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1.
目的:探讨弓形虫急性感染对雄性小鼠睾丸生精功能的影响。方法:将26只成年雄性小鼠随机均分为感染组和正常对照组;感染组腹腔注射0.3ml1×103/ml弓形虫速殖子,感染小鼠睾丸,正常组腹腔注射等量生理盐水,两组睾丸制成直接印片及病理切片,观察小鼠生精细胞的病理变化及弓形虫侵入生精细胞情况。同时比较两组睾丸乳酸脱氢酶同工酶、精子密度、精子活动率、精子畸形率。结果:感染组睾丸乳酸脱氢酶同工酶、精子密度、精子活动率、精子畸形率分别为53.19±18.04、(15.01±2.42)×106/ml、(8.26±2.57)%、(17.69±11.91)%,正常组为68.71±17.79、(23.87±6.66)×106/ml、(13.21±2.82)%、(11.30±6.60)%,两组比较差异均有显著性(P<0.05)。结论:弓形虫感染对雄性小鼠睾丸生精功能有一定的影响。  相似文献   

2.
不同浓度七氟烷对老年大鼠认知功能的影响   总被引:2,自引:1,他引:1  
目的 探讨不同浓度七氟烷对老年大鼠认知功能的影响.方法 18月龄雄性SD大鼠40只,体重500~650 g,随机分为3组,对照组(C组,n=8)吸入空气,1.5%七氟烷组(S1组,n=16)吸入1.5%七氟烷2 h,3.0%七氟烷组(S2组,n=16)吸入3.0%七氟烷2 h.于吸入七氟烷后1、7 d(T1.2)S1组和S2组随机取8只大鼠,采用Y型迷宫实验行认知功能测试,认知功能测试后12 h时处死大鼠,断头取脑,采用RT-PCR方法测定左侧海马N-甲基-D-天冬氨酸受体2B亚基(NR2B)mRNA表达,采用免疫组化法检测右侧海马NR2B蛋白表达.结果 与C组比较,S2组吸入七氟烷后1 d大鼠认知功能减退,右侧海马NR2B蛋白、左侧海马NR2B mRNA表达上调(P<0.05),S1.组上述指标差异无统计学意义(P0.05).结论 吸入1.5%七氟烷后老年大鼠认知功能无明显变化;吸入3%七氟烷后1 d老年大鼠认知功能减退,可能与其上调海马含2B亚基的NMDA受体表达有关.  相似文献   

3.
目的探讨淫羊藿苷对酒精致雄性小鼠生殖损伤的保护作用,为临床治疗酒精致男性不育提供理论依据。方法成年雄性小鼠随机分为正常组(蒸馏水)、模型组(酒精组)和给药组(酒精+淫羊藿苷组),灌胃5周后处死并制备附睾精子悬液,分别测定精子密度、精子活动率、存活率、精子畸形率;JC-1染色法检测线粒体膜电位改变;制备睾丸组织切片,观察睾丸组织病理改变。结果模型组小鼠精子密度、精子活动率和存活率明显低于正常组,精子畸形率明显增加;给药组精子密度、精子活动率和存活率较模型组明显升高,精子畸形率明显降低。线粒体膜电位分析,模型组去极化细胞(凋亡细胞)比例明显高于正常组;给药组去极化细胞(凋亡细胞)比例低于模型组。睾丸组织切片观察发现,与正常组比较,模型组生精细胞层数减少,结构紊乱稀疏;给药组生精小管结构明显改善。结论淫羊藿苷对酒精致雄性小鼠生殖损伤有一定保护作用。  相似文献   

4.
目的研究雄鼠睾丸Clock基因沉默后,小鼠精子顶体酶的活性及功能。方法在ICR小鼠睾丸内注射Clock干扰质粒干扰雄性小鼠睾丸节律基因Clock的表达,研究:(1)进行体外受精,观察精子驱散卵丘颗粒细胞情况及受精率等;(2)检测精子顶体内顶体蛋白酶、透明质酸酶活性及芳香基硫酸酯酶A(ASA)的含量。(3)将精子注射入卵母细胞,观察受精卵及胚胎发育情况。结果睾丸Clock基因沉默后,精子驱散卵丘颗粒细胞时间延长,受精率下降;精子顶体蛋白酶活性下降;透明质酸酶活性和ASA含量无明显变化;干扰组精子对卵母细胞及胚胎发育的影响小于未干扰组(P0.05)。结论干扰睾丸Clock基因表达后,影响精子顶体蛋白酶活性,从而影响雄性小鼠的生殖功能。  相似文献   

