邻苯二甲酸二丁酯宫内和哺乳期染毒对F_1代雄性大鼠的生殖发育毒性

目的　观察邻苯二甲酸二丁酯 (DBP)对F1代仔鼠的发育状况及性成熟期雄性仔鼠生殖系统损害情况 ,并期望得到现有文献中缺如的DBP对F1代仔鼠生殖发育毒性的最大无作用剂量 (NOAEL)。方法　选择在宫内暴露期和哺乳期 (受孕第 2天至仔鼠 2 1天断奶 ) ,通过灌胃方式给母鼠染毒 (DBP终浓度分别为 0、5 0、2 5 0和 5 0 0mg (kg·d) ,观察对仔鼠的影响。结果　DBP对母鼠无明显影响 ,中高剂量组 [2 5 0、5 0 0mg (kg·d) ]对F1代雄性仔鼠的出生体重、每窝活产数、体重增长及雄性仔鼠肛殖距有明显影响 ,对性成熟期雄性仔鼠生殖系统损害尤为严重 ,可观察到小睾丸、附睾发育不全甚至缺失、睾丸未降等现象 ,附睾尾精子参数和睾丸精子头计数及附睾、肝、肾、前列腺的脏器系数明显降低 ,而与激素合成相关的垂体系数却略有上升。低剂量组未观察到有害影响。结论　雄性生殖系统是DBP作用的主要靶器官 ,幼年敏感期所受的损害部分不可逆 ,并得到DBP经口染毒对F1代仔鼠生殖发育毒性的NOAEL为 5 0mg (kg·d)。据此 ,进一步提出DBP经口摄入的参考剂量 (RfD)为 5 0 0 μg (kg·d)。     

环境雌激素壬基酚对仔鼠精子的损伤作用

目的研究孕期暴露王基酚对雄性仔鼠精子的损伤作用。方法大鼠妊娠第14～19d灌胃染毒壬基酚（0、20、40、80、200mg／kg），仔鼠90d龄断头取血测睾酮，取睾丸和附睾称重，检测精子活动度和畸形率、附睾尾精子计数、睾丸每日精子生成量。结果与阴性对照组比较，80～200mg／kg组精子活动度、附睾尾精子计数、睾丸每日精子生成量显著下降，且与睾酮浓度正相关；精子畸形率与染毒剂晕正相关。结论孕期暴露壬基酚80mg／kg可损伤仔鼠生精功能。     

妊娠期和哺乳期双酚A暴露对子代雄性小鼠青春期启动及生精能力的影响

目的研究妊娠期和哺乳期双酚A(bisphenol A,BPA)暴露对子代雄性小鼠青春期启动及生精能力的影响。方法将24只健康清洁级C57BL/6妊娠小鼠按体重随机分为3组,分别为对照(含1%乙醇溶液)组和0.2、2.0μg/ml BPA染毒组,每组8只,单笼饲养。从妊娠第6天至哺乳期(仔鼠出生后21 d)结束,母鼠采用自由饮水方式进行染毒。断乳后,每组随机选取8只雄性仔鼠,断乳后正常喂养1个月。记录子代雄性小鼠青春期启动时间;统计小鼠的精子数和畸形精子数,并计算精子畸形率。结果与对照组比较,各剂量BPA染毒组子代雄性小鼠的青春期启动时间提前,精子计数减少,精子畸形率升高,除0.2μg/ml组精子计数外,差异均有统计学意义(P0.05)。且随着BPA染毒剂量的升高,子代雄性小鼠精子计数呈下降趋势,而精子畸形率呈上升趋势。结论妊娠期和哺乳期BPA暴露对子代雄性小鼠生殖功能具有明显不良影响,使其提前进入青春期并降低生精能力。     

