热应激诱导雄性大鼠生殖功能改变的实验观察

目的观察热应激诱导雄性大鼠生殖功能的改变,并初步探讨其生理机制。方法清洁级Wistar大鼠64只,随机分成4组,即正常对照组及环境温度分别为38℃、40℃、42℃的3组热应激组,将大鼠暴露于高温环境1h/d,连续14d。分别于高温暴露后7d和14d进行大鼠性行为能力的观察,包括扑捉潜伏期(capture incubation period,CIP)、扑捉次数(capture times,CT)、精子相对计数、精子畸形率;血清与睾丸组织中超氧化物歧化酶(SOD)和丙二醛(MDA)等指标的检测。结果与正常对照组比较,42℃高温暴露7d,14d以及40℃高温暴露14d后大鼠的扑捉潜伏期显著延长,扑捉次数显著减少(P0.05):精子相对计数明显减少(P0.05);精子畸形率明显增加(P0.05);血清和睾丸组织中SOD的活性显著降低(P0.05),MDA的含量显著增加(P0.05);38℃热应激组上述各项指标与正常对照组相比均未见明显变化。结论高温环境暴露后,产生的热应激可改变雄性大鼠的生殖功能,其作用机制可能与生殖细胞的氧化损伤有关。     

微波辐射对雄性小鼠生殖系统的影响

目的观察微波辐射对雄性小鼠生殖系统的影响,并初步探讨其作用机制。方法将48只雄性昆明小鼠随机分成微波辐射低、中、高强度组(微波辐射功率密度分别为5、10、15mW/cm~2强度)和对照组,对小鼠辐射1h/d,连续30d。微波辐射结束后进行小鼠性行为能力的观察扑捉潜伏期(capture incubation period,CIP)、扑捉次数(capture times,CT)、精子相对计数、精子畸形数、超氧化物歧化酶(SOD)和丙二醛(MDA)等指标的检测。结果 15mW/cm~2强度辐射后15d小鼠的扑捉潜伏期显著延长、扑捉次数显著减少(P0.05),10mW/cm~2强度辐射后30d小鼠的扑捉潜伏期显著延长、扑捉次数显著减少(P0.05);精子相对计数明显减少(P0.05);精子畸形率明显增加(P0.05);血清和睾丸组织中SOD的活性显著降低(P0.05);血清和睾丸组织中MDA的含量显著增加(P0.05);5mW/cm~2强度辐射组上述各项指标与对照组相比均未见明显变化。结论低功率微波辐射可对雄性小鼠生殖系统产生影响,其作用机制可能与生殖细胞的氧化损伤有关。     

巴戟天根两种提取物对微波损伤大鼠生精功能的影响

目的:探讨巴戟天根不同浓度提取物对微波损伤的雄性SD大鼠生精功能的影响。方法:40只健康雄性SD大鼠先分为正常对照组和辐射组,辐射后再将辐射组分为辐射模型组,巴戟天根水提物治疗组和巴戟天根醇提物治疗组,每组10只。辐射组应用微波信号发生器(900 HZ 1.0 W),功率密度为218μm/cm2,12 h/d,持续辐射2周。治疗组在辐射后分别给予巴戟天根水提物和巴戟天根醇提物20 g/(kg.d)持续灌胃2周。观察各组大鼠生长发育,扑捉潜伏期(CIP)和扑捉次数(CT),睾丸和附睾指数及精子形态学的差异,精子浓度、精子畸形率以及血清睾酮的浓度。结果:与正常对照组[(269.50±36.07)g]相比,辐射模型组[(254.77±20.38)g]大鼠体重稍降低,CIP延长及CT减少(P<0.05),精子浓度[(87.717±12.365)×106/ml]降低及精子畸形率[(0.126±0.100)×106/ml]明显升高(P<0.05);睾丸和附睾出现不同程度的病理损伤改变,睾丸指数降低,血清睾酮水平无明显变化。两治疗组较正常对照组体重显著下降(P<0.05),血清睾酮的水平显著升高,且与辐射模型组相比CT增加、CIP缩短、精子浓度显著升高、畸形率显著下降、血清睾酮的水平升高(P<0.05)。治疗组睾丸的病理性损伤显著修复,附睾管内除见大量精子外,还可见大量脱落的细胞。结论:巴戟天根的水提取物和醇提取物均可促进微波辐射损伤的生殖器官的修复以及精子的生成。     