5.
交变磁场照射对小鼠睾丸生殖功能的影响   总被引:2,自引:0,他引:2  
目的:探讨交变磁场的物理作用与生物学效应的关系,研究磁场对小鼠睾丸生殖功能的影响。方法:30只ICR雄性小鼠随机均分为正常对照组、X线照射组、弱磁场(1000Hz)组、强磁场(2000Hz)1h组和强磁场2h组。照射后7d处死小鼠,分析附睾精子活率,对睾丸组织切片行HE染色观察睾丸病理组织变化,以Johnsen评分标准,评定睾丸变化积分。结果:精子活率正常对照组为(42.37±10.24)%,X线照射组为(39.00±12.35)%,弱磁场组为(36.00±17.28)%,强磁场1h组为(10.72±5.67)%,强磁场2h组为(4.44±2.87)%,强磁场1h组和2h组与正常对照组比较,精子活率明显下降(P<0.01)。睾丸病理变化Johnsen评分随着交变磁场的加大和时间延长积分越低,睾丸损伤越严重。结论:强、弱磁场均引起小鼠睾丸功能破坏,导致生精小管损伤,间质、间质细胞损坏,基膜增厚,腔内生精细胞排列紊乱,凋亡、坏死和脱落增多,导致无精子发生。  相似文献   

6.
目的评价N-甲基-D-天冬氨酸受体(NMDA受体)在七氟烷麻醉致老龄小鼠海马神经元程序性坏死中的作用。方法清洁级健康雄性C57BL/6小鼠90只, 18月龄, 体重27~30 g, 采用随机数字表法分为3组(n=30):对照组(C组)、七氟烷麻醉组(S组)和七氟烷麻醉+NMDA受体拮抗剂盐酸美金刚组(S+M组)。S组和S+M组小鼠连续3 d吸入3%七氟烷2 h, S+M组于每次吸入七氟烷前1 h腹腔注射盐酸美金刚20 mg/kg, C组只吸入纯氧。分别于麻醉前1 d、麻醉后3和7 d时每组随机取10只小鼠行Morris水迷宫实验。Morris水迷宫实验结束后立即处死小鼠取海马, 于光镜下观察病理学结果, 采用流式细胞术测定神经元程序性坏死率和胞浆游离钙离子浓度([Ca2+]i), Wes-tern blot法检测NMDA受体亚型GluN2A、GluN2B和受体相互作用蛋白激酶1(RIP1)的表达。结果与C组比较, S组和S+M组麻醉后各时点逃避潜伏期延长, 穿越原平台位置次数减少, 海马[Ca2+]i和神经元程序性坏死率升高, GluN2A、GluN2B和RIP1表达上调(P<0...  相似文献   

7.
反复吸入七氟烷对老年大鼠认知功能的影响   总被引:2,自引:0,他引:2  
目的 评价反复吸入七氟烷对老年大鼠认知功能的影响.方法 健康Wistar大鼠24只,月龄18月,体重270-450 g,雌雄各半,随机分为3组(n=8):对照组(C组)、2%七氟烷组(S1组)和3%七氟烷组(S2组).C组不吸入七氟烷;S1和S2组分别吸入2%、3%七氟烷,100 min/d,连续5d.于干预结束后1-6d(T1-6)时进行水迷宫实验,记录T1-5时游泳时间和游泳距离及T6时第4象限探索时间和游泳距离.于最后1次水迷宫实验结束后60 min处死大鼠,取海马组织,采用RT-PCR法测定海马N-甲基肌天冬氨酸受体(NMDAR)、NR1和NR2B mRNA的表达.结果 与C组比较,S1组T1时游泳时间和游泳距离延长.T6时第4象限探索时间缩短,NMDAR mRNA表达上调(P<0.05),NRI和NR2B mRNA的表达差异无统计学意义(P<0.05).结论 反复吸入2%七氟烷不会导致老年大鼠认知功能减退;而反复吸入3%七氟烷可导致一过性认知功能减退.  相似文献   