孕期及哺乳期邻苯二甲酸二(2-乙基己基)酯经口染毒对雄性仔鼠生殖发育的影响

目的观察邻苯二甲酸二(2-乙基已基)酯(DEHP)对雄性仔鼠的生殖发育毒性作用。方法采用围生期毒性试验的研究方法,将清洁级SD大鼠随机分为阴性对照组(玉米油)和4个DEHP染毒组(125、250、500、1000mg/kg),采用宫内及哺乳期[受孕后第2天～仔鼠出生后第21天(PND21)]经口灌胃的方式染毒。记录比较雄性仔鼠肛殖距、不同发育阶段雄性仔鼠体重、睾丸、附睾重量、仔鼠出生后第50天(PND50)附睾尾精子总数、精子活率及精子畸形数。结果 125～500mg/kg组不同发育阶段仔鼠体重随染毒剂量增加而增加,500mg/kg组PND21体重与对照组比较,差异有统计学意义(P0.01),1000mg/kg组体重均低于同发育阶段对照组,PND21体重与对照组比较,差异具有统计学意义(P0.05)。1000mg/kg组不同发育阶段仔鼠睾丸重量明显降低,与对照组比较,差异有统计学意义(P0.01),附睾重量与对照组比较差异均无统计学意义(P0.05)。仔鼠出生后4天肛殖距不同程度缩短,除125mg/kg组外,其余各剂量组与对照组比较,差异均有统计学意义(P0.01)。PND50雄性仔鼠精子总数、精子活率均不同程度降低,精子畸形率不同程度增高,1000mg/kg组与对照组比较,差异有统计学意义(P0.05)。结论母鼠孕期及哺乳期暴露DEHP可影响雄性仔鼠生长、生殖发育。     

大鼠新生期暴露2,2',4,4',5,5'-六氯联苯对精子发生的影响

目的 探讨新生期SD大鼠暴露持续性有机污染物2,2',4,4',5,5'-六氯联苯(PCB153)对大鼠精子发生的远期效应.方法 大鼠出生当天(postnatal day O,PNDO),将所有雄性大鼠混合后,重新分为12只,窝.在出生1 d(PND1),按窝别随机分成对照组和处理组,每组24只雄性大鼠.自PND1开始连续7 d经口给予PCB153 0.025、0.250、2.500 mg/kg和等量溶剂对照玉米油.在PND8,每组随机选择16只大鼠称重和测肛殖距离后,经乙醚麻醉并处死,分离和称重睾丸后作组织学检查.剩余大鼠在PND21断奶并饲养至PND90,称重和测肛殖距离后经质量分数为10%的水合氯醛麻醉后解剖,分离并称重睾丸和附睾,其中睾丸用作组织学检查和精子头计数,附睾尾作精子计数.结果 从PND3至PND8,2.500 mg/kg剂量组体重与对照组相比明显下降,差异有统计学意义(P<0.05);在光学显微镜和电子显微镜下观察显示,PND8睾丸组织曲精小管结构疏松,精原细胞体积增大、变性并与管内结构相脱离.随着染毒剂量的增加,PND90睾丸每日精子生成量和附睾尾精子计数与染毒剂量呈剂量-反应关系(r值分别为-0.97和-0.99,P<0.05).0.250和2.500mg/kg剂量组的每日精子生成量分别为30x106/g睾丸和18×106/g睾丸,与对照组(36×106/g睾丸)相比,差异有统计学意义(P<0.05);0.250和2.500 mg/kg剂量组附睾尾精子计数分别为42×107/g附睾尾和18x107/g附睾尾,明显低于对照组(51×107/g附睾尾),差异均有统计学意义(P<0.05).结论 SD大鼠新生期暴露PCB153,可引起成年期睾丸生精功能障碍,导致每日精子生成量和附睾尾精子计数下降.新生期化学物暴露可能引起雄性大鼠生殖功能的远期损害.     

妊娠期二月桂酸二丁基锡暴露对子代雄性大鼠生殖系统的影响

目的探讨妊娠期二月桂酸二丁基锡(DBTD)暴露对子代雄性大鼠性成熟后生殖系统的影响及其作用机制。方法将16只健康SPF级妊娠Wistar大鼠随机分为4组,分别为溶剂对照(玉米油)组和低(10 mg/kg)、中(20 mg/kg)、高剂量(30 mg/kg)DBTD染毒组,每组4只。采用灌胃方式进行染毒,染毒容量为5 ml/kg,自妊娠第12～20天连续染毒。仔鼠出生后第70天,每组随机抽取10只雄性大鼠,称重后处死,测定睾丸和附睾重量及其脏器系数、附睾精子数以及血清中黄体生成素(LH)、卵泡刺激素(FSH)和睾酮(T)以及睾丸组织中睾酮(T)的水平,并观察睾丸组织病理学改变。结果各剂量DBTD染毒组子代雄性大鼠体重、附睾重量及其脏器系数、血清中LH和FSH水平与溶剂对照组相比,差异均无统计学意义。与溶剂对照组比较,高剂量DBTD染毒组子代雄性大鼠睾丸重量及其脏器系数,中、高剂量DBTD染毒组子代雄性大鼠附睾精子数较高,差异均有统计学意义(P0.05或P0.01)。且随着DBTD染毒剂量的升高,子代雄性大鼠睾丸重量及其脏器系数以及附睾精子数均呈升高趋势。与溶剂对照组比较,高剂量DBTD染毒组子代雄性大鼠血清T水平和各剂量DBTD染毒组子代雄性大鼠睾丸T水平均较高,差异有统计学意义(P0.05或P0.01)。结论在本实验染毒时间和剂量范围内,孕期DBTD染毒可干扰子代雄性大鼠体内T的合成和代谢,从而促进睾丸发育和精子形成。     

