男性不育精液中尿酸含量与生殖细胞凋亡的探讨

目的探讨人精液中尿酸含量与生殖细胞凋亡的关系.方法参照WHO标准方法,进行精液常规分析,按精子密度、活动率不同分为(正常、＜20、20～40、＞40)4个组.采用尿酸酶-过氧化物酶偶联法检测精液尿酸含量.用脱氧核苷酸末端转移酶(TdT)介导的缺口末端标记(TUNEL)和瑞-姬染色法,分别检测和观察生殖细胞的凋亡.结果75例不育者精液尿酸含量和生殖细胞的凋亡率分别为(263.87±57.15)μmol/L和(16.38±1.25)%与正常生育组(397.60±52.1)μmol/L、(4.61±1.23)%比较呈显著性差异(P＜0.01).精子密度和活动率随精液尿酸含量减少而降低,生殖细胞调亡率随之上升(P＜0.01).不育组精液尿酸含量与生殖细胞的凋亡地显著性负相关(r=-0.93,P＜0.05).凋亡的生殖细胞体积缩小,核染色质致密,凝聚在核周形成新月形,或核裂解形成凋亡小体.结论精液尿酸含量与生殖细胞的凋有着密切关系.低精液尿酸含量可使睾丸生殖细胞凋亡率增加,使精子密度和活率下降而致男性不育.     

人精液一氧化氮含量与男性不育的相关性

目的:研究精液中一氧化氮(NO)含量对精子凋亡的影响及其与男性不育之间的相关性.方法:采用精子质量检测系统对精液标本进行常规检查;应用硝酸还原酶法测定精液中NO的含量;应用瑞-姬染色和TdT介导的原位末端标记(TUNEL)法检测凋亡精子;观察凋亡精子的形态结构改变.结果:不育组精液中NO(58 37±14 14)μmol/l比正常生育组精液中NO(35 20±8 23)μmol/l含量高;正常生育组精子凋亡率9 67%±2 54%比不育组精子凋亡率33 98%±10 54%低.结论:不育组精液中精子的凋亡率随着NO含量的增高而增加.高浓度的NO导致精子凋亡率增加而致使男性生育力下降.     

人类精液中一氧化氮和尿酸含量检测的关系

目的探讨人精液中一氧化氮(N0)与尿酸含量的关系,对精了质量的影响。方法参照WHO标准方法,进行精液常规分析,按精子密度、活动率不同分为(正常、<20、20~40、>40)4个组。采用镀铜镉还原荧光法检测NO代谢产物硝酸盐(NO3-)。采用尿酸酶一过氧化物酶偶联法检测精液尿酸含量。结果70例不育组精液中尿酸含量和NO含量为(236.4±47.8)μmol/L、(78.7±1.6)μmol/L与正常生育组(398.6±52.3)μmol/L、(41.84±1.6)μmol/L呈显著性差异(P<0.01)。将尿酸含量与NO含量进行相关性分析,两者呈显著性负相关(r=-0.96,P<0.05)。不育各精子密度和活动率组精液尿酸含量随精子密度及活动率增加而上升,N0含量随之下降(P<0.01),结论精液尿酸含量测定可作为评价精子受活性氧损害的重要指标,证明尿酸对活性氧尤其在医学领域极为重视的NO损害精子具有保护性作用。     

饮酒与男性不育的关系研究

目的探讨长期高浓度过量饮酒者精液中一氧化氮（NO）含量其精子质量和生精细胞凋亡与不育的关系。方法随机将146例精液分为5组,采用硝酸还原酶法特异地将NO代谢产物硝酸盐（NO3^-）测还原成亚硝酸盐（NO2^-）总量代表NO水平。用脱氧核苷酸末端转移酶（TdT）介导的缺口末端标记（TUNEL）法和双目光学显微镜,分别检测和观察生精细胞的凋亡率及形态结构。用SQA-V全自动精子质量分析仪,测定精子质量。结果未饮酒生育组精液中NO的含量为（54.81±11.45）μmol/L,生精细胞的凋亡率（4.52±1.23）%,精子质量活率（80.24±0.17）%、活力a＋b（78.32±0.12）%、畸形率（5.30±0.13）%,与长期高浓度过量饮酒各组结果相比,均呈显著性差异（P〈0.01,见表2）。长期高浓度过量饮酒各组NO的含量和生精细胞的凋亡率呈显著的正相关（r=0.93）。凋亡的生精细胞核染色质浓缩于核周形成新月形,核裂解形成凋亡小体。结论长期高浓度过量饮酒者精液中NO的含量和生精细胞的凋亡率均升高,精子质量低下。提示长期高浓度过量饮酒可致机体NO过度产生而促使生精细胞凋亡致男性不育的因素之一。     