8.
目的 探讨长期低浓度吸入七氟烷对雌性小鼠生殖激素的影响. 方法 性成熟雌性昆明小鼠32只,按随机数字表法分为对照组和七氟烷组,其中七氟烷按吸入浓度分为30、100、300 ppm(parts per million,1×10-6)3组,每组8只.七氟烷组每天吸入对应浓度七氟烷6h,连续吸入4周,对照组吸入等量空气.实验前和4周后分别取小鼠静脉血用酶联免疫法检测血清促黄体生成素(serum luteinizing hormone,LH)、促卵泡成熟激素(follicle stimulating hormone,FSH)、雌二醇(estradiol-2,E2)浓度,组织学观察小鼠卵母细胞形态. 结果 对照组、30 ppm组和100 ppm组卵母细胞形态完整,胞质均匀;300 ppm组卵母细胞完整,但胞质出现空泡异常.实验后300 ppm组LH浓度为(3.15±0.52) U/L、FSH(4.9±1.6) U/L,较实验前及其他3组升高(P<0.05);而实验后300 ppm组E2浓度为(4.9±2.9) pmol/L,较实验前及其他3组也降低(P<0.05). 结论 慢性吸入低于100 ppm七氟烷对雌性小鼠生殖激素无影响,高于300 ppm可能有生殖损害.  相似文献   

9.
目的 通过对雄性新西兰兔精液中精子质量及受精能力的检测,观察睾丸大体形态及精子细胞超微结构的改变,探讨局部振动对雄性兔的生殖功能的影响.方法 将新西兰兔随机分为A组(接振强度为3.02m/s2)、B组(接振强度为6.13m/s2)、C组(接振强度为12.26m/s2)和1个对照组.于接振后30d测定精浆中精子的密度、活动力、活动率、畸形率,通过去透明带仓鼠卵-精子穿透试验和精子低渗膨胀试验评价精子的受精能力,光镜下观察睾丸组织学变化,电镜下观察睾丸精子细胞超微结构的改变.结果 接振试验后与对照组相比较,A、B、C 3个试验组新西兰兔精液精子活动率、活动力明显降低(P<0.01);精子的畸形率明显升高(P<0.05).精子的受精率及尾部肿胀的精子比率明显降低(P<0.05).睾丸生精细胞数量减少,精子细胞的部分细胞器破坏、裂解、坏死.结论 后肢接振试验可降低精子的活动力、活动率及卵子受精率及低渗肿胀率,增加精子的畸形率,睾丸组织中生精细胞减少,精子细胞的部分细胞器破坏、裂解、坏死,从而抑制精子的成熟,影响生殖功能.  相似文献   

10.
目的 观察通痹合剂对雄性大鼠性激素水平及生殖功能的影响.方法 27只成熟雄性SD大鼠,随机分成3组:正常组、合剂1组和合剂2组每组9只.对照组喂服生理盐水10ml/kg·d-1,合剂1组喂服合剂30g/kg·d-1,合剂2组喂服合剂10g/kg·d-1,60d后处死.检测睾丸系数、精子密度、形态、活力等及血清生殖激素(T、FSH、LH、E2).光镜观察睾丸和附睾组织的病理变化.结果 各组间血清生殖激素水平无统计学差异(P>0.05).与正常组比较,合剂1组睾丸系数、精子密度显著下降(P<0.01),合剂2组无统计学差异(P>0.05).给药组精子形态异常,活动力丧失.光镜下合剂1组睾丸组织严重损伤,合剂2组睾丸组织几乎无损伤.结论 通痹合剂具有明显的抗雄性生育作用,其影响程度呈剂量-效应关系.  相似文献   

11.
The reproductive toxicity of the insecticide methamidophos was studied in male mice. Adult male mice were treated by gavage with methamidophos at doses of 0, 1, 2 and 3 mg kg(-1) day(-1) for 4 weeks before mating with untreated females. Brain and skeletal muscle acetylcholinesterase activity was inhibited in the middle- and high-treated groups. Methamidophos treatment was associated with a decreased number of live foetuses and an increased number of dead and resorption foetuses at 2 and 3 mg kg(-1) day(-1) treated groups. The per cent morphologically normal spermatozoa were affected in the 2 and 3 mg kg(-1) day(-1) dose groups; however, sperm motility and count were decreased in the same treated groups compared to the control. Histological examination of brain, muscles, testes and epididymis revealed histological abnormalities in a dose-dependent manner. The current study demonstrated adverse effects of male methamidophos exposure on pregnancy outcome with effects on sperm parameters at 2 and 3 mg kg(-1) day(-1) .  相似文献   