宫内和哺乳期接触多氯联苯118和126对雄性仔鼠生殖功能影响

目的探讨宫内和哺乳期接触多氯联苯(PCB)118和PCB126混合物对雄性子代大鼠生殖功能的影响。方法根据浙江某地母乳混合样中PCB118和PCB126含量及比例,按10、100和500倍配制成剂量为0.096、0.96和4.8μg TEQ/kg的混合物,在孕15 d对SD大鼠进行一次经口染毒,对母鼠的体重、雄性子代各发育阶段的肛门生殖口距离(AGD)和体重、脏器重量、精子计数及血清中睾酮水平等指标进行评估。结果各剂量组对母鼠没有明显毒性,0.96和4.8μg TEQ/kg组雄性仔鼠出现体重增加迟缓、AGD及精子数减少现象;雄性生殖器官如附睾、前列腺和精囊的重量改变只发生在出生后70日龄(PND70)4.8μg TEQ/kg组和0.96μg TEQ/kg组(附睾);血清睾酮水平没有发生明显变化。结论宫内和哺乳期接触PCB118和PCB126混合物在未观察到母体毒性剂量下能延迟子代雄性大鼠生长发育进程,并对其生殖系统产生损害。     

哺乳期小鼠阿特拉津染毒对仔鼠精子存活率的影响

为研究哺乳期小鼠阿特拉津染毒对仔鼠精子存活率的影响,将16窝健康清洁级昆明小鼠[16只母鼠及其生后7d雄性仔鼠(每窝5～7只)]随机分为4组,分别为对照组(植物油)和低(50mg/kg)、中(100mg/kg)、高(200mg/kg)剂量阿特拉津染毒组,每组4窝。对母鼠进行灌胃染毒,染毒剂量为10ml/kg,每天1次,连续进行14d。仔鼠于生后7～20d通过母乳染毒阿特拉津,生后21～45d自由饲养。各窝母鼠分别于染毒0、7、14d称重;仔鼠于生后9、15、28d称重,称量睾丸重量,并计算脏器系数。在仔鼠生后45d,测定仔鼠附睾中精子的存活率。结果显示,染毒阿特拉津后,各组母鼠体重均略有下降,但差异无统计学意义。各组仔鼠的体重、睾丸重量及其睾丸系数间比较,差异均无统计学意义。与对照组比较,中、高剂量阿特拉津染毒组仔鼠精子存活率较低,差异均有统计学意义(P0.05);且随着阿特拉津染毒剂量的升高,仔鼠精子存活率呈下降趋势。表明阿特拉津可以通过母鼠乳汁,降低小鼠的精子存活率。     

P,P'-DDE宫内暴露致雄性子代大鼠的生殖毒性

[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8～15d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/mL],较对照组[(70.63±4.17)×106个/mL]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.     

