肾精亏虚对雄性小鼠及其雄性仔鼠生育力的影响

目的:观察肾精亏虚对雄性小鼠及其雄性仔鼠生育力的影响。方法:将30只6周龄雄性昆明小鼠随机均分为正常对照组、模型组和补肾组3组。模型组和补肾组采用房劳加惊恐的复合伤肾法制造肾精亏虚模型。补肾组每天给予0.16ml/10g体重的补肾填精方浓缩液灌胃。正常对照组及模型组予等量生理盐水灌胃,造模并给药21d。从造模结束次日起,所有小鼠与正常动情期雌鼠配对饲养5d后检测其精子密度及活动率。取出雌鼠待其分娩,分别计算各组配对雌鼠妊娠率和每胎生产数(仔鼠总数/妊娠并分娩的雌鼠只数)以评估父代小鼠生育力。雄性仔鼠饲养至6周龄时每组随机取出10只检测其精子密度及活动率。结果:模型组每胎生产数[(7.00±1.73)只]明显比正常对照组[(9.43±1.27)只]和补肾组[(8.80±1.10)只]低(P<0.05);模型组小鼠精子密度[(9.70±1.45)×106/ml]及活动率[(66.72±10.12)%]均明显低于正常对照组[(14.08±1.15)×106/ml,(81.75±3.56)%]和补肾组[(12.20±1.55)×106/ml,(78.55±4.38)%],P<0.01,而正常对照组与补肾组之间则没有差异(P>0.05);模型组仔鼠精子密度[(10.1±1.79)×106/ml]及活动率[(71.86±7.48)%]均低于正常对照组[(15.30±1.83)×106/ml,(79.86±5.68)%]和补肾组仔鼠[(14.20±2.21)×106/ml,(81.92±2.51)%],P<0.05,正常对照组与补肾组仔鼠之间没有差异(P>0.05)。结论:"惊恐、房劳"可以明显降低小鼠生育力,其仔鼠生育力亦可受累。补肾法可以阻断这种损伤的发生。     

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。     

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。     

益心康泰胶囊对老年SD大鼠生精功能及血清超氧化物歧化酶和丙二醛的影响

目的:观察益心康泰对老龄SD大鼠精子密度和活率,以及血清超氧化物歧化酶(SOD)和丙二醛(MDA)的影响,并探讨其可能的作用机制。方法:将老年(24月龄)SD雄性大鼠随机分为空白组、十一酸睾酮组、益心康泰高、中、低剂量组共5组,根据体重,分别给予10 ml/kg生理盐水、4 mg/kg十一酸睾酮悬浊液、0.6 g/kg、0.3 g/kg、0.15 g/kg益心康泰悬浊液灌胃,1次/d,30 d后,取附睾,剥离脂肪、包膜,剪碎放入37℃恒温水浴锅中预热的生理盐水试管内,利用CASA精子自动分析系统(伟力)检测精子各项常规参数。取血查血清SOD和MDA含量。并行睾丸组织HE染色,在光镜下观察睾丸组织形态学变化。结果:与空白对照组相比,高、中、低剂量益心康泰均能显著提高老年大鼠的精子密度[分别为(152.3±24.0)×106/ml、(334.5±97.7)×106/ml、(302.7±158.9)×106/ml、(221.4±75.6)×106/ml,P<0.05]和活率[分别为(26.5±2.0)%、(35.5±5.9)%、(33.1±5.4)%、(28.4±2.1)%,高、中剂量与空白组相比P<0.01],同时,高剂量组可以显著提高血清SOD含量[(22.0±5.3)U/ml,P<0.01],降低MDA含量[(13.6±4.6)nmol/ml,P<0.01];睾丸组织学检测显示,给药组相对于空白组细胞增殖更为活跃,可见较多分裂期细胞,管腔内成熟精子数目较多,间质稀少,血管丰富,间质细胞发育良好。结论:益心康泰可以通过影响SOD和MDA的含量而改善老年SD大鼠的生精功能。     

