吸烟对雄性小鼠睾丸间质细胞、睾酮及精子数量的影响

目的探讨吸烟对雄性小鼠的睾丸间质细胞、血清睾酮含量及附睾精子数量的影响。方法雄性小鼠50只,随机分为5组,即经吸烟处理后6周、12周(吸烟组),未经特殊处理的6周、12周小鼠(对照组),及吸烟6周后戒烟6周(戒烟组)小鼠。对5组小鼠睾丸组织进行HE染色,光镜下观察支持细胞、问质细胞形态及结构;免疫组化方法分别计数5组小鼠睾丸支持细胞及问质细胞数量;利用酶联免疫法(ELIsA)测定小鼠体内睾酮含量:用石墨炉原子吸收光谱法测定血清镉含量;同时计数附睾精子数。结果 HE染色可见吸烟6周小鼠睾丸问质细胞数量减少;吸烟12周小鼠睾丸问质细胞数量稀少甚至消失:而睾丸支持细胞数量及形态与对照组相比未见明显改变。免疫组化发现吸烟组小鼠睾丸支持细胞数量与对照组相比无显著差异(P0.05)。问质细胞数量随吸烟时间延长而显著减少(P0.01);小鼠血清中睾酮水平吸烟组明显低于对照组(P0.01),且随吸烟时间的延长而下降(P0.01):吸烟组小鼠附睾精子汁数较对照组显著下降(P0.01),并且与吸烟时间呈正相关(P0.01)。而戒烟组中,睾丸问质细胞、血清睾酮含量、附睾精子数量3组数据都较吸烟组增高。结论吸烟可导致睾丸间质细胞的破坏,影响体内睾酮的生成,进而导致生精障碍,而戒烟可逆转此现象。     

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。     

小鼠单侧睾丸损伤后环孢素A对Fas系统的影响

目的 :研究昆明小鼠 (KM小鼠 )单侧注射冰乙酸致睾丸损伤后环孢素A(CsA)对对侧睾丸生精功能和Fas系统表达的影响。　方法 :6 0只KM小鼠随机分为 4组 :A组为对照组 ,B组为单侧睾丸损伤组 ,C组为单侧睾丸损伤后 6h切除损伤睾丸组 ,D组为单侧睾丸损伤后 6h内开始腹腔注射CsA组。 4周后取对侧附睾尾 ,计数精子及其活率 ,对侧睾丸作石蜡切片苏木精 伊红染色和免疫组化链霉素抗生物素蛋白过氧化物酶连结 (SP)法检测Fas和FasL的表达。　结果 :D组附睾尾精子和活率计数显著高于B组 (P <0 .0 5 ) ,D组的FasL和Fas较B组显著降低 (2 4 .3± 7.0vs37.8± 5 .8和 17.8± 4 .3vs32 .4± 3.6 ,P <0 .0 5 )。　结论 :KM小鼠单侧睾丸损伤后CsA可以通过抑制Fas和FasL的表达 ,降低生精细胞凋亡 ,维持生精功能的稳定     

淫羊藿苷对模拟高原环境下雄性大鼠生殖系统损伤的保护作用研究

目的 研究淫羊藿苷对模拟高原环境下雄性大鼠生殖系统损伤的保护作用,并初步探讨相关作用机制。方法 选取30只12周龄雄性Wistar大鼠,随机分为平原对照组、高原模型组以及淫羊藿苷实验组,每组10只。平原对照组饲养于本院动物实验中心(海拔1 400 m),高原模型组以及淫羊藿苷实验组置入模拟海拔高度6 000 m高原环境动物实验舱;淫羊藿苷实验组给予100 mg/kg淫羊藿苷悬浊液于每日上午9时舱内灌胃,其余两组给予等体积生理盐水灌胃。模拟高原环境干预满30 d后麻醉取材,睾丸组织称重后一侧多聚甲醛固定用于进行苏木素-伊红(HE)染色观察大鼠睾丸组织形态学改变,一侧破碎匀浆处理用于检测超氧化物歧化酶(SOD)、丙二醛(MDA)氧化应激指标检测;附睾尾制备成精子悬液,检测精子质量。取大鼠血清检测睾酮(T)、黄体生成素(LH)、卵泡刺激素(FSH)等激素水平。结果 (1)高原模型组与淫羊藿苷实验组的体重增长显著低于平原对照组(P<0.05),且高原模型组睾丸指数显著低于平原对照组与淫羊藿苷实验组(P<0.05)。(2)HE染色结果示,高原模型组睾丸组织生精小管内各级生精细胞排列不...     

