苯并咪唑对雄性大鼠生育力的影响

目的探讨苯并咪唑对雄性大鼠生育力的影响及其作用靶点。方法将100只健康清洁级Wistar雄性大鼠随机分为4组,分别为低(20 mg/kg)、中(100 mg/kg)、高剂量(200 mg/kg)苯并咪唑染毒组和对照(0.5%吐温80溶液)组,每组25只。采用经口灌胃染毒方式进行染毒,染毒容量为10 ml/kg,每天1次,连续染毒80 d。染毒结束后,雌、雄大鼠以1∶1合笼,观察雌性大鼠妊娠情况,并计算雄性大鼠的交配率和生育力指数。测定精子活动率和精子数量及血清中促黄体生成素(LH)、卵泡刺激素(FSH)和睾酮(T)水平,采用流式细胞学术测定睾丸细胞周期的情况。结果与对照组比较,中、高剂量苯并咪唑染毒组雄性大鼠的交配率和G2期/M期的比例显著升高,生育力指数、精子活动率和精子数量以及睾丸细胞G0期/G1期及S期的比例显著降低,差异均有统计学意义(P<0.05,P<0.01);且随着苯并咪唑染毒剂量的升高,雄性大鼠的交配率和G2期/M期的比例均呈上升趋势,生育力指数、精子活动率和精子数量以及睾丸细胞G0期/G1期及S期的比例均呈下降趋势。与对照组比较,仅高剂量苯并咪唑染毒组雄性大鼠血清中LH水平显著降低,差异有统计学意义(P<0.05),且雄性大鼠血清中LH水平随着苯并咪唑染毒剂量的升高而下降;而各剂量苯并咪唑染毒组雄性大鼠血清中FSH、T水平均无显著变化。结论苯并咪唑对雄性大鼠具有明显的生殖毒性,可引起精子生成障碍,导致雄性大鼠生育力降低,甚至不育。     

小剂量氯化汞对小鼠的生殖毒性

目的观察小剂量氯化汞对雄性小鼠生殖功能的毒性作用以及氯化汞对小鼠精子数量和质量的影响。方法雄性ICR小鼠随机分为4组:阴性对照组,0.25、0.50、1.00mg/kg氯化汞组。分别以0.25、0.50、1.00mg/kg氯化汞腹腔染毒4周龄雄性小鼠每3天1次,共10次。50d后以雌雄2∶1合笼交配,观察雌鼠受孕率、生育子胎数、胎鼠重量,同时测定睾丸指数、附睾精子数量、精子活动率和精子畸形率。结果对照组、0.25、0.50和1.00mg/kg组合笼1周雌鼠受孕率分别为100%、100%、83.33%和66.67%,合笼3周雌鼠受孕率分别为100%、100%、83.33%和75%;其中1.00mg/kg组1周雌鼠受孕率显著低于对照组(P<0.05)。以上各组母鼠生育子胎数分别为127、142、113、95只,异常妊娠率分别为0%、1.41%、2.65%和4.21%;1.00mg/kg组异常妊娠率显著高于对照组(P<0.05)。0.50、1.00mg/kg组附睾精子数显著低于对照组和0.25mg/kg组(P<0.05);0.25、0.50、1.00mg/kg组睾丸指数、精子活动率与对照组比较差异无显著性(P>0.05)附睾精子畸形率显著高于对照组(P<0.05)。结论1.00mg/kg氯化汞染毒可降低雄性小鼠生育力,增加了受孕雌鼠异常妊娠率。氯化汞引起的这种雄性小鼠生育力的降低、异常妊娠率的增高可能与精子畸形率增高和精子数量下降有关。     

纳米二氧化钛对雄性小鼠生殖的影响

为探讨纳米二氧化钛对雄性小鼠生殖的影响,选择健康清洁级雄性昆明小鼠40只,随机分为正常对照组(生理盐水组)和纳米二氧化钛组(低、中、高剂量分别为10、50、250 mg/kg)染毒2周.观察小鼠染毒前后体重变化,进行精子计数、小鼠睾丸病理组织观察、睾丸和附睾乳酸脱氢酶的活力检测.结果显示,纳米二氧化钛染毒组小鼠的体重增...     