甲醛急性染毒对性成熟期雄性大鼠睾丸支持细胞结构和功能的影响

目的探讨甲醛急性染毒对性成熟期雄性大鼠支持细胞结构和功能的影响。方法选用性成熟期健康SD雄性大鼠24只,随机分为甲醛染毒高[10mg／（kg·d）]、中[1mg／（kg·d）]、低[0．1mg／（kg·d）]剂量和对照组4组。腹腔注射染毒3d后,利用透射电镜观察支持细胞的超微结构,利用逆转录聚合酶链反应（RT—PCR）测定雄激素结合蛋白（ABP）mRNA的相对表达量。结果①染毒3d后,高剂量甲醛染毒组精子数与对照组相比显著下降（P〈0．05）;中、高剂量甲醛染毒组精子活动率与对照组相比显著下降（P〈0．05）而精子畸形率与对照组相比显著升高（P〈0．05）;②中、高剂量甲醛染毒组大鼠支持细胞线粒体空泡化、核染色质边集;③各剂量甲醛染毒组的ABPmRNA表达水平与对照组相比均有明显的差异（P〈0．05）。相关检验发现甲醛染毒剂量与ABPmRNA表达水平显著负相关（r=-0．896,P〈0．05）。结论对支持细胞结构和功能的影响可能是甲醛雄性生殖毒性的重要机制。 献标志码：A     

大剂量5α还原酶抑制剂对雄性大鼠生精功能的影响

目的:研究高选择性5α还原酶抑制剂(爱普列特)在较大剂量时对雄性SD大鼠生精功能的影响。方法:32只8周龄雄性SD大鼠随机分为喂服淀粉的空白对照(C)组、喂服爱普列特1 mg/d(EL)组、喂服爱普列特5mg/d(EH)组及喂服非那甾胺(F)组,每组8只。观察大鼠睾丸重量、血清睾酮和双氢睾酮水平、附睾精子计数和配对雌性大鼠妊娠阳性数等变化情况。结果:与C组相比,F组或EH组均有①抑制前列腺生长和减轻睾丸重量的作用(P<0.05);②降低血清双氢睾酮而升高睾酮水平;③抑制大鼠精子数量,同时影响雄性大鼠生育能力。结论:大剂量高选择性5α还原酶抑制剂(爱普列特)可抑制雄性SD大鼠前列腺、睾丸重量,抑制精子生成并降低雄性大鼠生育力。     