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。     

中药生精冲剂对生精障碍小鼠治疗作用的实验研究

目的:研究生精冲剂对环磷酰胺所致生精障碍小鼠的治疗作用。方法:46只雄性昆明小鼠随机分为正常组(n=10)、模型组(n=12)、对照组(n=12)和中药组(n=12),后3组腹腔注射环磷酰胺,建立生精障碍模型。造模完成后,中药组和对照组分别灌胃中药生精冲剂[16 g/(kg.d)]和克罗米芬[21.6 mg/(kg.d)],正常组与模型组每天灌胃等量生理盐水,连续15 d。次日,测量睾丸重量,并计算睾丸指数;放射免疫法测定血清FSH、LH、T水平;对睾丸组织进行组织学观察。结果:中药组小鼠血清T[(7.046±0.291)nmol/L]、FSH[(2.947±0.587)mIU/ml]、LH[(3.254±0.492)mIU/ml]、睾丸指数[(3.958±0.342)g/kg]与模型组各检测值相比[(6.231±0.317)nmol/L、(5.428±0.719)mIU/ml、(5.155±0.460)mIU/ml、(3.525±0.462)g/kg]差异有显著性(P<0.05)。组织学观察中药组睾丸生精小管生精细胞层数及管腔内精子数明显高于模型组。结论:生精冲剂治疗小鼠生精障碍有效。     

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。     

长期吸入低浓度七氟烷对小鼠生殖功能的影响

目的 评价长期吸入低浓度七氛烷对小鼠生殖功能的影响.方法 ICR雄性小鼠加只,日龄60 d,体重20～25 g,随机分为4组(n=10):对照组(C组);S1-3组分别吸入0.003%、0.01%和0.03%七氟烷.每天2 h,每周连续5 d,持续8周后处死动物.取睾丸和附皋,测定精子活动率、精子数量、精子畸变率、睾丸组织总乳酸脱氢酶(LDH)及乳酸脱氢酶同工酶-X(LDH-X)的活性,并观察睾丸组织超微结构.结果 与C组比较,S3组精子活动率降低、畸变率升高、睾丸组织LDH-X活性降低(P<0.05),S1,2组各指标差异无统计学意义(P>0.05),仅S3组睾丸组织出现病理学改变.结论 长期吸入0.03%七氟烷可导致雄性小鼠生殖功能异常,而长期吸入≤0.01%七氟烷对生殖功能未见影响.     

季节因素对供精志愿者精液冷冻前后相关参数的影响

目的:本研究旨在了解季节因素对供精志愿者冷冻前后精液参数及前向运动精子冷冻复苏率的影响。方法:6414份精液样本均来自2006年9月～2008年6月在浙江省人类精子库捐精的1135例供精志愿者,年龄22～32岁;按取精时间划分为春、夏、秋、冬季组;对所有精液标本均进行精液常规分析,对其中达到精子库冷冻标准的精液进行分装、冷冻,并进行复苏后的精液常规分析。结果:精液量春季最多[(2.92±1.17)ml],明显高于夏、秋、冬3个季节[(2.71±1.07)、(2.74±1.15)、(2.83±1.15)ml],有显著性差异(P均<0.05);精子密度秋季最高[(105.60±39.76)×106/ml],明显高于春、夏、冬3个季节[(101.18±40.16)×106/ml、(93.54±35.10)×106/ml、(101.29±38.37)×106/ml],有显著性差异(P均<0.05);前向运动精子百分率春季最高[(58.49±10.04)%],明显高于夏、秋、冬3个季节[(57.60±8.97)%、(56.76±9.63)%、(56.60±8.56)%],有显著性差异(P均<0.05);夏季精液的前向运动精子冷冻复苏率最低[(66.98±15.68)%],明显低于春、秋、冬3个季节[(69.04±14.26)%、(69.35±13.42)%、(69.31±15.11)%],有显著性差异(P均<0.05);春季精液冷冻复苏后前向运动精子密度最高[(28.82±11.29)×106/ml],明显高于夏、秋、冬3个季节[(25.57±10.08)×106/ml、(26.97±9.68)×106/ml、(26.21±9.47)×106/ml],有显著性差异(P均<0.05);夏季精液冷冻复苏后前向运动精子百分率最低[(39.75±9.48)%],明显低于春、秋、冬3个季节[(41.87±9.28)%、(41.44±8.45)%、(41.03±9.13)%],有显著性差异(P均<0.05)。结论:季节因素对供精志愿者精液参数及前向运动精子冷冻复苏率有影响,春季精液量多、前向运动精子百分率高、冷冻复苏率高、冷冻复苏后前向运动精子密度高,是捐精的最佳季节。     