玉米赤霉醇染毒对雄性小鼠睾丸及生精功能的影响

目的研究玉米赤霉醇对小鼠生精功能的影响及可能机制。方法选择健康性成熟的雄性昆明种小鼠40只,随机分为对照组和染毒组(玉米赤霉醇25、50、100mg/kg),连续灌胃染毒35天后脱臼处死。检测睾丸、附睾、精囊腺重量及脏器系数,附睾尾精子数、精子的形态结构及活力,并观察睾丸组织病理学改变。结果玉米赤霉醇各染毒组小鼠的精囊腺系数及精子计数均低于对照组,差异有显著性(P<0.05);50、100mg/kg组精子活动率下降,与对照组比较差异有显著性(P<0.05);睾丸组织有明显的病理改变,生精上皮细胞排列疏松、紊乱,层次减少,成熟精子数明显减少。结论在本实验剂量条件下,玉米赤霉醇对小鼠生精功能有毒性作用。     

胚胎期毒死蜱和氯氰菊酯混合暴露对仔代雄性大鼠生殖功能的影响

目的 观察低剂量毒死蜱和氯氰菊酯联合染毒对仔代雄性大鼠生殖功能的影响及其机理。方法 健康Wistar大鼠雌雄按2∶1合笼,孕鼠分为对照组、毒死蜱组、氯氰菊酯组、毒死蜱和氯氰菊酯联合染毒组等4组,每组8只,孕l至孕8天染毒孕鼠。给予雄性仔鼠普通饮食喂养至成年。股动脉放血法处死仔鼠,迅速分离脏器,计算脏器系数,附睾尾精子计数,计算精子活动率、精子畸形率。测定血清生殖激素和乙酰胆碱酯酶活力,观察睾丸组织病理改变、生殖细胞凋亡和生精细胞端粒酶的表达。〖HTH〗结果 联合染毒组雄性仔鼠睾丸、附睾的体重比值显著性降低(P<0.05),附睾尾精子总数显著低于对照组,血清FSH高于对照组,T低于对照组(P<0.05)。联合染毒组雄性仔鼠睾丸少量曲细精管生精上皮退化变性,生精细胞脱落,生精细胞凋亡指数明显高于对照组(P<0.05)。结论 胚胎期毒死蜱和氯氰菊酯混合染毒对仔代大鼠的生殖系统有明显的增毒作用;对睾丸的损伤及性激素水平(FSH、T)的协同影响,可能是产生联合生殖毒性的机理之一;提示对毒死蜱和氯氰菊酯进行环境健康风险评价时应考虑这种协同作用。     

甲基丙烯酸甲酯对雄性大鼠生殖功能的影响

通过甲基丙烯酸甲酯染毒的雄鼠精子畸形试验、精子计数、活动精子百分率的检查、睾丸和附睾的脏器系数及光、电镜病理学检查以及血清睾酮（Ｔ） 、黄体生成素（ＬＨ） 的检测, 研究甲基丙烯酸甲酯对雄性大鼠生殖功能的影响。实验结果表明, 中、高剂量组（１－６８ ｇ／ｋｇ 和２－８０ ｇ／ｋｇ 组） 的精子数明显减少而精子畸形率明显增高; 高剂量组的活动精子百分率下降, 且染毒雄鼠的体重增重减少, 睾丸脏器系数显著下降, 血清Ｔ 下降; 中剂量组的血清ＬＨ 明显升高。提示甲基丙烯酸甲酯对雄鼠生殖功能有损害作用。     

膦氧氮丙啶对雄性小鼠的生殖毒性研究

膦氧氮丙啶(phosphine oxide,MAPO)对AMS雄性小鼠经口染毒60天,与正常雌鼠交配后,雄鼠染毒剂量≥10ppm时其生育率为0％,阴性对照及MAPO1ppm组雄鼠生育率为100％。对小鼠附睾精子数量检测,MAPO10ppm和100ppm组的精子数量分别为0.62和0.51×10~6/ml/10g附睾,明显低于对照组(2.59×10~6/ml/10g附睾)和MAPO1ppm组(2.06×10~6/ml/10g附睾),仅存的精子活动度极差,绝大多数是伴有畸形的死精子。畸形精子中以无定形等头部畸形居多。结果表明,MAPO对哺乳类动物也是一种雄性不育剂,对雄性小鼠生殖细胞具有潜在诱变危害。     