补肾助阳方对植物雌激素致勃起功能下降干预的实验研究

目的:研究补肾助阳方(养精胶囊)对大鼠阴茎勃起功能的影响机制。方法:成年雄性SD大鼠56只,随机分为7组,分别为空白对照组、大豆黄酮组、十一酸睾酮组、西地那非组及养精胶囊(高/中/低)剂量组。空白对照组给予生理盐水灌胃,其余各组100 mg/(kg·d)大豆黄酮灌胃30d。随后各实验组在给予大豆黄酮灌胃的同时,养精胶囊(高/中/低)剂量组分别给予1.26、0.63、0.315 mg/k/d剂量的养精胶囊组方,十一酸睾酮组给予4mg/(kg·d)剂量的十一酸睾酮,西地那非组给予2.5 mg/(kg·d)剂量的西地那非。分别在实验第0、30、60天观察各组大鼠阿扑吗啡诱导的自发勃起反应,记录勃起次数及勃起潜伏期,测定大鼠血清睾酮、黄体生成素水平,并观察大鼠阴茎海绵体组织切片。结果:实验第30天时,所有实验组大鼠阿扑吗啡诱导的勃起次数明显下降,勃起潜伏期延长,有统计学意义(P0.05)。第60天时,大豆黄酮组(1.39±0.42 vs 2.67±0.33)和大豆黄酮及低剂量养精胶囊组(1.33±0.49 vs 2.83±0.61)大鼠阿扑吗啡诱导的勃起次数明显下降(P0.05);阿扑吗啡诱导的大鼠勃起潜伏期只有大豆黄酮组[(16.33±3.11)min vs(8.50±0.93)min]和大豆黄酮及低剂量养精胶囊组[(15.50±3.21)min vs(8.63±1.54)min]明显延长(P0.05),其余各组变化不明显。实验第30天时,所有实验组大鼠血清睾酮、黄体生成素均有显著下降(P0.05)。实验第60d时,大豆黄酮组[(5.34±0.89)ng/ml vs(1.24±0.30)ng/ml]和大豆黄酮及低剂量养精胶囊组[(5.28±1.12)ng/ml vs(2.07±0.76)ng/ml]血清睾酮变化有统计学意义(P0.05)。两组的黄体生成素由(3.62±0.37)ng/ml、(3.79±0.28)ng/ml变为(2.09±0.12)ng/ml、(2.17±0.33)ng/ml,显著下降(P0.05)。切片结果显示对照组大鼠阴茎海绵体内海绵窦数目多,血管清晰可见。大豆黄酮加睾酮组、大豆黄酮加西地那非组和大豆黄酮加中、高剂量养精胶囊组大鼠海绵体与正常对照组相比,海绵窦数目减少。大豆黄酮组和大豆黄酮加低剂量养精胶囊组大鼠海绵体内海绵窦明显减少,血管少见。结论:使用高剂量养精胶囊治疗后,大鼠阴茎勃起功能恢复,对由植物雌激素引起的勃起功能下降有良好疗效。     

选择性5α-还原酶抑制剂与十一酸睾酮合用对雄性大鼠生殖功能的影响

目的: 观察 5α 还原酶抑制剂与十一酸睾酮合用对雄性大鼠的生殖功能影响,从而探讨双氢睾酮是否参与生精及精子成熟的激素调节过程。　方法: 设立对照组后,给雄性大鼠经食道喂饲选择性 5α 还原酶抑制剂非那甾胺,并肌肉注射十一酸睾酮。观察大鼠生殖腺重量与组织学变化,血清睾酮、双氢睾酮水平,附睾精子计数和配对雌性大鼠妊娠胎仔数等变化情况。　结果: 与正常对照组相比,①非那甾胺减轻雄性大鼠的前列腺、睾丸和附睾的重量。合用外源性长效睾酮可以拮抗非那甾胺对大鼠前列腺重量的抑制作用。②非那甾胺使大鼠血清睾酮水平上升,而双氢睾酮显著下降。加用十一酸睾酮后的FT组血清睾酮和双氢睾酮水平均明显高于F组。③较大剂量的非那甾胺对大鼠的附睾精子计数,精子活率均有抑制作用,而且使精子畸形率明显升高和配对雌鼠的妊娠胎仔数减少。④非那甾胺与十一酸睾酮合用对大鼠的附睾精子计数与活率的抑制作用并没有得到进一步加强,虽然精子畸形率进一步升高,但配对雌鼠的妊娠胎仔数比T组却显著增加。　结论: 5α 还原酶抑制剂非那甾胺可以通过减少双氢睾酮的生成对大鼠的生殖器官和功能产生抑制作用。非那甾胺加用大剂量外源性雄激素并没有出现更强的抑制效应,反而部分抵消外源性雄激素的抑制生殖效应。     