12.
Pesticides can be toxic to desirable plants and animals, including humans. The aim of this study was to investigate the reproductive effects of low doses of pesticides on male offspring of exposed pregnant mice. Three groups of five female mice were treated daily by oral gavage with dimethoate (5 mg kg(-1) per day), deltamethrin (5 mg kg(-1) per day) and their mixture at 5 mg kg(-1) per day from day 3 to day 21 of pregnancy. Fertility, sexual behaviour and a number of reproductive endpoints, such as organ weights, sperm evaluations and testicular histology, were examined on four adult male offspring of exposed pregnant mice. When compared with control, a dose of deltamethrin 5 mg kg j(-1) causes a decrease in the absolute and relative weight of the testes of exposed mice and it affects their fertility by reducing the density, mobility and vitality of sperm and increasing the number of abnormal forms of these cells (P ≤ 0.01). The same results were obtained in mice exposed to a dose of 5 mg kg j(-1) combination of dimethoate and deltamethrin. This study demonstrated that deltamethrin and combination of dimethoate and deltamethrin caused a decrease in the absolute and relative weight of the testes, which affected the sperm parameters of male offspring of exposed mice to a low dose of these pesticides during pregnancy.  相似文献   

13.
Objectives:To document the effect of progesterone exposure with large dose and long term on spermatogenesis,especially on the germ cell apoptosis in rats.This study was also to evaluate the toxicity of progesterone in the reproductive system when administered with large doses and long term in men.Methods:Groups of adult male SD rats were administered with 37.5,75 and 150 mg/kg depot-medroxyprogesterone acetate(DMPA)per two-weeks for 12 or 18 weeks.At the end of treatment,each male rat was paired with one adult female SD rat to estimate the reproductive function.Serum testosterone concentration was analyzed in duplicate by radioimmunoassay(RIA).The pathological changes of testes,epididymis,and prostate were checked under light microscopic,epididymis was also used for sperm count,and fresh testis tissue was used for apoptosis assessment by flow cytometry.Results:After treatment with DMPA,weights of gonad,the ratio of testes/body,the ratio of epididymides/body,and the ratio of prostate/body decreased significantly(P<0.01).The level of serum testosterone,sperm count,sperm activity decreased significantly(P<0.01)while abnormality of sperm increased significantly(P<0.01).The embryonic number in uterus of pairing female rat decreased significantly after DMPA treatment.Compared with control,the number and the ratio of apoptotic germ cell increased dramatically(P<0.01)along with dose increase or treating prolongation of DMPA,which analyzed by flow cytometry.Conclusion:In summary,in addition to inhibition of pituitary gonadotrophin and subsequently deprivation of androgen,progesterone(DMPA)inhibits spermatogenesis by the induced germ cell apoptosis.The reproductive toxicity of DMPA administrated with large doses and long term is confirmed.  相似文献   

14.
Testicular tumors in mice exposed in utero to diethylstilbestrol   总被引:3,自引:0,他引:3  
Treatment of pregnant women with diethylstilbestrol (DES) is associated with the subsequent development of reproductive tract abnormalities such as epididymal cysts, retained hypotrophic testes and sperm abnormalities in their male offspring. It recently has been suggested that prenatal DES exposure is associated with development of testicular seminoma in humans. Studies of in utero exposure of laboratory animals to DES are few, but previous reports from our laboratory have described several abnormalities in the reproductive tract of the mouse following prenatal DES exposure. To study the possible association of testicular tumors and prenatal DES exposure in mice, pregnant outbred CD-1 mice were injected subcutaneously with daily doses of DES (100 micrograms./kg.) on days nine through 16 of gestation. DES-exposed and age-matched control male mice were sacrificed at 10 to 18 months of age and examined for testicular lesions. In addition to the nonmalignant abnormalities reported in previous studies such as 91% cryptorchidism and degenerative changes, interstitial cell tumors were observed in nine mice among 277 mice treated prenatally with DES. Two of these lesions were benign tumors and five were interstitial cell carcinomas. Rete testis adenocarcinoma was seen also in 5% of these DES-treated animals and is described in another report. The overall incidence of testicular tumors is 8% in DES-exposed male mice. No comparable lesions were seen in 122 control male mice. These results suggest that the testicular lesions that can occur following prenatal DES exposure include neoplasia. The combined prevalence of DES-induced tumors of the corpus testis and rete testis in mice suggests the male offspring may be more at risk for developing carcinoma of the reproductive tract than the female offspring.  相似文献   