呕吐毒素对小鼠精液质量和生育力的影响

目的探讨呕吐毒素即脱氧雪腐镰刀菌烯醇(deoxynivalenol,DON)染毒对小鼠精液质量和生育力的影响。方法将40只2~3月龄健康清洁级昆明雄性小鼠按体重随机分为4组,分别为对照(玉米油)组和10、30、50 mg/kg DON染毒组,每组10只。采用腹腔注射方式进行染毒,染毒容量为10 ml/kg,每天1次,连续染毒7 d。与未染毒的雌性小鼠合笼(雌雄比为2∶1);于妊娠15 d时,检测雄性小鼠精液质量和雌性小鼠生育力的变化情况。结果与对照组比较,各剂量DON染毒组小鼠的精子畸形率升高,而精子存活率和顶体完整率降低,差异均有统计学意义(P0.01,P0.05);且随着DON染毒剂量的升高,小鼠的精子存活率和顶体完整率均呈下降趋势,而精子畸形率呈上升趋势。与对照组比较,各剂量DON染毒组小鼠睾丸总精子数和精子日生成量以及20和30 mg/kg DON染毒组小鼠的附睾尾总精子数均下降,差异均有统计学意义(P0.05,P0.01);且随着DON染毒剂量的升高,小鼠的总精子数、精子日生成量和附睾尾总精子数均呈下降趋势。与对照组比较,各剂量DON染毒小鼠可使交配母鼠的妊娠率、着床胚胎数、活胎数降低,而妊娠流产率升高,差异均有统计学意义(P0.05,P0.01);且随着DON染毒剂量的升高,与各剂量DON染毒小鼠交配母鼠的妊娠率、着床胚胎数、活胎数均呈下降趋势,而妊娠流产率呈上升趋势。结论 DON染毒可降低雄性小鼠精液质量和生育力。     

醋酸铅对雄性小鼠生殖功能的影响

给雄性小鼠灌胃染毒醋酸铅 10mg/kg、 2 0mg/kg和 40mg/kg ,每天 1次连续 3 5d。应用分光光度法测定血清和睾丸中酶活性 ,按标准方法测定小鼠生育力 ,并对睾丸、附睾进行组织病理学检查。结果表明 ,雄鼠受精率、雌鼠妊娠率、平均每窝活胎率及睾丸匀浆中的 β G和LDHx随染毒剂量增加而降低 ,死胎率和吸收胎率随染毒剂量增加而升高 ,与阴性对照组比较差异均有显著性 (P <0 0 5 ) ,并呈现明确的剂量 反应关系 ,r值依次为 -0 412、 -0 42 0、-0 5 3 7、 -0 5 3 8、 -0 617、 0 5 42和 0 5 3 5。雄鼠交配率 ,血清和睾丸匀浆中G 6 PD、ACP、LDH仅在 40mg/kg组与阴性对照组比较差异有高度显著性和显著性 (P <0 0 1或P <0 0 5 )。说明染毒醋酸铅≥ 2 0mg/kg剂量可损害雄性小鼠生殖功能。     

氯氰菊酯暴露对青春期雄性小鼠精子发生的影响

[目的]探讨氯氰菊酯暴露对青春期雄性小鼠精子发生的影响及其可能机制。[方法]选择30只5周龄雄性ICR小鼠,随机分为暴露组和对照组,于出生后35天（PND35）至PND70,每天给予暴露组小鼠氯氰菊酯（25mg/kg）灌胃染毒,对照组以等容积的玉米油灌胃。末次染毒16h后,处死小鼠,取附睾尾评价精子数量;取睾丸称重并进行组织病理学检查;免疫组织化学法检测睾丸间质细胞;放射免疫分析法检测血清和睾丸组织睾酮水平;蛋白质免疫印迹法测定睾丸组织类固醇激素合成急性调节蛋白（StAR）和睾酮合成关键酶蛋白表达水平。[结果]暴露组小鼠睾丸生精小管管腔内出现大空泡。与对照组相比,暴露组第Ⅶ-Ⅷ期生精小管所占百分比明显下降,附睾尾精子数量明显减少,血清和睾丸组织睾酮含量明显降低,睾丸组织生成StAR的表达明显下调,而氯氰菊酯对小鼠睾丸间质细胞数量无影响。[结论]青春期氯氰菊酯暴露后对小鼠精子发生有损害作用,这可能与睾丸睾酮合成的降低有关。     

Testicular apoptosis after dietary zinc deficiency: Ultrastructural and TUNEL studies