氰戊菊酯对大鼠精子及生殖激素的影响

目的探讨氰戊菊酯(Fen)对雄性大鼠精子计数、活力以及生殖激素的影响。方法成年雄性SD大鼠,分别以0、20、40、80mg/kg剂量的Fen连续灌胃染毒15和30d,按常规方法进行精子计数和精子活力检测,应用放射免疫法和化学发光免疫法测定大鼠血清卵泡刺激素(FSH)、黄体生成素(LH)、睾酮(T)、雌二醇(E2)和睾丸匀浆中T、E2水平。结果Fen染毒15d时,与0mg/kg组相比,40mg/kg剂量组精子数量明显减少(P<0.01),20和40mg/kg组睾丸匀浆中T水平显著降低(P<0.01,P<0.05),血清LH、FSH水平随染毒剂量的增加而升高,且FSH水平和染毒剂量有显著的剂量-效应关系(P<0.05);Fen染毒至30d时,各组间精子数量差异不显著,与0mg/kg组相比,40mg/kg剂量组(a+b)级精子活力显著降低(P<0.05),血清LH、FSH水平随染毒剂量的增加而升高,但差异不显著。结论Fen对雄性大鼠有明显的生殖毒性作用,能够改变血清和睾丸中的生殖激素水平。     

长期大量饮酒对大鼠阴茎组织结构和功能的影响

目的探讨长期大量饮洒对大鼠阴茎组织结构和功能的影响。方法将30只雄性大鼠随机分为对照组，20％酒精剂量组和40％酒精剂量组。分别以生理盐水，20％和40％食用酒精各2ml给大鼠灌胃，每日1次。3个月后，观察各组大鼠的性行为和药物诱发阴茎勃起的情况；用酶放大物理发光仪测定各组大鼠血清睾酮的含量；对阴茎平滑肌三色改良法染色，并利用图象分析管理系统，分别计算各组大鼠阴茎平滑肌的目标总面积和面密度。结果与对只照组相比，20％酒精剂量组大鼠性行为受到抑制（P〈0．05），大鼠血清睾酮含量降低（P〈0．05）；40％酒精剂量组人鼠性行为，药物诱发阴茎勃起实验均受到抑制（P〈0．05），血清睾酮含量和平滑肌细胞数量减少。结论大鼠长期大量饮洒后性功能障碍，其机制与血浆睾酮含量降低，阴茎海绵体平滑肌成分减少有关。     

枸橼酸西地那非对雄性大鼠性活动能力的影响

目的 :为了获得与临床相关的药物动力学资料 ,本实验通过给雄性大鼠枸橼酸西地那非灌胃后观察它们性活动的变化。　方法 :4 0只雄性SD大鼠 ,分成阴性对照组 (蒸馏水 )、枸橼酸西地那非低剂量组 ( 0 .0 8% )、中剂量组( 0 .2 4 % )和高剂量组 ( 0 .72 % )共 4组 ,与雌性大鼠成对合笼 ,观察并记录雄性大鼠捕捉潜伏期、爬高潜伏期、6 0min内捕捉次数和 6 0min内爬高次数。　结果 :与阴性对照组相比 ,西地那非高、中剂量组能极显著性提高雄性大鼠的捕捉次数 ,缩短捕捉潜伏期 (P <0 .0 1) ;高、中、低剂量组均能极显著性提高雄性大鼠的爬高次数 ,缩短爬高潜伏期(P <0 .0 1)。　结论 :西地那非能够显著提高雄性大鼠的性活动能力。     

Long-term effects of intrauterine exposure to mono-n-butyl phthalate on the reproductive function of postnatal rats

Purpose

Although it is well known that phthalate esters induce testicular dysfunction in both adult and immature rats, there have been few reports on the long-term effect of phthalate esters on the testicular function of male rats exposed to phthalate esters in utero. This study was designed to assess the long-term effects of the mono-n-butyl phthalate (MBP) ester on the testicular function of neonatal and adult rat offspring from pregnant dams exposed to phthalate esters during gestation.

Methods

Pregnant rats were administered MBP [0.5 g/(kg body weight/·d); 4 days] by gavage from the 15th to the 18th gestational day. Rats administered solvent only were used as control subjects. After the rats' puberty, using male pups whose testes descended normally, the authors examined their fertility while also measuring their testicular weights, mean seminiferous tubular diameter, and the developmental grade of the germ cells (Johnsen score) in their testes. Next, in neonatal rats, the authors measured the testicular concentration of the Mullerian inhibiting substance (MIS) protein using enzyme-linked immunoassay and the expression level of the MIS messenger RNA using the quantitative polymerase chain reaction method as a marker of the Sertoli cells' function. Next the concentration of testosterone protein using a radioimmunoassay as a marker of the Leydig cells' function was measured.