15.
醋酸铅对雄性小鼠生殖功能的毒性作用   总被引:6,自引:0,他引:6  
目的 探讨醋酸铅对雄性小鼠生殖功能的毒性作用。 方法 不同浓度醋酸铅 ( 1 .5、6及 2 4mg/kg)腹腔注射 4周龄雄性小鼠 ,共 1 0次。 50d后与正常雌鼠合笼交配 ( 1∶2 ) ,观察雌鼠受孕率、胚胎总数、异常胚胎数 (率 )、胎鼠重量 ;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、醋酸铅各组合笼 2 1d,雌鼠受孕率和胚胎总数无显著差异 (P >0 .0 5)。醋酸铅 2 4mg/kg组异常胚胎数 (率 )显著高于对照组和 1 .5mg/kg组 (P <0 .0 5) ,胎鼠重量和雄鼠睾丸指数显著低于对照组 (P <0 .0 5)。其他实验组异常胚胎率、胎鼠重量和雄鼠睾丸指数与对照组比较无显著性差异。各实验组附睾精子数显著低于对照组 (P <0 .0 5,P <0 .0 0 5) ,附睾精子畸形率显著高于对照组 (P<0 .0 5,P <0 .0 0 5) ,中、高浓度醋酸铅组附睾精子活动率显著低于对照组 (P <0 .0 5)。 结论 醋酸铅 2 4mg/kg处理雄鼠对睾丸、精子数量和质量、合笼雌鼠胚胎产生影响。 1 .5及 6mg/kg只影响精子数量和质量而不影响生殖功能和子代。合笼雌鼠异常胚胎率增高和胎鼠重量下降可能与醋酸铅引起精子质量下降有关  相似文献   

16.
OBJECTIVE: Given that anesthesia and surgery are known by their immunomodulatory effects, we aimed to compare the immune response after 1 or 3 anesthetic exposures to sevoflurane in a murine model without surgery. MATERIAL AND METHODS: Young adult male mice, non-controlled for body conformation, were exposed 1 (group S1) or 3 times (group S3) to 3% sevoflurane in oxygen (1.2 maximum alveolar concentration) for 40 minutes. Untreated animals were used as controls. Three days after in vivo exposure to sevoflurane, the cellular composition of peripheral blood and of the spleen were studied. We also studied the in vivo response to exogenous (sheep red blood cells: SRBC) and endogenous antigens (heat shock proteins: HSP 65 and HSP 70) as well as biomarkers of toxicity. RESULTS: The number of leukocytes in peripheral blood decreased in S3 animals, and the number of lymphocytes decreased in both groups. B cells in spleen decreased only in the S1 group, but an increased in vivo response to SRBC was seen in both S1 and S3 mice in comparison with the control animals. Re-exposure to sevoflurane led to a decrease in immunoglobulin G response only to HSP 70. Plasma markers of liver and kidney function did not change after anesthetic exposure. CONCLUSION: Changes in leukocyte populations in peripheral blood and in antibody-producing capacity occur after either a single exposure or repeated exposures to sevoflurane. However no changes occur in biomarkers of toxicity.  相似文献   