The present study was conducted in Wistar rats to determine whether prepubertal dietary zinc deficiency causes apoptotic changes in testes. Prepubertal male Wistar rats (40–50 gm) were divided into 3 groups: zinc control (ZC), pairfed (PF), and zinc deficient (ZD). Control and pairfed groups were given a 100 ppm zinc diet while the deficient groups received 1 ppm zinc diet for 2 and 4 weeks (w), respectively. Ultrastructural studies revealed several apoptotic features such as wavy basement membrane, displaced nuclei, chromatin condensation, plasma membrane blebbing, nuclear membrane dissolution, loss of inter-Sertoli cell junctional complexes, and intercellular bridges and deformed mitochondria. A variable spectrum of sperm defects had also been visualized e.g., acrosomal deformities such as decapitation and a ring of condensed chromatin around the nuclear periphery, deformed sperm heads with a condensed nucleus, tail-elements with superfluous cytoplasm, and damage to the mitochondrial sheath and aggregation of spermatozoa within the membrane. This was further supported by TUNEL studies. Apoptotic index, epididymal sperm concentration, motility, and fertility index also revealed a significant (P?<?0.05) decrease in zinc deficient groups (2 and 4 w) when compared with their respective control and pairfed groups. All the above findings are indicative that changes observed in the testes after dietary zinc deficiency are due to the onset of apoptosis. Increased apoptotic degeneration in testes may cause irreversible changes in the germ cells associated with decreased epididymal sperm concentration, motility, and fertility index which contributes to the low efficiency of spermatogenesis thereby indicating a possible role of zinc in fertility.     

The reversible antifertility effect of Piper betle Linn. on Swiss albino male mice

To study the antifertility effect of an extract (alcoholic) of the leaf-stalk of Piper betle Linn., one set of experiments with two different doses in Swiss male albino mice were evaluated. Initially, 500 mg of the leaf-stalk extractive for 30 days and then 1000 mg for next 30 days/animal/day/kg body weight were administered orally. The extract reduced fertility to 0% within 60 days. Suppression of cauda epididymal sperm count and motility (p <0.05) was observed. Biochemical parameters did not show any marked alterations in testosterone content in serum nor 17beta-hydroxysteroid dehydrogenase (17beta-HSD) activity in testes although fructose content in seminal vesicles was reduced as are the weights of reproductive organs. The cholesterol content in testes increased, although not appreciably. After cessation of drug (plant extract) treatment, the altered parameters recovered. Results suggest that the contraceptive effect of the extract of leaf-stalk of Piper betle Linn. is mainly on the maturation process of spermatozoa in epididymides without influencing hystemic hormonal profiles. Withdrawal of the extract restored all altered parameters including organ weights and fertility after 60 days.     

Antifertility effect of sulfasalazine in the male rat

Sulfasalazine, which has been used for treatment of ulcerative colitis in man, caused a dose-dependent and reversible reduction in fertility of the male rat. By five weeks after forced feeding with sulfasalazine in corn oil at daily doses of 300, 450 and 600 mg/kg, the fertility decreased to 60.9, 35.5 and 26.8% of the control rats, respectively. Besides, the number of cohabited female being successfully inseminated was significantly reduced especially at high dose. However, complete recoveries of the mating behavior and fertility were evident by three weeks after drug withdrawal. Number of spermatozoa in the caput, the corpus and the cauda epididymides were not changed, but motility of spermatozoa collected from the cauda epididymides was significantly decreased. The body weight and the weights of testes, epididymides, seminal vesicles, prostate glands and coagulating glands as well as the concentration of plasma testosterone were not altered by five weeks after drug treatment at a dose of 450 mg/kg. This study shows that sulfasalazine also has an antifertility action in the male rat without affecting the blood androgens as previously reported in male patients.     

Testicular apoptosis after dietary zinc deficiency: ultrastructural and TUNEL studies

The present study was conducted in Wistar rats to determine whether prepubertal dietary zinc deficiency causes apoptotic changes in testes. Prepubertal male Wistar rats (40-50 gm) were divided into 3 groups: zinc control (ZC), pairfed (PF), and zinc deficient (ZD). Control and pairfed groups were given a 100 ppm zinc diet while the deficient groups received 1 ppm zinc diet for 2 and 4 weeks (w), respectively. Ultrastructural studies revealed several apoptotic features such as wavy basement membrane, displaced nuclei, chromatin condensation, plasma membrane blebbing, nuclear membrane dissolution, loss of inter-Sertoli cell junctional complexes, and intercellular bridges and deformed mitochondria. A variable spectrum of sperm defects had also been visualized e.g., acrosomal deformities such as decapitation and a ring of condensed chromatin around the nuclear periphery, deformed sperm heads with a condensed nucleus, tail-elements with superfluous cytoplasm, and damage to the mitochondrial sheath and aggregation of spermatozoa within the membrane. This was further supported by TUNEL studies. Apoptotic index, epididymal sperm concentration, motility, and fertility index also revealed a significant (P?相似文献   

Effects of subchronic exposure of laboratory mice to benzylbutyl phthalate (BBP) on the quantity and quality of male germ cells

