二甲磺酸乙烷对成年大鼠精囊组织形态结构的影响

目的:研究二甲磺酸乙烷(EDS)注射对大鼠精囊不同组织结构体积的影响。方法:27只约90日龄雄性SD大鼠随机分成2组,对照组(n=14)一次性腹腔内注射生理盐水,EDS组(n=13)一次性腹腔内注射EDS75 mg/kg体重;7 d和12 d后取一侧精囊,制作甲基丙烯酸树脂包埋切片,用体视学方法估计精囊内各种结构的总体积。结果:EDS几乎完全破坏睾丸内的Leydig细胞,导致急剧睾酮缺乏。与7 d对照组(n=7)相比,7 d EDS组(n=6)精囊(包括附着在精囊上的凝固腺)的体积减少53%[(138.2±12.9)mm3vs(64.9±3.6)mm3,P<0.05],但该体积在7 d EDS组和12 d EDS组(n=7)之间无显著差异[(64.9±3.6)mm3vs(55.4±7.7)mm3,P>0.05]。与12 d对照组(n=7)相比,12 d EDS组腺腔、腺上皮、平滑肌层和外膜的总体积分别显著减少97%、80%、58%和67%。结论:EDS处理导致大鼠精囊腺腔、腺上皮、平滑肌层和外膜结构的严重萎缩。     

大鼠单侧精索扭转后保留同侧坏死睾丸对对侧睾丸和附睾的组织学影响

目的:将大鼠单侧精索持续扭转96 h,研究保留扭转侧坏死睾丸对对侧睾丸和附睾的影响,以说明延迟性的睾丸切除是否对对侧睾丸功能有保护作用。方法:将33只青春前期(21～42日龄)正常雄性SD大鼠,随机分为假手术对照组(n=11)、扭转保留组(n=12)和扭转切除组(n=10)。假手术对照组只对左侧睾丸行睾丸肉膜囊固定术,后两组扭转实验组用睾丸肉膜囊固定术固定维持扭转720°的睾丸、附睾,在扭转96 h后将扭转保留组扭转侧睾丸、附睾行复位及固定,而同时扭转切除组则将扭转侧睾丸、附睾切除。术后3个月抽取血液标本,ELISA测定大鼠血清睾酮、抗精子抗体浓度。同时取睾丸、附睾标本,石蜡包埋切片后作组织学观察,并利用体视学方法定量研究睾丸、附睾结构的体积以及生精小管直径。结果:3组大鼠血清睾酮值无统计学差异;仅扭转保留组造模后1例大鼠血清抗精子抗体阳性。光镜下定性观察发现精索扭转组睾丸间质细胞核较假手术对照组间质细胞核增大,假手术对照组、扭转保留组和扭转切除组睾丸结构有明显形态改变的数量分别为1、3、0只。扭转保留组对侧睾丸相对假手术对照组睾丸体积增加19%,相应附睾体积增加11%,扭转切除组对侧睾丸体积增加21%,附睾体积增加7%,且睾丸代偿性肥大具有统计学意义(P<0.05)。假手术对照组、扭转保留组和扭转切除组对侧睾丸生精小管体积分别为(1.15±0.07)、(1.30±0.04)、(1.35±0.05)cm3,3组间无显著性差异。3组大鼠对侧睾丸内间质体积分别为(0.25±0.02)、(0.36±0.02)、(0.34±0.03)cm3,精索扭转组和假手术对照组相比显著增加(P<0.05)。3组大鼠对侧睾丸内生精小管直径分别为(226.00±7.00)、(223.00±6.00)、(221.00±3.00)μm,无显著性差异(P>0.05)。结论:单侧精索长期扭转后对侧睾丸、附睾主要改变是单侧去势后的对侧代偿性肥大表现,是否切除对对侧睾丸和附睾组织学上无明显影响。     

成年大鼠睾丸间质细胞同种异体移植的实验研究

本实验在远交系大鼠间行睾丸间质细胞同种异体移植，为临床移植提供实验依据。将７０只成年雄性大鼠阉割。睾丸间质细胞分离、提纯后，作体外培养；培养第７天，将细胞移植到去势大鼠体内，定期测试受鼠血清睾酮。实验结果显示：细胞体外培养１８天仍能分泌睾酮；０．１ｍｏｌ／Ｌ二甲基亚砜能明显提高细胞睾酮分泌量；细胞移植后４个月，受鼠血清仍可测到较高水平的睾酮，而对照组大鼠血清睾酮低于测试下限。作者认为，体外培养和睾丸间质细胞分离后可能出现的主要组织相容性（ＭＨＣ）免疫原性的改变是细胞移植后存活较长的原因。     