孕期乙酸铅暴露对子代小鼠睾丸组织能量代谢酶活力的影响研究

目的评价孕期乙酸铅暴露对性成熟雄性子代小鼠睾丸组织能量代谢酶活力的影响,并探讨其对生殖系统损伤的作用机制。方法将清洁级健康昆明种孕小鼠32只按体重随机分为高剂量组（2000 mg/kg）、中剂量组（1000 mg/kg）、低剂量组（500 mg/kg）和对照组（蒸馏水）,每组8只。于妊娠第14天开始,每日灌胃染毒,灌胃剂量为10 ml/kg,持续至母鼠自然分娩。记录孕鼠染毒期间体重增量和分娩时间。待雄性仔鼠8周龄（性成熟）时,称重并处死,分离双侧睾丸和附睾,测定睾丸、附睾的重量及脏器系数、附睾精子数。检测睾丸组织中的碱性磷酸酶（AKP）、乳酸脱氢酶（LDH）、琥珀酸脱氢酶（SDH）、Ca-Mg-ATP酶、Na-K-ATP酶、总ATP酶活力。结果各组孕鼠分娩时间和体重增量间比较,差异均无统计学意义（均P>0.05）。中、高剂量组仔鼠体重、睾丸重量、睾丸脏器系数、附睾重量、附睾脏器系数均明显低于对照组（P<0.05）;各染毒组仔鼠附睾精子数、睾丸组织SDH酶、Na-K-ATP酶、Ca-Mg-ATP酶、总ATP酶活力均明显低于对照组（均P<0.01）;高剂量组仔鼠睾丸组织LDH酶、AKP酶活力均明显低于对照组（P<0.01）;且随着乙酸铅染毒剂量的增高,睾丸组织SDH酶、Na-K-ATP酶、Ca-Mg-ATP酶以及总ATP酶活力均呈下降趋势。结论在本研究的染毒时间和剂量范围内,孕期乙酸铅暴露可干扰雄性子代小鼠睾丸的能量代谢,继而使得精子生成减少。     

氯氰菊酯和甲基对硫磷混配对大鼠生殖发育的影响

[目的]探讨妊娠期氯氰菊酯和甲基对硫磷混配染毒,对母鼠的生殖毒性和对子代大鼠生殖和发育的影响。[方法]Wistar孕鼠112只随机均分为4组,于孕1～15天连续经口灌胃染毒不同剂量农药(两种农药以相当于0、1/300、1/95、1/30LD50的剂量等毒混配),对照组采用溶剂灌胃。56只孕鼠(每组14只)妊娠19天时处死,测定胚胎毒性;另56只孕鼠自然分娩,记录空孕率、每窝活产数、妊娠天数、平均产仔数和性别比;测量其371只仔鼠的体重增长和生长发育情况;10周龄时随机抽取雌鼠32只(每组8只)、雄鼠40只(每组10只)处死,称量生殖腺重量,计数睾丸每日生精量和附睾精子数。[结果]孕鼠胚胎毒性指标中仅高剂量组活胎比低于中剂量组和对照组(P<0.05);各剂量组分娩孕鼠的空孕率、妊娠天数、产仔数、平均活产数、仔鼠性别比与对照组相比无差异(P>0.05)。各剂量组仔鼠体重增长与对照组一致(P>0.05);高剂量组仔鼠出生第一天尾长比对照组长(P>0.05);雌性仔鼠的卵巢脏器系数与混配农药剂量之间存在剂量-效应关系(rs=0.3144,P=0.0172);各剂量组雄鼠睾丸每日精子生成量和附睾精子数与对照组相比无差异(P>0.05)。[结论]妊娠期甲基对硫磷和氯氰菊酯混配染毒,对母鼠有一定的胚胎毒性,并对仔鼠生长发育有轻微的影响。     

Dose dependent effects of inhaled ethylene oxide on spermatogenesis in rats.

Male Wistar rats were exposed to ethylene oxide (EO) at concentrations of 50, 100, or 250 ppm for six hours a day, on five days a week for 13 weeks. Dose effect relations of inhaled EO on spermatogenesis were evaluated from testicular and epididymal weights, histopathological changes and lactate dehydrogenase X (LDH X) activity in the testis, and sperm counts and sperm head abnormalities in the epididymis. At 250 ppm, a decrease in epididymal weights, slight degenerations in the seminiferous tubules, decreased sperm counts, and increased numbers of abnormal sperm heads in the tail of the epididymis were found; these were not seen at lower doses. When the abnormal sperm heads were classified into immature types and teratic types, the number of immature heads increased only at 250 ppm. On the other hand, the teratic type had increased at doses of 50 and 100 ppm EO when compared with the control group. Hence, subchronic inhalation of EO at low concentrations affects spermatogenesis in rats.     

Dose dependent effects of inhaled ethylene oxide on spermatogenesis in rats

Male Wistar rats were exposed to ethylene oxide (EO) at concentrations of 50, 100, or 250 ppm for six hours a day, on five days a week for 13 weeks. Dose effect relations of inhaled EO on spermatogenesis were evaluated from testicular and epididymal weights, histopathological changes and lactate dehydrogenase X (LDH X) activity in the testis, and sperm counts and sperm head abnormalities in the epididymis. At 250 ppm, a decrease in epididymal weights, slight degenerations in the seminiferous tubules, decreased sperm counts, and increased numbers of abnormal sperm heads in the tail of the epididymis were found; these were not seen at lower doses. When the abnormal sperm heads were classified into immature types and teratic types, the number of immature heads increased only at 250 ppm. On the other hand, the teratic type had increased at doses of 50 and 100 ppm EO when compared with the control group. Hence, subchronic inhalation of EO at low concentrations affects spermatogenesis in rats.     

