吸烟对大鼠生精细胞发育影响的研究

目的:探讨吸烟对大鼠生精细胞发育的影响。方法:自制吸烟机将大鼠制成被动吸烟模型,大鼠随机分成被动吸烟组(A、B组各10只)及相应对照组(C、D组各10只),A、B组被动吸烟8周,随后处死A组及相应对照组C组大鼠;B组停止被动吸烟后与其相应对照组D组继续观察48 d后处死。流式细胞术(FCM)检测各组大鼠生精细胞周期,放免法测定血睾酮(T)、黄体生成素(LH)水平,HE染色观察睾丸组织结构变化,透射电镜观察睾丸超微结构改变。结果:与C组比较,A组大鼠精子、精子细胞(18.76±3.58)%]和初级精母细胞(5.71±1.18)%]明显减少(P均<0.01),而精原细胞(55.98±5.35)%]增加(P<0.01),增殖指数降低(P<0.01)。A组大鼠生精小管壁变薄,层次减少,生精小管内精原细胞减少,精母细胞固缩。间质细胞内质网扩张脱颗粒,高尔基复合体减少,支持细胞脂滴和溶酶体增多。A组大鼠T、LH水平低于C组(P均<0.01)。B组大鼠停止被动吸烟后,精子、精子细胞、初级精母细胞比例和增殖指数上升,T、LH水平升高,但仍低于D组。结论:吸烟导致大鼠睾丸生精上皮损伤及间质细胞和支持细胞受损,同时伴有T和LH水平的下降,延缓生精细胞增殖,停止吸烟后生精功能有逐渐恢复的趋势。

Cigarette Smoking Affects Cyclogeny of Spermatogenic Cells in Rats

Objective: To determine the effects of cigarette smoking on the cyclogeuy of spermatogenic cells in rats. Methods : Rat models of passive smoking were established using a self-made smoking device, and then allocated randomly into two passive smoking groups (A and B, n = 10) and two corresponding control groups (C and D, n = 10). Groups A and B were exposed to cigarette smoke for 8 weeks, followed by the sacrifice of the rats in Groups A and C. And the animals in Groups B and D were killed 48 days after the cessation of passive smoking. The spermatogenesis cycle of each group of rats was detected by flow cytometry, the levels of testosterone (T) and luteinizing hormone (LH) measured by radio-immunity method, and the testis histopathology analyzed by HE staining and transmission electron microscopy. Results: Compared with Group C, Group A showed a significant decrease in the number of spermatids, spermatozoa (18.76±3.58] % ) and primary spermatoeytes (5.71±1.18] % ) (P < 0.01), but an obvious increase in the spermatogonias (55.98±5.35] %, P < 0.01), with a markedly decreased proliferation index (P < 0.01). The rats of Group A also exhibited pycnosis of spermatocytes, nucleus aberration of Leydig cells, expansion and degranulation of the endoplasmic retieulum, decreased Golgi apparatus, increased lysosomes and fat drops of Sertoli cells, as well as a reduction in the thickness of the wall and the layers of seminiferus tubules and the number of spermatogonia. The T and LH levels were significantly lower in Group A than in C (P <0.01). After the cessation of passive smoking, a remarkable increase was observed in the percentage of spermatozoa and primary spermatocytes and the levels of serum T and LH in Group B, although the latter were still lower than those of Group D. Conclusion : Smoking damages permatogenic epithelia, Leydig cells and Sertoli cells, reduces the T and LH levels, and block the proliferation of spermatogenetic cells. These changes can be partially reversed after cessation of smoking.