老年大鼠睾丸间质细胞结构和功能变化的实验研究

目的:研究老年SD大鼠(PADAM动物模型)睾丸间质细胞形态、分泌功能变化,探讨老年大鼠睾丸间质细胞的功能状态。方法:分别取青年SD大鼠和老年各20只,静脉血测定血清总睾酮和游离睾酮的浓度,并通过组织切片和透射电镜观察两个年龄组大鼠睾丸间质细胞形态学变化;此外,分别用hCG、Forskolin刺激体外培养的两个年龄组大鼠的睾丸间质细胞,比较培养基中睾酮和孕酮的浓度。结果:老年大鼠的血清总睾酮[(3.07±0.75)nmol/L]和游离睾酮[(0.71±0.65)nmol/L]均比青年大鼠[(10.89±6.11)nmol/L和(2.42±1.02)nmol/L]显著降低(P<0.05);细胞形态有较显著差异;体外培养的大鼠睾丸间质细胞分泌能力显著降低(P<0.05)。结论:老年SD大鼠血清睾酮和游离睾酮浓度显著低于青年SD大鼠,原因在于睾酮合成酶系统整体功能衰退。     

大鼠睾丸年龄性变化的定量组织学研究

本研究运用体视学原理,在光镜下对衰老大鼠睾丸各结构成份进行了定量观察研究,以探讨睾丸各结构成份年龄性变化与功能的关系。结果表明:1.随着年龄的增长,睾丸曲细精管的体密度(Vv)、表面积与体积之比(Sv/Vv)均明显降低(P<0.01);而线密度(Lv)则无明显变化(P>0.05)。2.老年组曲细精管的生精细胞除精原细胞的体密度(Vv)明显降低外,初级精母细胞和精细胞的体密度(Vv)均有较大的增加,差异显著(P<0.01)。3.间质体密度(Vv)、曲细精管基膜调和平均厚度(th)两个参数值在衰老大鼠睾丸中增大,间质中毛细血管的线密度(Lv)降低(P<0.01)。上述测量结果提示:衰老大鼠睾丸曲细精管的萎缩退化主要与精细胞发育障碍有关。此外,由于间质纤维化、曲细精管基膜调和平均厚度增大造成生精细胞在发育过程中营养物质的缺乏。     

老年大鼠睾丸间质细胞形态及睾酮合成功能变化的研究

目的 探讨衰老对睾丸间质细胞的形态及功能的影响.方法 青年(3月龄)及老年(24月龄)清洁级雄性SD大鼠各10只,麻醉后取血清检测总睾酮浓度,取睾丸组织用HE染色观察睾丸组织形态学变化,并用电镜观察睾丸间质细胞的超微结构改变.通过密度梯度离心分离原代睾丸间质细胞,并用LH刺激睾酮分泌后用Western blot比较青年组和老年组睾丸间质细胞类固醇合成快速调节蛋白(steroidogenic acute regulatory protein,StAR)表达水平的差异,并用ELISA法检测其睾酮分泌的差异.结果 HE染色显示老年大鼠睾丸呈老年退行性改变,电镜下观察到老年大鼠睾丸间质细胞线粒体水肿,线粒体嵴消失.老年大鼠血清睾酮水平显著低于青年组(P＜ 0.05).原代培养的睾丸间质细胞无论LH刺激与否,老年组细胞上清中睾酮浓度及StAR蛋白表达水平均显著低于青年组(LH刺激时P＜0.01,无LH刺激时P＜0.05).结论 衰老造成的睾丸间质细胞线粒体水肿及LH诱导的StAR蛋白表达水平下降与其睾酮合成能力降低密切相关.     