抑制Hedgehog信号通路对前列腺癌DU125细胞增殖及凋亡的影响

目的研究Hedgehog(Hh)信号通路阻断剂环王巴明对前列腺癌Dul45细胞增殖及凋亡的影响。方法体外培养DU145细胞,以10、50、100μmol/L的环王巴明作用24 h,MTT法检测环王巴明对DU145细胞增殖的影响,流式细胞技术检测环王巴明对DU145细胞凋亡的影响,RT-PCR检测环王巴明对DU145细胞Gli-1 m RNA表达的变化,Westernblot检测环王巴明对DU145细胞Gli-1蛋白表达的变化。结果 MTT检测结果表明10μmol/L环王巴明组(85.01±2.61)%、50μmol/L环王巴明组(76.71±3.13)%和100μmol/L环王巴明组(69.10±4.11)%细胞活性较空白对照组(99.97±0.21)%降低(P0.05);流氏细胞技术检测结果表明10μmol/L环王巴明组(15.12±0.21)%、50μmol/L环王巴明组(24.97±0.24)%和100μmol/L环王巴明组(31.26±0.26)%细胞总凋亡率较空白对照组(2.56±0.28)%升高(P0.05);RT-PCR检测结果表明10μmol/L环王巴明组(0.69±0.06)%、50μmol/L环王巴明组(0.69±0.06)%和100μmol/L环王巴明组(0.69±0.06)%Gli-1m RNA表达水平较空白对照组(0.92±0.11)%降低(P0.05);Western blot检测结果表明10μmol/L环王巴明组(0.79±0.06)%、50μmol/L环王巴明组(0.59±0.05)%和100μmol/L环王巴明组(0.41±0.04)%Gli-1蛋白表达水平较空白对照组(0.94±0.11)%降低(P0.05)。结论 Hedgehog信号通路阻断剂环王巴明可以抑制DU145细胞增殖、诱导DU145细胞凋亡,其作用机制可能与下调GLi-1表达有关。     

抑制Hedgehog信号通路对脑胶质瘤U87细胞增殖及凋亡的影响

目的研究Hedgehog(Hh)信号通路阻断剂环王巴明对脑胶质瘤U87细胞增殖及凋亡的影响。方法体外培养U87细胞,以10、50、100μmol/L的环王巴明作用24h,MTT法检测环王巴明对U87细胞增殖的影响,流式细胞技术检测环王巴明对U87细胞凋亡的影响,RT-PCR检测环王巴明对U87细胞Gli-1 mRNA表达的变化,Western blot检测环王巴明对U87细胞Gli-1蛋白表达的变化。结果 MTT检测结果表明10μmol/L环王巴明组(85.11±2.61)%、50μmol/L环王巴明组(76.81±3.13)%和100μmol/L环王巴明组(69.20±4.11)%细胞活性较空白对照组(99.87±0.21)%降低(P0.05);流氏细胞技术检测结果表明10μmol/L环王巴明组(15.22±0.21)%、50μmol/L环王巴明组(24.87±0.24)%和100μmol/L环王巴明组(31.36±0.26)%细胞总凋亡率较空白对照组(2.66±0.28)%升高(P0.05);RT-PCR检测结果表明10μmol/L环王巴明组(0.68±0.06)%、50μmol/L环王巴明组(0.48±0.06)%和100μmol/L环王巴明组(0.30±0.06)%Gli-1mRNA表达水平较空白对照组(0.92±0.11)%降低(P0.05);Western blot检测结果表明10μmol/L环王巴明组(0.78±0.06)%、50μmol/L环王巴明组(0.58±0.05)%和100μmol/L环王巴明组(0.40±0.04)%Gli-1蛋白表达水平较空白对照组(0.94±0.11)%降低(P0.05)。结论Hedgehog信号通路阻断剂环王巴明可以抑制脑胶质瘤U87细胞增殖、诱导U87细胞凋亡,其作用机制可能与下调GLi-1表达有关。     