Results

The pregnancy rate of the female rats coupled with MBP-treated male rats decreased significantly in comparison with that of the female rats coupled with control male rats (P < .01). Both the testicular weight and the Johnsen score in the MBP-treated group were decreased significantly more than those of the control group (P < .05). Neither the concentration of the MIS protein nor the expression level of the MIS messenger RNA in the MBP-treated neonatal testes differed from those of the control testes, whereas the concentration of testosterone protein in the neonate testes decreased significantly in the MBP-treated group in comparison with that of the control group (P < .01).

Conclusions

A prenatal short-time exposure to MBP induces a long-term effect on postnatal rats and impairs reproductive function in male offspring probably by inhibiting the Leydig cells' rather than Sertoli cells' function in the fetal period.     

Risperidone induced reproductive toxicity in male rats targeting leydig cells and hypothalamic–pituitary–gonadal axis by inducing oxidative stress

Risperidone (RIS), a commonly used drug during a lifetime for the treatment of schizophrenia, causes some adverse effects in the male reproductive system; however, there is no comprehensive reproductive toxicity study of RIS. For this purpose, male rats were administered orally for 1.25, 2.5 and 3 mg/kg RIS for 28 days and the sperm count, motility, morphology, DNA damage and the histological changes in testicular tissue were evaluated. Follicle-stimulating hormone (FSH), luteinising hormone (LH) and serum levels of testosterone, which are the main hormonal regulators of reproduction, and testicular glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and malondialdehyde (MDA) levels as the indicators of oxidative stress were determined. Normal sperm morphology was decreased in RIS groups and histopathological degeneration occurred in testis tissue dose-dependently. Serum LH levels were not altered; however, FSH and testosterone levels decreased in the high-dose group. Histopathologic examination showed RIS toxicity targeted Leydig cells, which might be associated with impairment of the hypothalamic–pituitary–gonadal (HPG) axis. GSH levels were decreased and MDA levels were increased in the high-dose group which was evaluated as indicators of oxidative stress. In conclusion, RIS caused reproductive toxicity in male rats by inducing oxidative stress and disrupting hormonal regulation.     

Effect of methanol extract of Ricinus communis seed on reproduction of male rats

Aim:To investigate the effect of methanol extract of Ricinus communis seed(RCE)on male rats reproductivefunctions.Methods:Thirty-two male albino rats were divided into four groups.Groups 1,2 and 3 were gavagedwith 0.2 mL of 2.5% tween 80(RCE vehicle;control)or 20 mg/(kg·d)and 40 mg/(kg·d)of RCE,respectively,for30 days,and group 4 was also gavaged with 40 mg/(kg·d)of RCE,but was allowed a recovery periold of 30 days.Five untreated female rats were cohabited with male rats in each group from day 25 of RCE treatment for 5 days,except group 4,where cohabitation began on day 25 of the recovery period.All male rats were sacrificed 24 h afterthe experiments.The female rats were laparatomized on day 19 of pregnancy and the number and weight of litterswere recorded.Results:There was a significant decrease(P<0.01)in the weight of the reproductive organs,sperm functions and serum levels of testosterone in RCE treated rats.There was disorganization in the cytoarchitec-ture of the testes,disruption of the seminiferous tubules and erosion of the germinal epithelium.The number andweight of litters of rats in groups 2 and 4 decreased significantly(P<0.05)but no changes were observed in group3.RCE caused no changes in liver,kidney,heart or body weights in male rats.Conclusion:RCE has a reversiblenegative impact on male reproductive functions,which appears to be mediated via gonadal disruption in testosteronesecretion.(Asian J Androl 2006 Jan;8:115-121)     