邻苯二甲酸二-(2-乙基)己酯致小鼠隐睾睾丸和附睾的组织病理学改变

目的 :探讨邻苯二甲酸二 (2 乙基 )己酯 (DEHP)引起的小鼠隐睾睾丸和附睾的组织病理学改变。　方法 :妊娠KM小鼠 4 0只 ,随机分成 5组 ,分别为正常对照组 8只、玉米油对照组 8只、己烯雌酚 (DES)组 8只、DEHP低剂量组 [DEHP 10 0mg/ (kg·d) ]9只和DEHP高剂量组 [DEHP 5 0 0mg/ (kg·d) ]7只。自妊娠第 12d开始到分娩后 3d ,分别持续经口给予DEHP 10 0mg/ (kg·d)、5 0 0mg/ (kg·d)和DES 10 0 μg/ (kg·d)及玉米油 ,观察仔代雄小鼠的隐睾发生率及隐睾睾丸和附睾的组织病理学改变。　结果 :DEHP 5 0 0mg/ (kg·d)组染毒小鼠的隐睾发生率显著增高 ,睾丸和附睾的体积明显减小、重量减轻 ;睾丸生精上皮发育明显异常 ,精曲小管变薄、萎缩 ,间质细胞异常增生 ,电镜下其隐睾精曲小管上皮和间质细胞均出现明显的超微结构改变。同时附睾管腔中的精子数显著减少甚至缺乏。　结论 :高剂量 [5 0 0mg/ (kg·d) ]DEHP可能具有与DES类似的作用 ,是一种诱发隐睾的重要因子。小鼠在孕期及哺乳期接触DEHP后可引起雄性仔鼠性分化异常 ,诱导隐睾发生、睾丸生精上皮损害和生精过程障碍 ,从而对雄性仔鼠生育力产生不利影响。以上作用存在明确的量 效关系。     

异丙苯过氧化氢体内致大鼠睾丸和附睾过氧化的初步研究

目的:建立异丙苯过氧化氢(cHP)体内过氧化模型,探讨cHP体内过氧化对大鼠睾丸组织和附睾精子的影响,及对精子核DNA断裂的影响。方法:90日龄雄性W istar大鼠52只,设cHP 1/10 LD50、1/6 LD50、1/4 LD503个剂量组和对照组,cHP 1/10 LD50、1/6 LD50组和对照组每组大鼠12只,1/4 LD50组大鼠16只。用无菌生理盐水稀释70%cHP水剂配制,按2 m l/kg经腹腔每日1次注射,对照组给同体积生理盐水,观察一般中毒症状和体征。连续1周,最后1次给药24 h后处死动物。分光光度法测定睾丸组织匀浆、附睾头部和尾部精子丙二醛含量,用单细胞凝胶电泳检测睾丸生精上皮细胞、附睾头部和尾部精子核DNA断裂发生率,计数附睾尾部精子活动率,睾丸和附睾常规石蜡切片,苏木精-伊红染色观察病理变化。结果:给予cHP大鼠活动稍差,无死亡,1/6 LD50、1/4 LD50 cHP组体重降低明显(P<0.001)。1/6 LD50、1/4 LD50 cHP组大鼠睾丸和附睾精子丙二醛浓度均明显高于对照组,附睾尾部精子活动率均明显降低,睾丸生精上皮细胞和附睾头部精子核DNA断裂发生率明显高于对照组,附睾尾部精子核DNA断裂的发生率与对照组差异无显著性(P>0.05)。1/10 LD50 cHP组大鼠体重变化、睾丸丙二醛浓度、附睾尾部精子活动率、睾丸生精上皮细胞和附睾精子核DNA断裂与对照组比较,差异均无显著性(P>0.05)。结论:1/6 LD50、1/4 LD50 cHP能在体内使大鼠睾丸和附睾精子发生过氧化,并使细胞核DNA发生断裂,核DNA断裂的主要部位可能在睾丸组织,对附睾尾部精子核DNA断裂无明显影响。     

血管内皮生长因子和其受体Flt-1在青春期大鼠睾丸、附睾及附睾内精子上的表达研究

目的:通过对血管内皮生长因子(VEGF)及其受体Flt-1在大鼠睾丸、附睾及附睾内精子上表达的研究,探讨其在雄性生殖系统中的作用。方法:免疫组化SP法和免疫荧光法检测20只青春期SD大鼠睾丸、附睾及精子上VEGF和Flt-1蛋白的表达情况。结果:VEGF和Flt-1在大鼠睾丸和附睾组织及精子上均有特征性表达。睾丸内VEGF蛋白表达于生精细胞、精子细胞发育中的顶体、Sertoli和Leydig细胞胞质内;Flt-1只见于精子细胞发育中的顶体及Leydig细胞胞质中。附睾中VEGF表达于各段上皮主细胞胞质内,而Flt-1表达于头、尾段上皮主细胞胞质内,体部免疫染色阴性;两者在附睾上皮亮细胞、晕细胞和基细胞中均为阴性表达。免疫荧光染色显示,VEGF和Flt-1共同定位于附睾内精子头部的顶体,尾部的颈、中和主段。结论:VEGF和Flt-1蛋白在大鼠睾丸、附睾及精子中的特异性表达提示,他们可由不同生精上皮细胞、间质细胞和附睾主细胞产生,可能以自分泌或旁分泌的形式单独或共同作用于睾丸和附睾的生殖细胞或Leydig细胞,直接或间接地影响精子的发生、发育和成熟过程,并与精子的活动和受精能力有关。     