抑制Hedgehog信号通路对食管癌细胞EC9706增殖及凋亡的影响

目的研究Hedgehog(Hh)信号通路阻断剂环王巴明对食管癌EC9706细胞增殖及凋亡的影响。方法体外培养食管癌EC9706细胞,以10、50、100μmol/Lol/L的环王巴明作用24 h,MTT法检测环王巴明对EC9706细胞增殖的影响,流式细胞技术检测环王巴明对EC9706细胞凋亡的影响,RT-PCR检测环王巴明对EC9706细胞Gli-1 mRNA表达的变化,Western blot检测环王巴明对EC9706细胞Gli-1蛋白表达的变化。结果 MTT检测结果表明10μmol/Lol/L环王巴明组(86.11±2.61)%、50μmol/Lol/L环王巴明组(77.81±3.13)%和100μmol/Lol/L环王巴明组(70.20±4.11)%细胞活性较空白对照组(99.97±0.21)%降低(P0.05);流氏细胞技术检测结果表明10μmol/Lol/L环王巴明组(16.22±0.21)%、50μmol/Lol/L环王巴明组(25.87±0.24)%和100μmol/Lol/L环王巴明组(32.36±0.26)%细胞总凋亡率较空白对照组(2.76±0.28)%升高(P0.05);RT-PCR检测结果表明10μmol/Lol/L环王巴明组(0.78±0.06)%、50μmol/Lol/L环王巴明组(0.58±0.06)%和100μmol/Lol/L环王巴明组(0.40±0.06)%Gli-1mRNA表达水平较空白对照组(0.93±0.11)%降低(P0.05);Western blot检测结果表明10μmol/Lol/L环王巴明组(0.68±0.06)%、50μmol/Lol/L环王巴明组(0.48±0.05)%和100μmol/L环王巴明组(0.30±0.04)%Gli-1蛋白表达水平较空白对照组(0.75±0.11)%降低(P0.05)。结论 Hedgehog信号通路阻断剂环王巴明可以抑制食管癌EC9706细胞增殖、诱导U87细胞凋亡,其作用机制可能与下调GLi-1表达有关。     

一氧化氮对鼻咽癌CNE-2细胞增殖与凋亡的影响

目的:探讨外源性NO对CNE-2细胞增殖与凋亡的影响.方法:分别用不同浓度NO供体药物硝普钠(sodium nitroprusside,SNP)干预CNE-2细胞,观察细胞形态学变化、检测细胞的抑制率及细胞的凋亡和坏死率.结果:SNP以浓度依赖性方式抑制CNE-2细胞增殖,SNP 100,200,400,600,800,1600,3200μmol/L各组细胞抑制率与药物浓度呈正相关;SNP以浓度依赖性方式促进CNE-2细胞凋亡,SNP(1000μmol/L)组细胞凋亡率较SNP(600μmol/L)组显著增高(P<0.05).结论:外源性NO能抑制CNE-2的增殖,促进CNE-2的凋亡,其抑制效应与NO浓度呈正相关.     

