE) staining and TdT-mediated dUTP nick end labeling (TUNEL) methods; discontinuity density gradient centrifugation to separate different types spermatogenic cells and flow cytometry method (FCM) to detect its apoptotic percentage.The results showed that the apoptosis of spermatogenic cells had a significant time-course relationship after 0.075 Gy X-ray whole body irradiation (WBI) in mice. Spermatogone cell apoptosis increase 6 h after irradiation with 0.075 Gy X-rays, reached its peak 12～18 h and subsequently decrease; spermatocyte cell apoptosis began to increase 6～12 h after irradiation with the same dose irradiation, reached its peak 18 h, and subsequently began to decrease. The apoptotic percentages of spermatids and spermatozoa at every time point after irradiation were relatively lower than those of spermatogonia and spermatocytes, and the apoptotic percentages didn't have significant difference between every time point and 0 h point. The results indicate that 0.075 Gy irradiation could cause the DNA damage of spermatogenic cells, selectively promote the spermatogone and spermatocyte apoptosis, and subsequently significantly decrease the abnormal cell number because of the activation of self-repair mechanisms and swallowing effects of macrophages and nearby cell.In addition, the apoptotic percentages of spermatogonia and spermatocytes had a significant dose-effect relationship 12 h after LDR WBI, but nonlinear, and the former apoptotic peak obviously higher than that of the latter. Spermatogone cell apoptotic percentages significantly increased after 0.025 Gy irradiation. The apoptotic percentage... |
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