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[目的]探讨宫内暴露p,p’-DDE对雄性子代生殖毒性的影响。[方法]母鼠交配成功后,将其随机分为对照(玉米油)组和100 mg/kg p,p’-DDE染毒组,每组8只。染毒组于孕第8~15 d采用灌胃方式给予100 mg/kg p,p’-DDE处理,对照组孕鼠给予等容积玉米油。孕鼠自由分娩,观察仔鼠个数和出生性别,测量雄性仔鼠肛殖距及检查乳头存留情况;计算睾丸的脏器系数;利用计算机辅助精子分析系统测定雄性仔鼠的精子质量各相关指标;酶联免疫吸附法测定雄性子代血清睾酮水平。[结果]染毒组仔鼠肛殖距[(0.94±0.12)cm]较对照组仔鼠肛殖距[(1.11±0.13)cm]有所缩短,乳头存留率(34%)较对照组(0%)明显上调,精子数目[(50.00±4.62)×106个/m L],较对照组[(70.63±4.17)×106个/m L]明显降低,精子活力[(62.42±3.32)%],较对照组[(76.75±2.68)%]明显下降,差异均有统计学意义。2组雄性仔鼠雌雄比例、睾丸脏器系数、血清睾酮水平、睾丸重量差异均无统计学意义。[结论]宫内暴露p,p’-DDE可诱导雄性仔鼠出现雌性化特征,精子数目和活力下降,导致雄性子代生殖毒性。
[Objective] To investigate the effect of intrauterine exposure of p, p’-DDE on reproductive toxicity of male offspring. [Methods] After mating successfully, female rats were randomly divided into control (corn oil) group and 100 mg / kg p, p’-DDE exposure group, with 8 rats in each group. The rats in the exposure group were given 100 mg / kg p, p’-DDE by intragastric administration on the 8th to 15th day of pregnancy, and the pregnant rats in the control group were given the same volume of corn oil. Pregnant mice were given free labor, the number of pups and their sex at birth were observed, the male and female offspring of male pups were measured, and the preservation of the nipples was measured. The organ coefficients of testis were calculated. The related parameters of spermatozoa were determined by computer-assisted sperm analysis Serum testosterone levels were measured by enzyme-linked immunosorbent assay. [Results] The anal interspice was significantly shorter than that of the control group [(1.11 ± 0.13) cm] [(0.94 ± 0.12) cm], and the retention rate of the nipple was 34% (50.00 ± 4.62) × 106 / m L compared with the control group [(70.63 ± 4.17) × 106 / m L], and the sperm motility was (62.42 ± 3.32)% ], Compared with the control group [(76.75 ± 2.68)%], the differences were statistically significant. There was no significant difference in male and female ratio, testicular organ coefficient, serum testosterone level, testicular weight difference among male pups in two groups. [Conclusion] Intrauterine exposure to p, p’-DDE induces fecundity in male offspring, with decreased sperm count and viability, leading to reproductive toxicity in male offspring.