白藜芦醇对神经母细胞瘤SH-SY5Y增殖的影响

目的:探讨白藜芦醇(Resveratrol,Res)对人神经母细胞瘤SH-SY5Y增殖变化规律和生长状况的影响。方法:通过不同浓度(0.15～500)μmol/LRes作用于SH-SY5Y,检测药物作用5d后各组细胞增殖率和细胞生长状态,同时通过增殖率曲线获得其半数生长抑制浓度(IC50)和杀伤浓度,并对各组细胞进行Hochest染色,检测其细胞凋亡情况。结果:Res5μmol/L组细胞增殖率为(117.00±15.30)%显著高于空白对照组(P0.05),15μmol/L组细胞增殖率为(31.33±2.89)%,50、150、500μmol/L组,细胞出现负增长。Res对SH-SY5Y的IC50为12.78μmol/L,细胞杀伤浓度(即增殖率为0%)为19.88μmol/L。Res50～500μmol/L各组内,部分细胞皱缩,突起减少或消失,并出现凋亡细胞。结论:Res在0.15～500μmol/L浓度范围内对SH-SY5Y的增殖影响存在浓度依赖性,并依次表现为促进增殖、抑制增殖和杀伤细胞三个方面效应。其中杀伤细胞效应与促进SH-SY5Y的凋亡启动相关。     

多靶点抑制剂西奥罗尼增强人胶质瘤细胞放射敏感性的机制

目的:探索多靶点抑制剂西奥罗尼对人胶质瘤细胞放射敏感性的影响及其机制。方法:利用CCK-8实验和集落形成实验测定西奥罗尼对人胶质瘤U251细胞和T98G细胞增殖能力的影响。进一步,对U251细胞和T98G细胞进行药物和(或)X射线处理,设对照组、西奥罗尼(2.5μmol/L)组、4 Gy辐照组和西奥罗尼(2.5μmol/L)联合4 Gy辐照组,流式细胞术检测4组细胞的细胞周期和凋亡变化;通过Western blot检测4组细胞周期和凋亡关键蛋白的表达量;通过免疫荧光实验,探索西奥罗尼联合辐照对DNA损伤和修复的影响;最后通过Western blot检测DNA损伤修复关键蛋白的表达量。结果:与对照组相比,西奥罗尼显著抑制U251细胞和T98G细胞的增殖,半数抑制浓度(IC50)分别为7.773μmol/L和24.68μmol/L;随着X射线剂量的增加,细胞存活率在X射线辐照组和联合组中均显著降低,并且联合组在不同射线剂量的细胞存活率均低于单独辐照组,西奥罗尼的辐射增敏比(SER)分别为1.387和1.384。U251细胞对照组、西奥罗尼(2.5μmol/L)组、4 Gy辐照组和西奥罗尼(2.5μmol/L)联合4 Gy辐照组中处于G2/M期的细胞比例分别为(17.68±0.98)%、(18.93±0.03)%、(16.31±0.58)%和(23.96±1.18)%;4组细胞的总凋亡率分别为(8.04±0.24)%、(17.04±0.75)%、(9.34±0.50)%和(21.22±0.38)%。T98G细胞对照组、西奥罗尼(2.5μmol/L)组、4 Gy辐照组和西奥罗尼(2.5μmol/L)联合4 Gy辐照组中处于G2/M期的细胞比例分别为(2.05±0.71)%、(5.70±0.34)%、(5.14±0.33)%和(6.54±0.13)%;4组细胞的总凋亡率分别为(11.35±0.39)%、(13.23±0.18)%、(17.43±0.30)%和(21.32±0.64)%。免疫荧光实验发现,在30 min,γH2AX荧光灶点在单纯辐照组和联合组中均十分明显,并且联合组的荧光强度更强;在6 h和24 h,γH2AX荧光灶点在X射线辐照组中逐渐减少,而在联合组中可以观察到γH2AX的荧光强度依然较强。结论:西奥罗尼通过诱导G2/M期阻滞、促进凋亡、诱导DNA损伤及延迟DNA修复来增强人胶质瘤细胞的放射敏感性。     

一氧化氮对大鼠睾丸生殖细胞凋亡作用的研究

目的：探讨一氧化氮（NO）对大鼠睾丸生殖细胞凋亡的影响。方法 采用MTT法观察NO对细胞增殖的抑制作用，透射电镜分析细胞结构变化，末端脱氧核苷酸转移酶（TdT）介导的原位末端标记法（TUNEL）及琼脂糖凝胶电泳检测生殖细胞DNA变化以进一步分析细胞凋亡的特征。结果：MTT法及DNA末端标记法检测表明，NO可抑制细胞增殖，诱导生殖细胞的凋亡，并呈剂量及时间依赖性，NO组细胞凋亡率明显高于对照组（P〈0．01）。透射电镜观察NO处理20h后的生殖细胞，其核染色质凝集、附着于核边缘呈新月形，核固缩、碎裂形成凋亡小体，符合凋亡细胞特征性改变。结论：一氧化氮具有促使生殖细胞凋亡形成的作用，这对不育症的研究有重要的价值。     

