학술논문

乙烯利对子代雄鼠睾丸病理结构及生精细胞凋亡的影响 / Effect of Ethephon on testicular pathology and apoptosis of spermatogenic cell in offspring male rats
Document Type
Academic Journal
Source
中华实用儿科临床杂志 / Chinese Journal of Applied Clinical Pediatrics. 34(10):777-780
Subject
乙烯利
睾丸
生精细胞
凋亡指数
Ethephon
Testis
Spermatogenic cell
Apoptotic index
Language
Chinese
ISSN
2095-428X
Abstract
目的 探讨乙烯利对子代雄鼠睾丸组织病理及生精细胞凋亡的影响.方法 选取45日龄健康雌性SD大鼠24只,根据随机数字表法分为对照组和低、中、高剂量乙烯利组,再选取同龄健康雄性大鼠与之合笼交配.每日分别以不同浓度乙烯利水溶液或9g/L盐水对各组雌鼠灌胃,并在妊娠期和哺乳期继续灌胃.子代雄鼠7日龄及14日龄时分别从各组随机选取10只处死.取睾丸组织行HE染色,光镜下观察睾丸组织形态变化;采用末端转移酶标记技术(TUNEL法)标记凋亡细胞,利用荧光显微镜检测睾丸生精细胞凋亡指数(AI).结果 仔鼠7日龄时,对照组睾丸内部结构发育良好,生精小管排列整齐紧凑.低剂量乙烯利组睾丸生精小管管腔略小,生精细胞较对照组排列稍松散;中剂量乙烯利组显示睾丸生精小管排列稍紊乱,细胞间隙增大.高剂量乙烯利组睾丸发育差,生精小管管径明显减小,生殖细胞排列紊乱.低剂量乙烯利组生精细胞AI[(0.54±0.10)%]与对照组[(0.53±0.09)%]相比,差异无统计学意义(P>0.05),中剂量乙烯利组生精细胞AI[(0.63±0.11)%]、高剂量乙烯利组生精细胞AI[(0.81±0.06)%]均高于对照组,差异均有统计学意义(均P<0.01).低剂量乙烯利组生精细胞AI[(0.54±0.10)%]低于中剂量乙烯利组生精细胞AI[(0.63±0.11)%],差异有统计学意义(P<0.05);中剂量乙烯利组生精细胞AI低于高剂量乙烯利组生精细胞AI,差异有统计学意义(P<0.01).14日龄时,各组生精细胞AI分别为(0.54±0.08)%、(0.65±0.11)%、(0.77±0.11)%和(0.88±0.10)%,对照组、低剂量乙烯利组、中剂量乙烯利组、高剂量乙烯利组仔鼠生精细胞AI逐渐升高,差异均有统计学意义(均P<0.01).结论 高剂量乙烯利可引起仔鼠睾丸生殖细胞排列紊乱、生精细胞凋亡增加,导致仔鼠生育能力降低.
Objective To investigate the effect of Ethephon on the testis pathological structure and apoptosis of spermatogenic cell in offspring male rats.Methods Twenty-four healthy female SD rats of 45 days old were randomly divided into control group,low-dose Ethephon group,medium-dose Ethephon group and high-dose Ethephon group according to body weight.The male rats of the same age were selected to mate with female rats.The rats were fed with Ethephon solution of different concentrations or 9 g/L saline every day,and they were continued to be fed with Ethephon during pregnancy and lactation.At the age of 7 days and 14 days,10 offspring male rats were randomly selected from each group and were put to death.The testicular tissue was stained with HE,and the morphological changes in the testis were observed with light microscope;the apoptotic cells were labeled with terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL method) and the apoptosis index(AI) of testis spermatogenic cells was detected with fluorescence microscope.Results At the age of 7 days,the testis internal structure of the control group developed well,and the spermatic tubules were neatly and compactly arranged.In the low-dose Ethephon group,the seminiferous tubules of the testis were slightly smaller and the spermatogenic cells were loosely arranged compared with the control group.In the medium-dose Ethephon group,the testis seminiferous tubules were slightly disordered and the cell gap increased.In the high-dose Ethephon group,the testis development was poor,the diameter of seminiferous tubules decreased significantly,and the spermatogenic cells arrangement was in disorder.There was no statistically significant difference in spermatogenic cell AI between the low-dose group [(0.54 ± 0.10)%] and the control group[(0.53 ±0.09) %] (P > 0.05),while the spermatogenic cell AI in the medium-dose Ethephon group [(0.63 ± 0.11) %]and the high-dose Ethephon group [(0.81 ± 0.06) %] were higher than that in the control group,thus there exists a statistically significant difference (all P <0.01).The spermatogenic cell AI in the low-dose Ethephon group [(0.54 ±0.10) %] was lower than that in the medium-dose Ethephon group [(0.63 ± 0.11)%],and the difference was statistically significant (P < 0.05).The spermatogenic cell AI in the medium-dose Ethephon group was higher than that in the high-dose Ethephon group,and the difference was statistically significant (P <0.01).At the age of 14 days,the spermatogenic cells AI in control group,low-dose Ethephon group,medium-dose Ethephon group and high-dose Ethephon group were (0.54 ± 0.08) %,(0.65 ± 0.11) %,(0.77 ± 0.11) %,and (0.88 ± 0.10) %respectively,and the spermatogenic cells AI in all groups increased gradually,in which the differences were statistically significant (all P < 0.01).Conclusions Excessive dose of Ethephon can induce pathological changes in testicular tissue and increase the apoptosis of spermatogenic cells,resulting in low fertility of offspring rats.