雄激素受体敲除后雄性小鼠的泌尿生殖系统表型

目的　了解敲除雄激素受体 (AR)后雄性小鼠的泌尿生殖系统表型。　方法　采用Cre lox技术 ,雌性Flox AR小鼠与雄性ACTB Cre小鼠交配 ,PCR方法检测子代小鼠尾巴的基因型 ,筛选出AR敲除小鼠 5只 ,5只AR未被敲除的小鼠作为对照。比较 2组小鼠的泌尿生殖系统表型 ,测量肛门生殖器距离、睾丸重量、血清睾酮及雌二醇浓度。　结果　AR敲除 (ARKO)组小鼠肛门生殖器距离为 (0 .5± 0 .1)cm ,对照组为 (1.1± 0 .1)cm。ARKO组前列腺、精囊、附睾及球海绵体肌均缺如 ,睾丸显著缩小 ,重量 (0 .0 0 6± 0 .0 0 1) g ;对照组前列腺、精囊、附睾及球海绵体肌发育正常 ,睾丸重量为 (0 .0 86± 0 .0 0 2 ) g。ARKO组血清睾酮浓度 (0 .0 5 6± 0 .0 4 5 )nmol/L ,雌二醇浓度 (1390 .1± 2 94 .3) pmol/L ,对照组睾酮浓度 (0 .84 3± 0 .736 )nmol/L ;雌二醇浓度 (786 .2± 15 0 .8) pmol/L。差异均有统计学意义 (P <0 .0 5 )。　结论　敲除雄激素受体后 ,小鼠前列腺、精囊、附睾及球海绵体肌缺如 ,睾丸缩小 ,雄激素水平降低 ,雌激素水平升高 ,提示AR在雄性小鼠泌尿生殖系统发生及雄激素水平调节中发挥重要作用。     

果糖二磷酸锶盐对雷公藤多甙所致的大鼠少精子症的治疗作用

目的:研究果糖二磷酸锶盐(FDP-Sr)对雷公藤多甙(GTW)所致雄性大鼠少精子症的治疗作用。方法:雄性SD大鼠随机分成3组:模型组,FDP-Sr组,正常组,每组10只。模型组灌胃GTW 30 mg/(kg.d)连续40 d造成大鼠少精子症模型;FDP-Sr组经过GTW造模后,灌胃FDP-Sr 200 mg/(kg.d),连续30 d;实验期间正常组则给予蒸馏水。观察3组大鼠的性腺指数(包括睾丸、附睾、包皮腺、精囊腺)、附睾精子数量及活动率、睾丸组织病理形态学,并测定血清睾酮水平,以及睾丸内酸性磷酸酶(ACP)、乳酸脱氢酶(LDH)、琥珀酸脱氢酶(SDH)的活性。结果:睾丸和精囊腺指数(%):正常组:0.71±0.04,0.29±0.04;模型组:0.37±0.04,0.25±0.05;FDP-Sr组:0.45±0.07,0.31±0.06,与模型组相比,显著提高(P<0.05);附睾精子的数量(×106/m l):正常组:59.87±11.28;模型组:11.06±2.53;FDP-Sr组:20.95±4.98,与模型组相比,明显增加(P<0.05);血清睾酮含量(ng/L):正常组:85.31±7.41;模型组:65.33±2.90;FDP-Sr组:75.32±5.34,与模型组相比,明显增加(P<0.05);ACP、LDH、SDH的活性(U/g prot):正常组:95.64±19.27,9 574.73±3 578.06,6.39±1.93;模型组:58.42±12.38,4 820.77±1 535.22,3.48±0.91;FDP-Sr组:83.74±21.30,7 649.01±3 123.02,5.59±1.75,与模型组相比,明显增加(P<0.05)。另外,经FDP-Sr治疗后,睾丸生精上皮损伤明显改善。结论:FDP-Sr对大鼠少精子症有明显改善,其治疗效果与FDP-Sr改善睾丸功能密切相关。     