Histological changes of the testis and epididymis in adult rats as a result of Leydig cell destruction after ethane dimethane sulfonate treatment： a morphometric study

Aim： To quantitatively study the histological changes of the testis and epididymis as a result of a drastic reduction of testosterone secretion. Methods： Fourteen adult Sprague-Dawley rats were injected intraperitoneally with ethane dimethane sulfonate （EDS, 75 mg/kg） and the same number of animals were injected with normal saline as a control. At days 7 and 12 （after treatment）, respectively, half of the animals from each group were killed. The testes and epididymides were removed and tissue blocks embedded in methacrylate resin. The cell number per testis was estimated using the stereological optical disector and some other parameters were obtained using other morphometric methods. Results： The EDS treatment resulted in an almost complete elimination of Leydig cells but had no effect on the numbers of Sertoli cells per testis. At day 7 after EDS treatment, many elongated spermatids were retained in the seminiferous epithelium and many round spermatids could be seen in the epididymal ducts. At day 12, a looser arrangement of spermatids and spermatocytes became evident, with apparent narrow empty spaces being formed between germ cells in an approximately radial direction towards the tubule lumen; the numbers （per testis） of non-type B spermatogonia and spermatocytes were similar to controls, whereas that of type B spermatogonia increased by 59%, and that of early round, elongating and late elongated spermatids decreased by 37%, 72% and 52%, respectively. Conclusion： The primary spermatogenic lesions following EDS administration were （i） spermiation failure and （ii） detachment of spermatids and spermatocytes associated with impairment in spermiogenesis and meiosis.     

Alterations of gene profiles in Leydig-cell-regenerating adult rat testis after ethane dimethane sulfonate-treatment

Only occupying about 1%–5% of total testicular cells, the adult Leydig cell (ALC) is a unique endocrine cell that produces androgens. Rat Leydig cells regenerate after these cells in the testis are eliminated with ethane dimethane sulfonate (EDS). In this study, we have characterized Leydig cell regeneration and messenger ribonucleic acids (mRNA) profiles of EDS treated rat testes. Serum testosterone, testicular gene profiling and some steroidogenesis-related proteins were analyzed at 7, 21, 35 and 90 days after EDS treatment. Testicular testosterone levels declined to undetectable levels until 7 days after treatment and then started to recover. Seven days after treatment, 81 mRNAs were down-regulated greater than or equal to two-fold, with 48 becoming undetectable. These genes increased their expression 21 days and completely returned to normal levels 90 days after treatment. The undetectable genes include steroidogenic pathway proteins: steroidogenic acute regulatory protein, Scarb1, Cyp11a1, Cyp17a1, Hsd3b1, Cyp1b1 and Cyp2a1. Seven days after treatment, there were 89 mRNAs up-regulated two-fold or more including Pkib. These up-regulated mRNAs returned to normal 90 days after treatment. Cyp2a1 did not start to recover until 35 days after treatment, indicating that this gene is only expressed in ALCs not in the precursor cells. Quantitative polymerase chain reaction, western blotting and semi-quantitative immunohistochemical staining using tissue array confirmed the changes of several randomly picked genes and their proteins.     

Protective effects of vitamin E on ethane dimethane sulfonate-induced testicular toxicity in rats

Aim： To evaluate the protective/ameliorative effects of vitamin E （vit E） on ethane dimethane sulfonate （EDS） induced testicular toxicity in rats. Methods： The rats were assigned to eight groups, seven rats in each, and were injected intraperitoneally with vehicle, a single dose of ethane dimethane sulfonate （EDS） （75 mg/kg bodyweight）, vit E （100 mg/kg bodyweight） or EDS ＋ vit E for 3-7 days. Thereafter, the rats were weighed, anaesthetized with ether and killed by cervical dislocation. The left testis weights were recorded and the relative testis weights were calculated. The left testes were processed for routine paraffin embedding. Three right testes from each group were taken randomly and then processed for routine electron microscopy. Tissue sections were examined using light and electron microscopy, and were scored for histopathological changes. Results： Vit E coadministration did not prevent the bodyweight loss on days 3 and 7. However, vit E administration prevented the EDS-induced testicular-weight loss in rats that received vit E for 3 days but not 7 days. The relative testis weight was higher on day 3 （instead of on day 7） than other groups. Nevertheless, the testis histology was not markedly protected by vit E in the EDS-treated rats. Detailed microscopic assessment showed few Leydig cells and abundant fibroblast-like cells indicating only some protection. Conclusion： Vit E cotreatment showed partial protective effects on the testicular weight and testicular histology in rats that received EDS.     