Rohypnol-induced sexual dysfunction is via suppression of hypothalamic-pituitary-testicular axis: An experimental study in rats

Sexual activity is an essential part of reproductive functions and needed for the maintenance of fertility. Drugs, particularly substances of abuse, impair male reproductive function either by interrupting hormonal functions or through the nonhormonal pathways. This study evaluated the impact of Rohypnol use in sexual behaviour. Materials and methods: Thirty adult male Wistar rats of comparable weights (180–200 g) were randomly allocated into three groups, the control and low-dose and high-dose Rohypnol-treated groups. The control group received 0.5 ml of distilled water, while the low- and high-dose Rohypnol-treated groups received 2 mg/kg b.w and 4 mg/kg b.w of Rohypnol via oral lavage once daily for 28 days. Rohypnol significantly increased mount latency, intromission latency, ejaculation latency and post-ejaculatory interval, as well as lowered mount frequency, intromission frequency and ejaculation frequency. Rohypnol-induced sexual dysfunction was found to be associated with significant suppression of circulatory follicle-stimulating hormone, luteinising hormone, testosterone and oestrogen. The present study reveals that Rohypnol induces sexual dysfunction through suppression of hypothalamic – pituitary – testicular axis. It also implicates Rohypnol as a potential candidate for drug-induced infertility.     

Effects of photoperiod on the ultrastructure of Leydig cells in rat

The aim of this study was to examine effects of photoperiod on the ultrastructure of Leydig cells in rat. For this purpose, 21 male Wistar rats were used. Animals were divided into three groups: Control rats in group I were kept under 12 hrs light: 12 hrs dark conditions (12L: 12D) for 10 weeks. Animals in group II were exposed to long photoperiods (18L: 6D), while rats in group III were exposed to short photoperiods (6L:18D) for 10 weeks. At the end of the experiment, all animals were killed by decapitation and blood samples were obtained. Serum testosterone levels were determined with the use of a chemiluminescent enzyme immunoassay. The testes of all rats were removed and weighed, then processed for light and electron microscopy. For morphometric comparison, diameters of seminiferous tubules in each group were measured. In rats exposed to long photoperiods, testicular weights, diameters of seminiferous tubules and serum testosterone levels were significantly increased as compared to those in control rats, whereas exposure of rats to short photoperiods resulted in a significant decrease of testicular weights, diameters of seminiferous tubules and serum testosterone levels as compared to those in control rats and rats maintained in long photoperiods. The amount of mitochondria and cytoplasmic secretory granules were increased in the cytoplasm of Leydig cells of rats exposed to long photoperiods. Furthermore, an increase in extensiveness of rough endoplasmic reticulum in the cell cytoplasm was noticed in this group, whereas a decrease in mitochondria and cytoplasmic secretory granules of the Leydig cell cytoplasm was seen in rats exposed to short photoperiods. The results of our study indicate that testicular functions increase after exposure to long photoperiods and decrease after exposure to short photoperiods.     

Interferon alpha-2b may impair testicular histology including spermatogenesis in a rat model

Interferon-alpha has been used in various diseases at the reproductive ages. However, the effect of interferon-alpha on testicular histology has not been studied in literature. The aim of this study was to investigate the effects of interferon alpha-2B on testicular histology including spermatogenesis in a rat model. Seventeen adult male Wistar albino rats were divided into 3 groups: Six rats received 7.500 units (5 MIU/m2) of interferon alpha-2B (Intron), considered clinical treatment dose range. Six rats received 30.000 units (20 MIU/m2) of interferon alpha-2B (Intron), considered high treatment dose. Five rats served as a control group receiving 0.5 mL of saline injection. All injections were done intraperitoneally 3 times weekly for 3 weeks under inhalation anesthesia. All rats underwent bilateral orchiectomy 30 days after the experiment. Histological examination included the mean seminiferous tubular diameter (STD), germinal epithelial cell thickness (GECT), and testicular biopsy score (TBS). The mean STD was significantly lower in the low-dose interferon and high-dose interferon groups than in the control group (p = 0.008 and p = 0.004, respectively). The mean GECT was significantly lower in the low-dose interferon and high-dose interferon groups than in the control group (p = 0.008 and p = 0.004, respectively). The mean TBS was significantly lower in the low-dose interferon group (p = 0.05) and the high-dose interferon group (p = 0.01) than in the control group. The decreases in the mean values of the STD, GECT and TBS were not related to the interferon dose. Interferon alpha-2B may impair testicular histology even in clinical widely used treatment dose. Therefore, men at the reproductive ages should be fully informed for the use of interferon-alpha in the treatment of various diseases.     