bcl—2癌基因反义硫代磷酸寡脱氧核苷酸诱导HL60细胞凋亡

目的 不同浓度ｂｃｌ－２癌基因反义硫代磷酸寡脱氧核苷酸９ＡＳ－ＰＳ－ＯＤＮ,ＡＳＰＯ）对ＨＬ６０细胞凋亡的诱导作用。方法 ＡＳＰＯ与ＨＬ６０细胞共培养后,用吖啶橙（ＡＯ）染色法,流式细胞仪ＤＮＡ倍体分析,电镜观察、ＤＮＡ片段电沪等方法进行观察。结果 ＡＳＰＯ组与正义组比较能特异诱导ＨＬ６０细胞的凋亡,且于培养２４５小时即可出现,此时ＡＳＰＯ５、１０、２０μｍｏｌ／Ｌ浓度各组的凋亡率分别为：（９．７     

人精子膜功能完整性与精液参数的关系

目的探讨精子膜功能完整性与精液参数的关系。方法收集503例精液样本,其中对照组149例,不育组354例。根据WHO标准分析精子密度、活率、活力、精液白细胞浓度、精子形态和精子尾部低渗膨胀(HOS)率。结果不育组精子尾部低渗膨胀率显著低于对照组(P<0.05)。与对照组相比,HOS正常不育组和HOS异常不育组形态正常精子率、密度、活力、活率均显著降低(P<0.05),头部异常精子率、精液白细胞浓度显著增高(P<0.05);此外,HOS正常不育组的尾部异常精子率显著高于对照组,其精子活力、活率均显著高于HOS异常不育组(P<0.05)。精子HOS与精子密度、活力、活率呈显著正相关,与精液白细胞浓度呈显著负相关(P<0.05)。结论精子膜功能可能与精液参数密切相关,精子膜功能是评价男性生育力的重要指标。     

NO介导的小鼠胸腺细胞中线粒体的变化在细胞凋亡过程中的作用

目的研究一氧化氮(NO)介导的胸腺细胞凋亡中线粒体膜电位(ΔΨm)和心磷脂(CL)含量变化的特点。方法以S-亚硝基-N-乙酰青霉胺(SNAP)作为NO的供体诱导胸腺细胞凋亡,以地塞米松(DEX)作为阳性对照药物;设空白对照组、SNAP组和DEX组3个实验组;经膜联蛋白V(annexinVmAb)和碘化丙啶(PI)染色后,用流式细胞术(FCM)检测细胞磷脂酰丝氨酸(PS)外翻;用3,3’-二已基噁羰花青碘化物[DiOC6(3)]和PE-anti-annexinVmAb检测凋亡中ΔΨm变化;用壬基吖啶橙(NAO)和PE-anti-annexinVmAb检测凋亡中线粒体CL变化。结果SNAP作用后6h,胸腺细胞出现典型的细胞凋亡特征,多数annexinV阳性的细胞出现皱缩。DEX组ΔΨm降低且未凋亡的细胞比例显著高于空白对照组(P<0.01);而SNAP组该群细胞所占比例与空白对照组比较,差异无统计学意义(P>0.05)。各组中约40%~50%的DiOC6(3)阴性细胞同正常细胞的大小。SNAP组CL含量降低的凋亡细胞所占比例显著高于对照组(P<0.01),未见CL含量降低且未凋亡的细胞群。空白对照组和SNAP组中分别有(48.32±3.96)%、(43.64±4.90)%的细胞CL含量降低但大小同正常细胞。结论NO介导的小鼠胸腺细胞的凋亡过程,依次为磷脂酰丝氨酸外翻、线粒体去极化、CL氧化及细胞皱缩。同DEX模型组相比较,NO介导的小鼠胸腺细胞线粒体的变化为凋亡过程中较晚期的变化。     