吡哆素L-2-吡咯烷酮-5-羧酸酯雄性生殖毒性及机制研究

目的:研究吡哆素L-2-吡咯烷酮-5-羧酸酯(Metadoxine,MTDX)对雄性大鼠的生殖毒性及机制。方法:灌胃染毒雄性成年SD大鼠0,250,500和1000 mg/kgMTDX,每天1次,连续4周。染毒结束后观察性腺和附属性腺脏器系数、精子质量、组织形态学和血清睾酮等指标的变化。Hershberger方法检测MTDX抗雄激素活性作用:40只4周龄雄性SD大鼠行双侧睾丸切除手术,2周后,除1组皮下注射花生油并灌胃给予蒸馏水外,其余3组去势大鼠每天皮下注射丙酸睾酮(TP,1 mg/kg),并同时灌胃给予蒸馏水或MTDX(500,1000 mg/kg),连续7 d,观察雄激素依赖组织重量的变化。对体外培养睾丸碎块合成睾酮的影响:利用离体组织培养和放射免疫技术,观察不同浓度MTDX对体外培养睾丸碎块合成睾酮的影响。结果:1000 mg/kg剂量组大鼠睾丸、附睾、前列腺和精囊腺脏器系数明显降低;精子数量和精子存活率减少,精子活力降低,精子畸形率增高,血清T无变化;500 mg/kg剂量组在睾丸相对重量、精子数量和精子活力方面与对照组比较有显著性差异。在Hershberger实验中,1000 mg/kg组大鼠的精囊腺、前列腺以及球海绵体肌的脏器系数值均显著低于对照组。MTDX各剂量组睾丸培养液中睾酮的含量与对照组相比均没有显著性差异。结论:MTDX能引起雄性大鼠生殖毒性,这种毒性作用可能与其具有抗雄激素样作用有关。     

Evaluation of the toxic potentials of cypermethrin pesticide on some reproductive and fertility parameters in the male rats

Adult male Sprague-Dawley rats were exposed to tap water containing 0, 8,571, 17,143, or 34,286 ppm cypermethrin for 12 weeks. Based on water consumption per animal per day the rats received 13.15, 18.93, and 39.66 mg cypermethrin, respectively. Fertility was significantly reduced in male rats ingesting cypermethrin at a concentration of 13.15 and 18.93 mg in that the number of females impregnated by them was significantly reduced. The number of implantation sites was significantly reduced in females mated with males that had ingested cypermethrin at a concentration of 39.66 mg. A significant reduction in the number of viable fetuses was observed in females impregnated by the exposed males at all three doses of cypermethrin. The body weight gain was significantly lower in the treated males. Ingestion of cypermethrin at a concentration of 18.93 or 39.66 mg per day resulted in a significant increase in the weights of testes and seminal vesicles. Preputial gland weights were increased at all three concentrations of cypermethrin. Epididymal and testicular sperm counts as well as daily sperm production were significantly decreased in exposed males. The serum levels of testosterone, follicle-stimulating hormone and luteinizing hormone were significantly reduced in males exposed to 39.66 mg per day. Ingestion of cypermethrin at 18.93 and 39.66 mg/animal/day also resulted in a significant decrease in the perimeter and number of cell layers of the seminiferous tubules. The testes of treated animals were infiltrated with congested blood vessels with marked hemorrhage and a significant accumulation of connective tissue surrounding the seminiferous tubules, which contained a large number of immature spermatids. These results clearly demonstrate the adverse effects of cypermethrin pesticide on fertility and reproduction in male rats. Received: 1 January 2001/Accepted: 28 May 2001     

The toxic effects of sodium fluoride on the reproductive system of male rats

The present study was undertaken to evaluate the effect of fluoride toxicity on the reproductive system of male rats. Sexually mature male Wistar rats were exposed to 2, 4, and 6 ppm sodium fluoride in their drinking water for 6 months ad libitum. Sperm motility and density in cauda epididymis were assessed. Biochemical and histological analysis were performed in reproductive organs. Fluoride treatment brought about a significant decrease in the weight of testis, epididymis, and ventral prostate. The sperm motility and density were significantly reduced. There was a marked reduction in the number of primary spermatocyte, secondary spermatocyte, and spermatids. The Sertoli cell counts and their cross sectional surface areas were significantly decreased. The Leydig cell nuclear area and the number of mature Leydig cells were also significantly decreased. The protein content of the testis and epididymis were significantly reduced. Fructose in the seminal vesicles and cholesterol in testes were increased significantly. In conclusion, sodium fluoride administrated in drinking water of 2, 4, and 6 ppm concentration for 6 months to male rats adversely affected their fertility and reproductive system.     