青春期前邻苯二甲酸二丁酯持续暴露对大鼠睾丸发育的影响

目的:研究青春期前邻苯二甲酸二丁酯(DBP)持续暴露对睾丸发育的影响。方法:21日龄断乳青春期前雄性SD大鼠随机分为对照组(n=24)和实验组(n=54),每日分别用玉米油或DBP玉米油溶液灌胃,DBP暴露剂量分别为50mg/(kg.d)(低剂量组,n=18)、200mg/(kg.d)(中剂量组,n=18)和600mg/(kg.d)(高剂量组,n=18),各组动物持续暴露14、21、28d后(即PND35,PND42和PND49)断颈处死。记录大鼠体重变化,检测睾丸重量和体积、附属性器官重量及附睾精子,化学发光免疫分析法检测血清睾酮含量,苏木精-伊红染色观察睾丸组织形态学变化,测量生精小管平均直径及进行睾丸活检评分。结果:低剂量组PND35少量生精小管生精细胞排列紊乱,PND42和PND49睾丸、附属性器官发育及生精功能正常;中剂量组PND35和PND42生精细胞排列紊乱、数目减少,PND49生精小管内可见各级生精细胞及精子,睾丸未见萎缩,附属性器官发育正常;高剂量组大鼠体重增长减缓,血清睾酮水平低下,睾丸生精小管变性萎缩,生精上皮发育阻滞,生精细胞大量凋亡坏死,青春期大鼠睾丸萎缩,无精子,附睾、前列腺和精囊等附属性器官发育迟缓。结论:青春期前DBP持续暴露可损害睾丸组织发育和正常生精功能形成,其毒性效应具有剂量依赖性,高剂量DBP持续暴露引起的睾丸毒性在青春期前发育过程中不可修复,而低中剂量暴露引起的睾丸毒性在PND49之前可完全或部分逆转性恢复。     

The hormonal regulation of premeiotic steps of spermatogenesis in the newborn rat

.he effect of high doses of testosterone propionate (TP) on the development of the first spermatogenic wave was systematically analyzed to determine the period of maximal susceptibility to testosterone. Two mg of TP were administered daily to groups of immature male rats, starting from birth, or days 5, 10, 15, and 20 until day 35 of life. Animals injected from birth or day 5 showed severe testicular atrophy, with reductions of more than 70% of testicular weight, diminished tubular diameters, and spermatogenic arrest during the meiotic prophase. Groups treated from days 10 or 15 showed increasing testicular weights with qualitatively normal spermatogenesis. When treatment started at 20 days, completely normal testicular development was achieved. To test the responsiveness of the neonatal hypothalamo-pituitary axis to TP administration, groups of 5-day-old male rats received daily injections of TP, and plasma FSH was determined at ten, 20, and 35 days. FSH levels were not detectable at ten and 20 days, and extremely depressed at 35. A group of 5-day-old male rats was injected simultaneously with 2 mg of TP and 14 IU of FSH (human menopausal gonadotropin: 71 IU of FSH and 80 IU of LH/ml) until day 35. Testicular weights and tubular diameters were increased compared to controls, and spermatid differentiation had proceeded to more mature steps than those seen in control animals. Inhibition of testicular development by neonatal TP administration was paralleled by a sharp decrease in circulating FSH levels and reversed by FSH replacement.(ABSTRACT TRUNCATED AT 250 WORDS)