The importance of the Leydig cells in the vascular response to hCG in the rat testis

The increase in permeability of the testicular blood vessels following an injection of hCG into rats is abolished completely if the animals are treated 3 days earlier with ethane dimethane sulphonate (EDS), a compound that effectively eliminates Leydig cells from the testes. As there is other evidence that androgens or prostaglandins are not involved in this vascular response, further studies will be necessary to determine whether these data mean that another vasoactive substance is secreted by the Leydig cells or whether the EDS also eliminates other cells besides the Leydig cells, for example the mast cells found in the vicinity of the testicular artery.     

Effect of unilateral cryptorchidism on the intertubular tissue of the adult rat testis: evidence for intracellular changes within the Leydig cells

Adult male rats were made unilaterally cryptorchid for 1, 2 or 4 weeks, and the morphological response of the Leydig cells was then studied using morphometric assessment of total Leydig cell volume and number per testis in abdominal and scrotal testes. Serum hormone levels were measured and the steroidogenic properties of isolated Leydig cells were evaluated by in-vitro stimulation with hCG and interstitial fluid (IF) obtained from normal rat testes. Total Leydig cell volume and number per testis were not altered in abdominal vs scrotal testes, although the volume of the abdominal testis was 46, 29 and 21%, respectively, of the volume of the contralateral scrotal testis after 1, 2 and 4 weeks. This reduction was accompanied by significant (P less than 0.05) elevation of the serum levels of FSH and LH, although serum testosterone levels were unchanged from the normal range. Despite the lack of quantitative alterations in Leydig cell morphology, hCG- and IF-stimulated testosterone production was significantly (P less than 0.01) greater by abdominal Leydig cells when compared with scrotal Leydig cells derived from the same animals. Ultrastructural examination of Leydig cells in situ suggested an increase in volumetric density of mitochondria in abdominal Leydig cells. Together with the enhanced steroidogenic responses of these cells, these findings suggest that disruption of spermatogenesis in the cryptorchid testis is accompanied by intracellular activation of Leydig cells. Since these effects were not exhibited by Leydig cells from the scrotal testis it is concluded that local factors within the cryptorchid testis are responsible, at least in part, for regulation of Leydig cell activity.     

Quantitative （stereological） study of incomplete spermatogenic suppression induced by testosterone undecanoate injection in rats

Aim: To evaluate the key lesions in spermatogenesis suppressed partially by testosterone undecanoate(TU) treatment. Methods: Adult male SD rats were treated with vehicle or TU (19 mg/kg) injection (i.m.) every 15 days for 130 days. The numbers of all types of cells (nuclei) in the seminiferous tubules and the interstitial tissue were estimated using a contemporary stereological tool, the optical disector. Results: In response to TU treatment, the numbers of non-type B spermatogonia, type B sperrnatogonia and late elongated spermatids per testis were reduced to 51%, 66% and 14% of the controls, respectively. The conversion ratios from type B spermatogonia to early spermatocytes and pachytene spermatocytes were not significantly affected and the ratios to the later germ cell types fell to 51%-65% of the controls. Less than 1.0 % of immature round spermatids were seen sloughing into the tubule lumen, 4.0% of elongated spermatids retained in the seminiferous epithelium, and about half of the elongated spermatid nuclei appreciably malformed. Leydig cells were atrophied but their number and the peritubular myoid cell number per testis were unchanged. Conclusion: Double inhibition of spermatogenesis (i.e. inhibition at spermiation and spermatogonial conversion to type B spermatogonia), a scenario seen in the monkey and human following gonadotrophin withdrawal, was not sufficiently effective for a complete spermatogenic suppression in the rat after TU treatment, probably due to ineffective inhibition of the Leydig cell population and therefore the intra-testicular test-osterone levels. (Asian J Androl 2004 Dec; 6: 291-297)     