不同生精功能障碍无精子症患者行ICSI后胚胎发育潜能的研究

目的:分析不同生精功能障碍的无精子症患者行ICSI后其胚胎发育潜能。方法:149例患者分为生精功能正常组,轻度、中度和重度生精功能障碍组,采用经皮附睾精子抽吸术(PESA)或经皮睾丸精子抽吸术(TESA)抽取不同生精功能障碍患者的精子行ICSI,记录和分析胚胎的正常受精率、卵裂率、优良胚胎形成率以及妊娠率。结果:PESA与TESA组比较,正常受精率(%)为74.9±19.6 vs 66.3±22.7(P>0.05),卵裂率(%)为96.7±8.6 vs 92.8±19.8(P>0.05),优良胚胎率(%)为43.5±26.2 vs 35.0±29.4(P>0.05)以及妊娠率(%)为44.0 vs 52.0(P>0.05),均无统计学差异。生精功能障碍从正常组到重度组的正常受精率(%)变化依次为77.8±18.4、68.4±18.5、73.5±19.8、51.4±27.9,其中轻度生精功能障碍与正常生精组有差异(P<0.05),重度生精功能障碍组与其他各组有统计学差异(P<0.05);胚胎卵裂率(%)变化依次为96.7±9.2、96.5±15.0、93.9±12.1、93.7±11.1,各组无统计学差异;优良胚胎率(%)变化依次为47.1±25.8、40.3±27.6、36.2±23.1、15.0±24.6,重度生精障碍组与其他各组有统计学差异(P<0.05);妊娠率(%)依次为54.8%、50.0%、13.6%、10.0%,有统计学差异(P<0.05)。结论:采用PESA或TESA行ICSI在正常受精率,卵裂率,优良胚胎率以及妊娠率上较均无明显差异。随着患者生精障碍程度的加重,受精率、优良胚胎率以及妊娠率均显著下降,而卵裂率却无明显区别。     

Activity of testis angiotensin converting enzyme (ACE) in ejaculated human spermatozoa

Testicular angiotensin converting enzyme (ACE) isozyme is likely to play important functional roles in male reproduction. Several studies have shown that ACE is released from human spermatozoa during capacitation and that ACE is associated with reduced sperm motility. Recently, we established an assay to detect testicular ACE activity in human spermatozoa. The purpose of this study was to determine if testicular ACE activity is related to sperm motility in human ejaculates. Semen samples were collected from 80 infertile patients. According to the semen characteristics, they were divided into four (WHO) categories. Enzyme activities of ACE in spermatozoa (testicular ACE) and seminal plasma (somatic ACE) were spectrophotometrically determined. Total testicular ACE activity in spermatozoa was measured by solubilization of spermatozoa with Triton X-100. Membrane testicular ACE activity was measured in a sperm : PBS suspension. Sperm concentration and sperm motility were 136.6 +/- 154.1 x 10(6)/mL and 58.6 +/- 23.4%, respectively (mean +/- SD). Enzyme activities of membrane testicular ACE, total testicular ACE and somatic ACE were 0.273 +/- 1.219 microU/10(6) spermatozoa, 0.35 +/- 1.34 microU/10(6) spermatozoa and 684.7 +/- 226.6 mU/mL, respectively. A negative correlation was observed between sperm motility and membrane testicular ACE activity (p < 0.05). Membrane testicular ACE activity in 44 normal semen samples was 0.04 +/- 0.02 microU/10(6) spermatozoa, whilst that in 36 abnormal semen samples was 0.24 +/- 0.42 microU/10(6) spermatozoa. There was a significant difference between these two groups (p < 0.01). Membrane testicular ACE in sperm samples from normozoospermic men was significantly lower than that from oligoasthenozoospermic men (p < 0.05). These findings suggest that testicular ACE is released from normal functional spermatozoa for them to have fertilizing ability.     