Apoptosis in human sperm: its correlation with semen quality and the presence of leukocytes

BACKGROUND: Apoptosis plays an important role in regulating spermatogenesis. However, the biological significance of apoptosis in ejaculated sperm is not yet clear. This study set out to investigate how apoptosis correlates with semen quality and the presence of seminal leukocytes. METHODS: Fifty-seven semen samples from the male partners of infertile couples were classified as normal or abnormal according to World Health Organization guidelines. Flow cytometry was used to evaluate sperm populations and seminal leukocytes. Preliminary flow cytometry analysis using 6-carboxyfluoresceindiacetate (6-CFDA), which identifies live cells, and propidium iodide (PI), which stains only dead cells, was performed in order to pinpoint the sperm region accurately. Having thus gated the sperm population, bivariate Annexin V/PI analysis was then carried out in order to measure the percentage of apoptotic and necrotic sperm and the apoptotic index (the ratio between apoptotic:live sperm). Leukocytes were counted by the standard peroxidase test and by flow cytometry using monoclonal antibody (mAb) anti-CD45 or anti-CD53. RESULTS: No significant differences in the apoptotic index and the percentage of live and apoptotic sperm were detected between the subjects with normal and abnormal semen. A significant inverse correlation between sperm concentration and the apoptotic index was observed only in the normal sperm group. There was no correlation between the concentration of leukocytes, detected either by peroxidase or by mAb anti-CD45 or anti-CD53, either with the percentage of apoptotic sperm or with the apoptotic index. In contrast, the ratio between CD45 positive leukocytes and sperm showed a significant correlation with the apoptotic index. A weaker correlation was found when leukocytes were counted by peroxidase, while no correlation was observed using mAb anti-CD53. CONCLUSIONS: Sperm apoptosis did not seem to be correlated with semen quality. In the absence of genito-urinary infection, one of the main functions of seminal leukocytes is probably to provide for the removal of apoptotic sperm.     

Trimetazidine inhibits cardiomyocyte apoptosis in a rabbit model of ischemia-reperfusion

The effects of trimetazidine on cardiomyocyte apoptosis and hemodynamics in a rabbit model of ischemia-reperfusion were determined. Thirty male New Zealand white rabbits were randomly divided into sham, control, and treated groups (n = 10). Trimetazidine (2 mg/kg(-1)/day(-1)) was fed for 2 weeks to treated animals before the procedure. Control and treated groups were subjected to a 30-min coronary occlusion followed by a 2-h reperfusion. Mean arterial pressure, left ventricular systolic pressure, and maximum rate of left ventricular pressure rise were significantly higher in the treated group than in the controls (P < 0.01, < 0.01, and < 0.05, respectively), whereas left ventricular end-diastolic pressure was significantly lower in the treated group than in the controls (P < 0.01). As compared with the sham group, controls had a significantly higher apoptotic index (22.10% +/- 2.85% vs 0.51% +/- 0.31%, P < 0.01) and malondialdehyde (MDA) concentration (18.52 +/- 1.51 vs 5.75 +/- 0.95 micromol/, P < 0.01), and significantly lower serum superoxide dismuase (SOD) levels (66.40 +/- 7.92 vs 89.25 +/- 1.36 microU/L, P < 0.01). Trimetazidine pretreatment apparently decreased apoptotic index (11.37% +/- 2.53%, P < 0.01 vs the sham or control) and MDA concentration (5.49 +/- 0.74 micromol/L, P > 0.05 vs sham, P < 0.01 vs control), and increased SOD levels (88.81 +/- 2.81 microU/L, P > 0.05 vs sham, P < 0.01 vs control). The caspase-3 activation and mitochondrial cytochrome c release were also higher in controls than in the treated group (P < 0.01). The apoptotic indices were negatively correlated with SOD and positively correlated with MDA in the groups, suggesting that trimetazidine may be a useful drug in preventing cardiomyocyte apoptosis and ischemia-reperfusion injury.     