Is testosterone involved in the initiation of spermatogenesis in humans? A clinicopathological presentation and physiological considerations in four patients with Leydig cell tumours of the testis or secondary Leydig cell hyperplasia

The purpose of this study was to evaluate the role of testosterone on the puberal development of spermatogenesis and to present additional clinicopathological data which bring about new information to this controversial subject. Four pre-pubertal patients are presented, 2 of them bearing Leydig cell tumours of the testis in the form of nodular masses. In both cases seminiferous tubules in the immediate vecinity to the tumours showed complete development of spermatogenesis, while those located away from the tumours were infantile in nature. Gonadotrophic levels were within the normal pre-pubertal range in these 2 cases. In one of the patients, testosterone concentration in the testis showed higher values than normal, and a concentration gradient was detected between the tumoral nodule and non-tumoral parenchyma. The 3rd patient had a pineal choriocarcinoma producing high amounts of hCG and consequently a diffuse hyperplasia of Leydig cells with high levels of plasma testosterone. Seminiferous tubules showed development up to pachytene spermatocytes. The last case was a precocious puberty in a boy with a tumour of the 3rd ventricle area. He had elevated levels of testosterone in the testis and plasma. In the testicular biopsy, stimulation of Leydig cells was detected. The seminiferous tubules showed mature Sertoli cells and pachytene spermatocytes. FSH levels were abnormally low. These 4 cases present in common different situations in which abnormally high amounts of testos-happens in the immature rat, the interaction between testosterone and gonadotrophins is essential for the normal initiation of spermatogenesis in normal puberty. Considerations are discussed on the possible synergistic role of gonadotrophins or other factors in relation with stimulation of seminiferous tubules by testosterone.     

Morphometric analysis of the components of the neonatal and the adult rat testis interstitium

Leydig cells in the foetal rat testis are still present at birth and it has been hypothesized that they commence to degenerate immediately after birth, based on the decrease in their volume density (v/v%) with age. In this study the interstitium of the rat testis was studied quantitatively at 1, 5, 10, 15, 20 and 90 days after birth: the latter are considered to be adults. The absolute volumes of connective tissue cells and blood vessels increased with age. The absolute volumes of macrophages and lymphatic spaces were greater at 90 days than at any other age. The absolute volume of foetal Leydig cells per testis was unchanged from 1 to 15 days, despite a decrease in the % volume occupied per testis. The number of foetal Leydig cells per testis did not decline from days 1-20 although on day 20 an average foetal Leydig cell was smaller in volume than at earlier ages (days 1-15). Adult Leydig cells were recognized at day 10 and their absolute volume and number per testis increased from 15 to 90 days. Adult Leydig cells were similar in morphology to foetal Leydig cells at 20 days except for a reduced volume of cytoplasmic lipid.     

Effects of a chronic treatment with testosterone on the morphology of the interstitial cells of the rat testis: an ultrastructural stereologic study

The suppressive effects of chronic testosterone administration on the rat testicular interstitial cells (Leydig cells) were investigated by stereological methods. The volume of cells, nuclei, mitochondrial compartment and smooth endoplasmic reticulum (SER), as well as the surface area of SER and mitochondrial cristae decreased significantly as a function of the duration of treatment. The decrease in the SER volume accounted for about 75–80% of that in the cell volume. These findings lend support to the view that SER is the subcellular organelle more responsive to the changes in the functional activity of rat Leydig cells.     

Quantitative （stereological） study on the spermatozoal storage capacity of epididymis in rats and monkeys

Aim: To investigate the spermatozoal production rate of the testis and the spermatozoal storage capacity of the epi-didymis in monkeys and rats. Methods: The number of the late spermatids (steps 13 - 14 in the monkey or steps15 - 19 in the rat) per testis and the number of spermatozoa per epididymis were estimated in 6 normal adult monkeys(Macaca fascicularis) and 6 normal adult SD rats on 25 um-thick methacrylate-embedded sections using a contempo-rary unbiased and efficient stereological method-the optical disector. The diameter and length of the efferent ductulesand ductus epididymidis and the volume of the epididymal fluid in the tubules were also estimated. Results: The totalnumber of the late spermatids per testis was 2902 ±749 (million, x ±s) in the monkey, or 179 ±31 in the rat; thenumber of spermatozoa per epididymis was 3235 ±1835 in the monkey, or 241±76 in the rat. Conclusion: A largenumber of spermatozoa was densely packed and stored in the ductus epididymidis; the epididymal transit t