17.
Aim: To evaluate the effect of oxidative stress on the spermatogenesis and lactate dehydrogenase-X (LDH-X) activity in mouse testis. Methods: For creating different levels of oxidative stress in mice, three selenium (Se) level diets were fed in separate groups for 8 weeks. Group 1 animals were fed yeast-based Se-deficient (0.02 ppm) diet. Group 2 and Group 3 animals were fed with the same diet supplemented with 0.2 ppm and 1 ppm Se as sodium selenite, respectively. After 8 weeks, biochemical and histopathological observations of the testis were carried out. LDH-X levels in the testis were analyzed by western immunoblot and ELISA. Results: A significant decrease in testis Se level was observed in Group 1 animals, whereas it was enhanced in Group 3 as compared to Group 2. The glutathione peroxidase (GSH-Px) activity was significantly reduced in both the liver and testis in Group 1, but not in Group 2 and 3. A significant increase in the testis glutathione-S-transferase (GST) activity was observed in Group 1,whereas no significant change was seen in Groups 2 and 3. Histological analysis of testis revealed a normal structure in Group 2. A significant decrease in the germ cell population in Group 1 was observed as compared to Group 2 with the spermatids and mature sperm affected the most. Decrease in the lumen size was also observed. In the Se-excess group (Group 3), displacement of germ cell population was observed. Further, a decrease in the LDH-X level in testis was observed in Group 1. Conclusion: Excessive oxidative stress in the Se deficient group, as indicated by changes in the GSH-Px/GST activity, affects the spermatogenic process with a reduction in mature sperm and in turn the LDH-X level. (Asian J Androl 2004 Sep; 6: 227-232)  相似文献   

18.
Four groups (minimum of 10/dose group) of male Dutch-belted rabbits were treated daily with dibromoacetic acid (DBA) via drinking water beginning in utero from gestation day 15 to adulthood; target dosages were 1, 5, and 50 mg DBA/kg body weight. Developmental, prepubertal as well as postpubertal reproductive sequelae were evaluated. One (out of 22), 2 (out of 32), and 1 (out of 21) male offspring in the 1, 5, and 50 mg DBA/kg groups were unilaterally cryptorchid. There were no significant differences in serum follicle-stimulating hormone, luteinizing hormone, and testosterone (basal concentrations or in response to exogenous gonadotropin-releasing hormone) in both prepubertal and adult rabbits. Chronic exposure to DBA adversely affected the mating abilities of some rabbits. The number of sperm produced was not affected, but spermiogenesis was disrupted, resulting in unique sperm acrosomal-nuclear malformations even at the 1-mg dose level. Concentrations of SP22, a specific sperm membrane fertility protein, in detergent extracts of ejaculated sperm were significantly lower (P < .05) in all DBA-treated groups compared with controls. The conception rates following artificial insemination of a constant number of sperm for 1, 5, and 50 mg DBA/kg groups were 55% (10/18), 65% (13/20), and 55% (9/16), respectively, vs 85% (17/20) for control group. Histologic lesions in testes characterized by spermatogenic arrest predominantly at the round spermatid stage, pyknosis of differentiating germ cells, and ultimate degeneration and desquamation leaving focal vacuolation in seminiferous epithelium were evident in DBA-treated groups. Thus, male rabbits exhibit reproductive toxicity with exposure to DBA during reproductive development at dosages as low as 1 mg/kg body weight.  相似文献   

19.
Spermatogenesis, fertility and sexual behavior in a hypospadiac mouse model   总被引:2,自引:0,他引:2  
PURPOSE: Administering of flutamide to pregnant mice causes hypospadias in male offspring. We investigated spermatogenesis, fertility and sexual behavior in this hypospadiac mouse model. MATERIALS AND METHODS: Male offspring exposed to flutamide during the embryonic period were divided into hypospadiac group 1 and normal external genitalia group 2. Control group 3 consisted of male offspring not exposed to flutamide. We analyzed the spermatogenesis, epididymides sperm motility, in vitro fertilization rate and sexual behavior of each mouse. RESULTS: There were no significant differences in the weight of the testes or mean seminiferous tubular diameter in the groups. The number of apoptotic germ cells per unit area was not significantly different in the 3 groups. In groups 1 to 3 there were no significant differences in the mean epididymides sperm motility rate plus or minus standard deviation (62.6% +/- 10.0%, 57.2% +/- 7.0% and 67.0 +/- 7.6%) or in the in vitro fertilization rate (52%, 48% and 48%, respectively). However, there were significant differences in groups 1 to 3 in mean mounting frequency (0, 29 +/- 4.0 and 12.4 +/- 4.5 times per hour) and mean intromission frequency (0, 24.4 +/- 3.5 and 3.8 +/- 1.5 times per hour, respectively). Females coupled with group 1 or 2 male mice did not achieve pregnancy. CONCLUSIONS: These results suggest that spermatogenesis, sperm motility and fertilization in vitro were unaffected in hypospadiac mice but sexual motivation and arousal were deficient.  相似文献   

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