Testicular toxicity of chlorpyrifos (an organophosphate pesticide) in albino rat

Organophosphates are among the most widely used synthetic insect pesticides. The widespread use of organophosphates has stimulated research into the possible existence of effects related with their reproductive toxic activity. Present study was therefore, undertaken to assess the effects of chlorpyrifos on testes, the main organ of male reproduction. Chlorpyrifos at the dose levels of 7.5, 12.5 and 17.5 mg/kg b. wt./day was administered orally to male rats of Wistar strain for 30 days to evaluate the toxic alterations in testicular histology, biochemistry, sperm dynamics and testosterone levels. The body weight of animals did not show any significant change, however, a significant reduction was observed in testes. Chlorpyrifos also brought about marked reduction in epididymal and testicular sperm counts in exposed males and a decrease in serum testosterone concentration. Histopathological examination of testes showed mild to severe degenerative changes in seminiferous tubules at various dose levels. Fertility test showed 85% negative results. A significant reduction in the sialic acid content of testes and testicular glycogen was noticed, whereas the protein and cholesterol content was raised at significant levels. All these toxic effects are moderate at low doses and become severe at higher dose levels. From the results of the present study it is concluded that chlorpyrifos induces severe testicular damage and results in reduction in sperm count and thus affect fertility. Small changes in sperm counts are known to have adverse affects on human fertility. Therefore, application of such insecticide should be limited to a designed programme.     

Suppression of fertility in male albino rats following the administration of 50% ethanolic extract of Aegle marmelos

BACKGROUND: Plants have served as a natural source of antifertility substances. The reactivated interest in the evaluation of some lead plants for fertility prompted us to undertake studies on the antifertility potential of Aegle marmelos leaves. STUDY DESIGN: Fifty percent ethanolic extract from the leaves of A. marmelos (AMLEt) was prepared. The effect of A. marmelos leaf extract on the reproductive system of male albino rats was investigated at three different doses, namely, 100, 200 and 300 mg(-1) kg (-1) day(-1) for each rat for 60 days. Recovery was also investigated after a withdrawal of 120 days. RESULTS: All the major accessory sex organs shed weight postadministration of the extract. There was a marked reduction in motility and density of the sperm derived from cauda epididymis of the treated animals. A. marmelos reduced fertility of male rats by 100% at the 300-mg dose level. Serum testosterone levels also decreased significantly in all the experimental groups. The protein, glycogen and lipid peroxidation content of the testes was significantly reduced at the highest dose level; a highly significant increase in testicular cholesterol was observed along with a highly significant reduction in the sialic acid contents of testes, epididymis and seminal vesicles. Blood tests did not point to distress in any of the vital organs. Withdrawal of the extract restored all the altered parameters including organ weights, fertility, testosterone levels and tissue biochemistry to control levels after 120 days. CONCLUSIONS: Taken together, it is inferred that the leaf extract of A. marmelos (AMLEt) suppresses fertility in male rats. Complete recovery of fertility was observed following the withdrawal of drug. Absence of any deleterious effect on the vital organs points to the safe use of the extract.     

Decrease in sperm number after treatment of rats with Austroplenckia populnea

The purpose of this study was to evaluate the effects of a hexanic extract (HE) made from leaves of A. populnea collected in Botucatu, State of S?o Paulo, and Nova Lima, State of Minas Gerais, Brazil, at a range of doses during 7 and 14 days, on the male reproductive system of rats. The treatment did not affect the body weight, nor absolute organ weight. The serum testosterone levels, testicular sperm head counts, daily sperm production, and sperm morphology did not differ from that of the control groups. The spermatogenesis and the morphometric parameters of cauda epididymidis were not affected by the treatment. Cauda epididymis sperm number was significantly reduced in the group that received HE of Nova Lima, 1 g/kg/day, during 14 days, from the control group.