The aim of the study was to investigate the effect of 8-weeks exposure of male mice to benzyl butyl phthalate (BBP) on the sperm count and quality of gametes. Pzh:Sfis male mice exposed per os to 450 mg/kg bw (1/16 LD50) and to 1800 mg/kg bw (1/4 LD50) of BBP in olive oil were used in the study. Control mice were treated with olive oil only. Groups of animals were killed 4 and 8 weeks after the start of exposure and 4 weeks after he end of exposure. Sperm count, motility, morphology and DNA damage in gametes were estimated in the study. Sperm counts were diminished 4 and 8 weeks after the start of exposure to BBP. In the same time decrease in sperm motility and dose-dependent increase in the frequency of abnormal sperm heads and slight increase in DNA damage were noted. 4 weeks after the end of exposure, slight decrease in sperm counts in the group of 1/4 LD50 was observed, only. Correlation between sperm count and testes and epididymes weight were noted. Themost sensitive to BBP exposure occurred spermatozoa and spermatids.     

锰对雄性小鼠生殖毒性的研究

采用一组试验方法研究了硫酸锰对雄性小鼠生殖系统的影响。实验结果表明，硫酸锰能引起早期精细胞和骨髓嗜多染红细胞微核发生率增加，精子数量减少，活动精子率下降，精子畸形率增高，精子尾部低渗肿胀率下降，血清睾酮含量下降，ＬＨ升高。本研究提示硫酸锰对哺乳动物雄性生殖细胞和体细胞有遗传损伤效应，对小鼠精子有毒性作用，并对血中性激素有影响．     

Effects of microquantities of cyproterone acetate released through Silastic capsules on the histology of the epididymis of the rat

The histological changes in the epididymis of rats exposed to microquantities of cyproterone acetate released from subcutaneously implanted Silastic capsules are recorded. A gradual reduction in the height of the epithelium, depletion of secretory granules, vacuolation of cells and nuclear pycnosis were observed in the caput and cauda epididymides at 4 months after implantation of the capsules. These degenerative changes reached their optimum at 6 months but returned to normalcy 15 days after removal of the capsules. Stainability of the acrosomes of the spermatozoa with PAS decreased significantly 4 and 6 months after implantation of the capsules; such epididymal spermatozoa were non-motile and non-viable. These results demonstrate a clear dissociation of the dose of antiandrogen needed to cause selective inhibition of epididymal function without interference with libido or the functions of the testes and accessory glands and indicate a new approach to control of fertility in the male.     

Melatonin prevents damage elicited by the organophosphorous pesticide diazinon on mouse sperm DNA

Toxic effects of pesticides are commonly associated with DNA damage. To evaluate the effect of the organophosphate diazinon on sperm DNA and to test whether melatonin could prevent this damage, male mice were intraperitoneally treated with melatonin, diazinon (1/3 or 2/3 LD50) or both; cauda epididymal spermatozoa were obtained on days 1 and 32 postinjection and tested for DNA alterations. On day 1, sperm from diazinon-treated mice showed augmented DNA breakages and reduced chromatin packaging, whilst DNA damage increased only in the diazinon 2/3 LD50 group. Micronucleus test of bone marrow cells demonstrated somatic cell chromosomal damage in both diazinon-treated groups. Pretreatment with melatonin before diazinon acute administration improved all parameters studied on day 1 pi. The organophosphorous pesticide diazinon is a dose-dependent testicular toxicant that alters the sperm DNA structure; melatonin is able to prevent this damage.     

Citrus limon extract: possible inhibitory mechanisms affecting testicular functions and fertility in male mice

The effect of oral administration of 50% ethanolic leaf extract of Citrus limon (500 and 1,000?mg/kg body weight/day) for 35 days on fertility and various male reproductive endpoints was evaluated in Parkes strain of mice. Testicular indices such as histology, 3β- and 17β-HSD enzymes activity, immunoblot expression of StAR and P450scc, and germ cell apoptosis by TUNEL and CASP- 3 expression were assessed. Motility, viability, and number of spermatozoa in the cauda epididymidis, level of serum testosterone, fertility indices, and toxicological parameters were also evaluated. Histologically, testes in extract-treated mice showed nonuniform degenerative changes in the seminiferous tubules. Treatment had adverse effects on steroidogenic markers in the testis and induced germ cell apoptosis. Significant reductions were noted in epididymal sperm parameters and serum level of testosterone in Citrus-treated mice compared to controls. Fertility of the extract-treated males was also suppressed, but libido remained unaffected. By 56 days of treatment withdrawal, alterations induced in the above parameters returned to control levels suggesting that Citrus treatment causes reversible suppression of spermatogenesis and fertility in Parkes mice. Suppression of spermatogenesis may result from germ cell apoptosis because of decreased production of testosterone. The present work indicated that Citrus leaves can affect male reproduction.