Effect of lead chloride on spermatogenesis and sperm parameters in mice

Aim: To evaluate the effect of acute lead chloride exposure on testis and sperm parameters in mice.Methods: PbC12, 74 mg/kg, was daily administered to sexually mature male mice for 3 days and the effects on the testicular histology and ultrastructure as well as the motility and density of spermatozoa in cauda epididymis were observed. An additional group of mice were treated for 1-3 days and were allowed to recover for 32 days to determine the reversibility of lead-induced changes. Results: The testicular weight, seminiferous tubular diameter and sperm counts were significantly decreased following 3 days of PbCl2 treatment, but were unaffected by shorterterm exposures. The changes caused by lead are mostly reversible. Conclusion: Acute lead chloride exposure injures the fertility parameters of male mice and the effects are partially reversible. (Asian JAndrol 2004 Sep; 6: 237-241)     

Early apoptotic changes in human spermatozoa and their relationships with conventional semen parameters and sperm DNA fragmentation

Aim： To investigate whether early apoptotic changes in spermatozoa can be significant markers for sperm quality. Methods： Two early apoptotic changes in the semen of 56 men were assessed using Annexin V （AN）/propidium iodide （PI） staining for phosphatidylserine externalization and JC-1 staining for mitochondrial membrane potential （MMP）. The results were compared with conventional semen parameters and DNA fragmentation identified using the TUNEL assay. Results： The different labeling patterns in the bivariate Annexin V/PI analysis identified four distinctive spermatozoa populations. The percentage of AN^-/PI^- spermatozoa positively correlated with conventional semen parameters and MMP, but negatively correlated with TUNEL （＋） spermatozoa. As for the AN^-/PI^＋ fraction, we found an opposite result in comparison to AN^-/PI^- spermatozoa. The level of early apoptotic AN^＋/PI^- spermatozoa negatively correlated with MMP and sperm motility. The level of late apoptotic AN^＋/PI^＋ spermatozoa negatively correlated with conventional semen parameters and MMP, and positively correlated with TUNEL （＋） spermatozoa. MMP positively correlated with conventional semen parameters, but negatively correlated with TUNEL （＋） spermatozoa. Conclusion： Although early apoptotic AN^＋/PI^- spermatozoa only negatively correlates with sperm motility, the differences in proportion of each subpopulation of spermatozoa （especially, the percentage of AN^-/PI^- spermatozoa）, and decreased MMP might be significant markers for diagnosing male infertility. They possibly bring additional information to predict the outcome of in vitro fertilization. （Asian J Androl 2008 Mar; 10： 227-235）     

Impaired reproductive function of male rats infected with Toxoplasma gondii

Toxoplasmosis is one of the classical conditions known to have an adverse effect on female reproductive functions, but a few investigations into male reproductive parameters have been performed. This work was carried out to study the effects of Toxoplasma gondii on reproductive function in male rats. Male rats were infected with the RH strain of T. gondii tachyzoites, and following every 10 days from 10 to 70 postinfection (PI), the percentage of body weight to testis weight ratio as well as epididymal sperm parameters (number, motility, viability, and morphology rates), serum testosterone (ST), intratesticular testosterone (ITT), serum lactate dehydrogenase (SLDH), intratesticular lactate dehydrogenase and fructose in seminal vesicles and coagulating glands were measured. The results of the study showed sperm motility, viability and concentration rates were significantly decreased temporary after infection up to 70 days. Sperm abnormality was also increased during these days. In addition, temporary alteration in ST, ITT, SLDH, intratesticular LDH and fructose in seminal vesicle and coagulating gland was observed PI. These findings suggest that toxoplasmosis can cause impermanent impairment on the reproductive parameters of male rats.     

In vivo study of LDH isoenzyme activities in heart, liver and testis cytosols of gossypol-treated rats

LDH isoenzyme activities of heart, liver and testis homogenates were measured in rats treated for 15 or 30 days with 30 mg gossypol acetic acid/kg body weight daily, a dose which severely suppressed sperm motility. No differences in LDH activities of the examined organs were found in comparison with control animals. LDH-X, the main LDH isoenzyme in spermatozoa and testicular germ cells from primary spermatocytes onwards was also unaffected. These results contrast with in vitro experiments on human, rabbit, and boar spermatozoa, purified bovine LDH-X and rat testis homogenate which show dose-dependent inhibition of LDH-X after incubation with gossypol. Our results therefore suggest that inhibition of LDH by gossypol is not the primary cause of sperm immotility.     