淫羊藿苷对酒精致雄性小鼠生殖损伤的影响

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。     

急性弓形虫感染对雄性小鼠睾丸生精功能影响的初步研究

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。     

交变磁场照射对小鼠睾丸生殖功能的影响

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。     

L-肉碱对糖尿病大鼠生精细胞凋亡及附睾精子数量和活动率的影响

目的:探讨L-肉碱(LC)对糖尿病(DM)大鼠生精细胞凋亡及附睾精子数量和活动率的影响。方法:24只雄性SD大鼠随机均分为3组,一组作为对照组,剩余两组分别注射链脲佐菌素(STZ,65 mg/kg)建立DM模型。建模成功后,各组大鼠分别给予如下灌胃剂量:对照组:生理盐水;DM模型组:生理盐水;LC组:300 mg/kgLC溶液,连续灌胃6周。末次给药24 h后,麻醉处死所有大鼠,分别进行附睾精子计数并检测精子活动率,流式细胞术检测各组大鼠睾丸生精细胞凋亡情况。结果:用LC治疗后的大鼠附睾头、尾精子活动率(%)分别为53.7±1.8和60.3±1.6,显著高于DM模型大鼠(分别为32.2±2.0和40.5±1.4,P<0.05),但低于对照组大鼠精子活动率63.1±2.4和68.9±1.3。与对照组附睾尾精子相对计数[(37.8±1.1)×106/100 mg]相比,DM组显著减少[(25.5±1.1)×106/100 mg],且具有统计学差异(P<0.05);LC治疗后大鼠附睾尾精子相对计数[(32.0±1.5)×106/100 mg]比DM组显著增加(P<0.05),但仍低于对照组。与对照组生精细胞凋亡率[(3.7±1.3)%]相比,DM组生精细胞凋亡率[(52.5±4.4)%]显著上升(P<0.05);经LC治疗后,LC组大鼠生精细胞凋亡率为(35.3±3.5)%,比DM组显著降低(P<0.05),但仍显著高于对照组。结论:LC(300 mg/kg)灌胃DM大鼠6周,可以减少DM大鼠生精细胞凋亡,增加附睾精子数量,提高精子活动率。     

Antispermatogenic and hormonal effects of Crotalaria juncea Linn. seed extracts in male mice

Aim: To evaluate the antifertility activity of various extracts of Crotalaria juncea seeds in male mice. Methods: Adult male mice were gavaged the petroleum ether, benzene and ethanol extracts of C. juncea seeds, 25 mg·(100g)-1·day-1 for 30 days. On day 31 the animals were sacrificed by cervical dislocation and the testes, epididymis, vas deferens, seminal vesicles, prostate gland, bulbourethral gland and levator ani were dissected out and weighed. The organs were processed for biochemical and histological examination. Results: In petroleum ether, benzene and ethanol extracts treated rats, there was a decrease in the weights of testis and accessory reproductive organs. The diameters of the testis and seminiferous tubules were decreased. Spermatogonia, spermatocytes and spermatids in the testis and the sperm count in cauda epididymis were also decreased. There was a significant reduction in the protein and glycogen contents and an increase in the cholesterol content in the testis, epididymis and vas def     

Antifertility effect of ethanolic extract of Amalakyadi churna in male albino mice

Aim: To evaluate the antifertility activity of the ethanolic extract of Amalakyadi churna by oral administra-tion in male albino mice. Methods: The ethanol extract of Amalakyadi churna at the dose of 250 mg/kg and 400 mg/kg body weight was administered orally for 30 days to adult male mice. On day 31, the mice were sacrificed and the testis and accessory reproductive organs were removed and weighed. The organs were processed for biochemical estimation and histological work. Results: Treatment with Amalakyadi chuma resulted in decrease in the weights of testis and accessory reproductive organs. The diameters of testis, seminiferous tubules and Leydig cell nucleus were decreased. The spermatogenic elements, like spermatogonia, spermatocytes and spermatids in the testis were re-duced significantly as well as the sperm count in cauda epididymis. There was a significant reduction in the protein,glycogen, DNA and RNA contents and the activity of acid phosphatase in the testis of extract treated mice compared with the control. The cholesterol content and the alkaline phophatase activity were increased significantly in treated mice. Conclusion: Amalakyadi churna extract arrests spermatogenesis in male mice without noticeable side effects.(Asian J Andro12003 Sep; 5: 247-250)     

印楝油复合物对雄性小鼠的抗生育作用研究

目的探讨印楝油复合物对雄性小鼠的抗生育作用。方法昆明种雄性小鼠口服印楝油复合物2ml/kg.d~(-1),在灌胃1周、2周和3周后。分别将正常性成熟雌鼠与雄鼠合笼,观察和统计怀孕率。灌胃至21d时,剖检灌胃雄鼠,采取睾丸和附睾组织固定,进行病理学和组织化学研究,并计算凝血时间和肉芽肿。结果印楝油复合物对附睾有一定程度的损伤,其靶器官为精母细胞和精子细胞,精原细胞未见明显损伤,睾丸间质疏松,附睾腔内精子密度降低,酸性磷酸酶和碱性磷酸酶活性增强。对血凝时间影响显著,具有一定的抗炎作用。结论印楝油复合物具有明显的抗生育作用,作用机制可能是通过影响生精细胞的代谢过程,从而引起生精细胞代谢障碍致使生精细胞发生变性、坏死。     