Cumulus cells are required for the increased apoptotic potential in oocytes of aged mice

Recent studies with female ICR mice have suggested that oocyte DNA fragmentation is one reason for poor oocyte quality and lower fertility associated with ageing. Since it was not determined if this increased 'apoptotic' potential in aged oocytes is due to changes within the oocyte itself or within the microenvironment of cumulus cells (CC) surrounding the germ cell, we sought to clarify if CC were required to affect the rate of apoptosis in oocytes maintained in vitro. Intact cumulus-oocyte complexes (COC) were retrieved by superovulation of virgin female ICR mice at 7 weeks ('young') or 34-35 weeks ('aged') of age. One-half of the COC in each group were incubated at 37 degrees C in human tubal fluid medium under paraffin oil for 24 h. The other half of the COC in each group were denuded of CC and incubated under the same conditions (denuded oocytes; DO). Following incubation, COC were stripped of adherent CC by gentle pipetting. All DO were then fixed and checked by light microscopy for morphological changes characteristic of apoptosis. In young mice, the presence of CC had no significant effect on oocyte death rate (18 +/- 9% and 14 +/- 6% apoptotic oocytes in COC and DO, respectively; P > 0.05). However, in aged mice the percentage of CC-enclosed oocytes that underwent apoptosis was significantly greater as compared to the death rate in DO (48 +/- 3% versus 19 +/- 8% apoptotic oocytes, respectively; P < 0.05). This increased death potential was due to the presence of CC since the occurrence of apoptosis in DO of aged versus young mice was not significantly different (19 +/- 8% versus 14 +/- 6% apoptotic oocytes, respectively; P > 0.05). These results demonstrate that the age-dependent acceleration of apoptosis in oocytes maintained in vitro requires the CC.      

Correlation between semen parameters and sperm aneuploidy rates investigated by fluorescence in-situ hybridization in infertile men

Spermatozoa from 32 infertile patients and 13 controls with normal semen parameters were analysed using dual and triple colour fluorescence in-situ hybridization (FISH) techniques, in order to investigate the rates of aneuploidy for chromosomes 13, 18, 21, X and Y. The patients were divided into three groups according to their karyotypes or the karyotypes of their offspring: 15 were infertile men with abnormal semen parameters and normal karyotypes (group 1), 13 were infertile men with abnormal karyotypes and normal or abnormal semen (group 2) and four were infertile men with abnormal semen and normal karyotypes but whose wives conceived a child (or a fetus) with a numerical chromosomal abnormality through an intracytoplasmic sperm injection cycle (group 3). Patients with abnormal semen parameters showed a significantly higher aneuploidy rate for the investigated chromosomes in their spermatozoa compared to controls (P < 0.005). Our data suggest the presence of a correlation between poor semen parameters and an increase in aneuploidy rate of chromosomes 13, 18, 21, X and Y in spermatozoa (r = -0.81071, P < 0.002); therefore the risk of a chromosomal aneuploidy in spermatozoa seems to be inversely correlated to sperm concentration and total progressive motility. Patients with abnormal karyotypes showed a higher incidence of diploidy and chromosomal aneuploidies compared to controls (P < 0.002). This strongly suggests the presence of an interchromosomal effect of the cytogenetic rearrangement. Men who fathered a child with an abnormal karyotype through intracytoplasmic sperm injection did not present a higher aneuploidy rate for the investigated chromosomes in spermatozoa compared to patients with infertility due to a similar male factor but showed higher incidence of chromosomal aneuploidy compared to normal controls.     

不育男性精子膜表面抗精子抗体水平与精液主要参数及精子功能的相关性

目的探讨男性不育症患者精子膜表面抗精子抗体与精液主要参数的相关性。方法收集男性不育症患者350例,均采用免疫珠法测定精子膜表面抗精子抗体(AsAb,IgA或IgG型),根据结果分为AsAb阳性组(43例)和阴性组(307例)。结果在这350例男性不育症患者中精子膜表面抗精子抗体检出率为14.00%。AsAb阳性组患者的精液主要参数(精液密度、活动率、活动力、精液量)均低于AsAb阴性组患者,两组间比较差异具有显著性(P<0.05)。结论精子膜表面抗精子抗体与精液主要参数及精子功能下降有明显相关性,是导致男性免疫性不育的重要因素之一。