育亨宾对雄性瑞士白化小鼠的生殖、细胞和生化毒性(英文)

目的:研究育亨宾(Yohimbe)对瑞士白化小鼠生殖细胞的影响。方法:用不同剂量(188,375和750mg/[kg·day])的育亨宾水性悬浮液灌胃处理成年雄性小鼠,持续90天。检测下面的参数:(1)生殖器官重量,(2)精子的活动力和数量,(3)怀孕率和平均受精卵附着数,(4)精子形态,(5)睾丸染色体的细胞学,(6)蛋白质,RNA,DNA,丙二醛,非蛋白质的硫氢化合物(NP-SH)和激素的生化评估。结果:育亨宾处理使精囊重量、精子的活动性和精子数量、受精卵附着前和受精卵附着后的重量的显著增加,雄性生殖能力降低。精子畸形和染色体变异方面的数据进一步证实了这一结果。生化评估数据也显示睾丸细胞中的丙二醛,NP-SH 的消耗,蛋白质,RNA 和 DNA 增加了。结论:本研究结果表明,自由基可能是通过 yohimbine(Yohimbe 的主要成分)对神经传递素,包括去甲肾上腺素的影响产生细胞毒性和生殖毒性。这些数据提示要谨慎使用 Yohimbe。     

Involvement of A1 adenosine receptors in the acquisition of fertilizing capacity

Ejaculated mammalian spermatozoa acquire competence to fertilize oocytes by a two-step process: capacitation followed by acrosome reaction. The biochemical and biophysical modifications occurring in vivo in the female reproductive tract can be reproduced in vitro, and previous studies have suggested a capacitative role for adenosine A(1) receptor (A(1)R). Mice with a targeted disruption of the Adora 1 gene (A(1)R-/- mice) provide a useful model for better understanding the role of the A(1)R in fertility. Murine spermatozoa express A(1)R in the head, neck, midpiece region, and tail. The number of capacitated spermatozoa incubated in human tubal fluid was significantly reduced in A(1)R-/- compared with A(1)R+/+ and A(1)R+/- spermatozoa. The difference between A(1) R+/+ and A(1)R-/- mouse spermatozoa was mainly in the time necessary to reach the maximum percentage of capacitation. A(1)R+/+ murine sperm obtained the full state of capacitation within 90 minutes whereas A(1)R-/- sperm required 240 minutes. Caffeine, a known antagonist of A(1) and A(2A) adenosine receptors, lowered the number of capacitated sperm and affected the time of capacitation in a dose-dependent manner, mimicking the effects of the lack of A(1) receptors. Although number, motility, and viability of A(1)R-/- murine sperm was not significantly different from A(1)R+/+ mouse spermatozoa, a significant reduction of the number of pups produced by A(1)R-/- male mice suggests that A(1) receptors must be fully operative to accomplish the optimal degree of capacitation and thereby fertilization.     

Inflammatory-associated obstructions of the male reproductive tract

A history of urogenital inflammation occurs in 5-12% of men attending infertility clinics. Usually, infection has a detrimental effect on sperm quality by reducing concentration and motility, and possibly affecting the number of morphological normal spermatozoa. In addition, infection may be the source of auto-antibodies against spermatozoa, found in about 8% of the infertile male population. In contrast to the situation in women, there is no clear evidence that male accessory gland infections can result in epididymal blockage or vassal obstruction, with the exception of genital tuberculosis. Although Chlamydia trachomatis is a well-documented source of chronic prostatitis, the infection does not seem to cause obstruction of the reproductive tract, as it does in women. If male urogenital infection causes obstruction it is most likely located at the level of the ejaculatory ducts. Chronic prostatitis has been proved to cause scarring of the prostatic and ejaculatory ducts, resulting in low seminal volume with low fructose and alpha-glucosidase. Many of these men present with severe oligozoospermia or azoospermia, normal size testis and normal gonadotrophins. We performed an excisional testicular biopsy in all men presenting with <1 million spermatozoa per millilitre and found that 39 of 78 (50%) had a normal spermatogenesis. A history of male accessory genital infection was found in 12% of the men and 10% had abnormalities found on transrectal ultrasound of the prostate (like oedema, dilatation of the seminal vesicles and ejaculatory ducts) intraprostatic calcifications and dilatation of the periprostatic venous plexus. Ejaculatory duct obstruction is a common cause of male infertility and infections are present in at least 22-50% of these men. Transurethral resection of the ejaculatory ducts may result in a significant improvement of the sperm quality and in spontaneous pregnancies in up to 25% of the couples. In case of failure sperm aspiration from the epididymis and intracytoplasmic sperm injection is the treatment of choice.