5-氟脲嘧啶诱发的小鼠睾丸形态学早期变化

目的:通过观察化疗药物5-氟脲嘧啶诱发小鼠睾丸组织形态学早期变化特点,提出一种简易实用的小鼠少精/弱精/无精模型制备方法,为相应生精机制研究和药物疗效观察提供方法学建议。方法:小鼠尾静脉一次性注射化疗药物5-氟脲嘧啶(250mg/kg),分别在注射前,以及注射后第3、7、11、14天取小鼠睾丸,制备石蜡切片,HE染色观察形态学变化。结果:小鼠睾丸内完整致密排列的生精小管管壁中各级精母细胞/精子细胞,在注射5-氟脲嘧啶之后第3、7、11天呈现进行性减少,管壁进行性变薄,在第11天达到最低点,并可见管壁明显肿胀和裂纹;第14天生精小管肿胀基本消失,但裂纹依然存在,可见精母细胞明显增多,但未见成熟精子。结论:小鼠尾静脉一次性注射5-氟脲嘧啶可能是一种简单、有效的化疗药物诱发生殖功能损伤动物模型制备方法。     

Effect of nitrofurazone on the reproductive organs in adult male mice

Aim: To study the effect of 5-nitro-2-furaldehyde semicarbazone (nitrofurazone), a derivative of nitrofuran, on male reproductive organs of Parkes (P) strain mice. Methods: Mice were given nitrofurazone orally at a dose of 64mg/kg body weight per day, for 10 and 20 days, and were killed 24 h and/or 56 days after the last treatment. Histological appearance of testis, motility and number of spermatozoa in cauda epididymidis, and biochemical indices in epididymis and seminal vesicle were evaluated. Results: Histologically, testis showed marked regressive changes in the seminiferous tubules in mice treated with nitrofurazone. Ten days after treatment, there was much depletion of germ cells in the seminiferous tubules, and the germinal epithelium was lined mainly with Sertoli cells, spermatogonia, spermatocytes, and a few round spermatids; intraepithelial vacuoles and multinucleated giant cells were also observed in tubules. By 20 days, regressive changes in the seminiferous tubules were further pronounced, and pachytene spennatocytes were the most advanced germ cells noticed in the tubules. In severe cases, the tubules were lined with a thin layer of Sertoli cells and spermatogonia. The treatment also caused marked reductions in the motility and number of spermatozoa in the cauda epididymidis, in weight and the level of fructose in the seminal vesicle, and in sialic acid level in the epididymis. Fifty six days after drug withdrawal, the alterations induced in the reproductive organs returned to control levels. Conclusion: Our results suggest that nitrofurazone treatment in P mice induces marked alterations in the male reproductive organs, and that the alterations are reversible following cessation of treatment.     

Effect of pineal indoles on testicular histology of mice

The effect of late afternoon injections of melatonin, 5-methoxytryptamine, 5-methoxytryptophol, and 5-methoxyindole-3-acetic acid on testicular histology in mice were examined. Melatonin and 5-methoxytryptophol injections caused a reduction in the diameters of seminiferous tubules. The tests of melatonin-treated animals underwent some detectable regressive changes in the seminiferous tubules, whereas administration of 5-methoxytryptamine or 5-methoxytryptophol appeared to cause atrophy in some tubules. The percentage of aspermic tubules in melatonin-treated and methoxytryptamine-treated mice was significantly higher than that of the control. In involuted testes, some seminiferous tubules contained only Sertoli cells together with spermatogonia and spermatocytes, but no discernible spermatids and spermatozoa. Regressing spermatids and cell debris were frequently observed in the tubules. The tested of mice that received daily injections of 5-hydroxytryptophol and 5-methoxyindole-3-acetic acid were indistinguishable from those of the controls.     

Acute effects and long-term sequelae of 1,3-dinitrobenzene on male reproduction in the rat. II. Quantitative and qualitative histopathology of the testis

This study determined the quantitative and qualitative histopathologic effects of a single oral dose of 1,3-dinitrobenzene (48 mg/kg) on the rat testis from 1 to 175 days postexposure. The testis was damaged severely by hour 24, as evidenced by increased numbers of regressive seminiferous tubules that exhibited degenerating pachytene spermatocytes, chromatin margination in spermatids, giant cells, deformed spermatid heads, retained spermatids, and reduced numbers of meiotic figures. The major effects during the first 48 hours posttreatment were degeneration or exfoliation of pachytene spermatocytes and round spermatids and the retention of step 19 spermatids. These regressive effects continued until 24 days, after which the tubules either recovered or became atrophic. At the end of the study (175 days), three males were normal, one had regressed testicles, and three males had atrophic tubules (15 to 45%). Several cellular abnormalities were common throughout the period. In addition, the frequency of the stages of spermatogenesis was altered, an indication of a disturbance in the kinetics of spermatogenesis. 1,3-Dinitrobenzene produced profound and specific lesions in the seminiferous tubules, and recovery was slow and incomplete. Atrophic tubules seemed to form if the normal cellular associations were not reestablished within 24 days, possibly due to the inability of Sertoli cells to reorganize the synchrony of germ cell development.     

Effects of estradiol-17β and bisphenol A administered chronically to mice throughout pregnancy and lactation on the male pups＇ reproductive system

AIM: To assess the effect of estradiol-17beta (E(2)) and bisphenol A (BPA) administered chronically by implanting a silicone tube throughout pregnancy and lactation on male pups' reproductive system in ICR mice. METHODS: Female mice were implanted with a tube filled with 10 ng, 500 ng, 1 microg, or 10 microg of E(2), or 100 microg or 5 mg of BPA, before mating. The tube was kept in the mice throughout pregnancy and lactation, until the pups had weaned at 4 weeks of age. During the period, E(2) was released from the tube at 120 pg or 6, 12 or 120 ng/day, and BPA at 1.2 or 60 microg/day. RESULTS: Most of the mice given 1 microg and 10 microg of E(2) did not maintain their pregnancy. However, the other groups showed high rates of birth, more than 70%. At age of 4 weeks, the male pups were killed. Body weight and reproductive organ weights (testes, epididymides and accessory reproductive glands) in the treated groups did not differ from the control values, whereas the percentage of seminiferous tubules in the testis with mature spermatids was significantly lower in the groups given 10 ng and 500 ng of E(2) and 5 mg of BPA than that in the control. CONCLUSION: Chronic exposure to E(2) and BPA might disrupt spermatogenesis in male pups.     

Spermatogenesis in Snell dwarf, little and congenitally hypothyroid mice

The status of spermatogenesis in Snell dwarf, little and congenitally hypothyroid mice was studied. In all of these mice with a hormone deficiency the seminiferous tubules were smaller in size and contained fewer spermatogonia, spermatocytes, spermatids and spermatozoa than did those of normal control mice. There was no substantial difference in the Johnsen score between the hormone-deficient mice and normal control mice, but the former had underdeveloped seminiferous tubules with a corresponding paucity of germ cells, which may be partly responsible for the infertility of these mice. In the present study, growth hormone and thyroxine were administered separately to growth hormone-deficient and thyroxine-deficient mice, respectively. Such replacement therapy brought about an increase in cell counts of the seminiferous tubules and in sperm counts in both groups.     

Reversible antifertility effect of aqueous leaf extract of Allamanda cathartica L. in male laboratory mice

The efficacy of oral administration of aqueous leaf extract of Allamanda cathartica (150 mg kg⁻¹ body weight day⁻¹ for 14, 28 and 42 days) in inducing infertility and changes in various male reproductive endpoints was evaluated in Parkes strain mice. The effect of the treatment on organ weight, histopathology, sperm parameters, testosterone level, haematology, serum biochemistry and on fertility indices was assessed. Histologically, testes in extract-treated mice showed nonuniform degenerative changes in the seminiferous tubules as both affected and normal tubules were observed in the same sections. The treatment also had adverse effects on motility, viability, morphology and on number of spermatozoa in the cauda epididymidis. Serum levels of testosterone, alanine aminotransferase, aspartate aminotransferase and creatinine, haematological parameters and liver and kidney histoarchitecture were, however, not affected by the treatment. Fertility of the extract-treated males was also suppressed, although the libido remained unaffected. By 56 days of treatment withdrawal, however, the above parameters recovered to control levels. Our results thus suggest that A. cathartica treatment causes reversible suppression of fertility in male mice, without causing detectable toxic effects.