生精冲剂对实验性精索静脉曲张大鼠生精细胞凋亡状况的影响

目的:探讨实验性精索静脉曲张大鼠睾丸生精细胞凋亡状况以及生精冲剂对其凋亡的影响。方法:将60只成年雄性W istar大鼠随机抽出20只为对照组,其余按石津和彦改良法制成左精索静脉曲张大鼠模型,再随机分为模型组20只,治疗组20只。用末端脱氧核苷酸转移酶介导的原位缺口末端标记法(TUNEL)检测睾丸生精细胞凋亡。结果:模型组大鼠睾丸生精细胞凋亡指数明显高于对照组(P<0.01)和治疗组(P<0.01),治疗组与对照组比较有明显差异(P<0.01)。结论:实验性精索静脉曲张大鼠睾丸生精细胞凋亡增加,这可能是影响生育力的机制之一;生精冲剂能够减少精索静脉曲张大鼠睾丸生精细胞凋亡,对睾丸生精功能具有保护作用,进而可提高睾丸的生殖能力。     

生殖股神经在单侧隐睾鼠对侧睾丸损害中的作用机制

目的：探讨生殖股神经在单侧隐睾鼠模型对侧睾丸损害中的作用机制。方法：建立单侧隐睾鼠模型（21d龄），切断该侧生殖股神经，120d后观察对侧睾丸的生精细胞凋亡及细胞乳酸含量变化。结果：切断生殖股神经后对侧睾丸生精细胞凋亡减少，乳酸含量降低，乳酸含量与细胞凋亡呈正相关。结论：单侧隐睾症对侧睾丸损伤可能与其神经传导反射性血流减少引起生精细胞凋亡有关。     

雄激素与精子发生的关系

雄激素被认为在精子发生中具有重要作用.近年的动物实验以及临床研究提示,雄激素可以导致严重少精子或者无精子症,内源性睾酮可以引起生精细胞凋亡,与生精细胞阻滞高度相关.本文对近年的材料进行分析后,认为雄激素与精子发生的关系在于,雄激素可以引起生精细胞凋亡,造成细胞重排,对精子发生起到调节作用.     

人类凋亡生精细胞超微结构研究

目的 :研究人类生精细胞凋亡的超微结构特征。　方法 :10例不育男性 ,年龄 2 8～ 36岁 ,手淫留取精液标本 ,生理盐水洗涤离心 ,戊二醛固定 ,树脂包埋 ,超薄切片 ,电镜观察。　结果 :①生精细胞及精子存在多形态的超微结构异常 ;②生精细胞凋亡的发生是一连续过程 ,电镜下根据其形态变化可分为 3个阶段 :即凋亡发生的初始阶段 ,首先出现生精细胞核染色质浓缩 ,电子密度高 ,核膜间隙宽 ,局部核膜下或核双层膜间形成空泡 (出芽 ) ;第 2阶段出现核膜膨胀折叠 ,互相融合形成花环状结构 ;第 3阶段表现核膜、胞核裂解 ,细胞形成凋亡小体和残余体 ;③精子凋亡表现为顶体结构异常 ,浆内形成空泡 ,细胞器部分或全部消失 ,胞核浓缩呈细杆状 ,体积缩小 ,核周缘电子密度减低 ;④组织细胞、粒细胞吞噬凋亡的生精细胞或精子并形成髓鞘样结构。　结论 :①生精细胞和精子发生凋亡是男性不育病人常见的异常现象 ;②生精细胞凋亡早期胞核的“出芽”方式有 2种 :即核膜下和核膜间形成囊泡 ,在这过程中 ,核表面先出现针状突起 ,然后转变为光滑 ;③凋亡的生精细胞或精子最后被组织细胞或粒细胞吞噬 ;④对不育男性精液电镜检查 ,了解生精细胞的亚微结构 ,对该病的诊断和治疗具有重要价值。     

单侧隐睾大鼠生殖股神经在对侧睾丸损害中的作用机制研究

目的 :探讨单侧隐睾大鼠模型生殖股神经在对侧睾丸损害中的作用机制。　方法 :建立单侧隐睾大鼠模型 (2 1d龄 ) ,切断该侧生殖股神经 ,12 0d后观察对侧睾丸的生精细胞凋亡变化及组织乳酸含量变化。　结果 :切断生殖股神经后 ,对侧睾丸生精细胞凋亡为 (5 .76± 0 .76 ) % ,与对照组 (17.2 8± 1.36 ) %相比明显减少 (P <0 .0 5 ) ;乳酸含量也由 (2 .19± 0 .2 4 )mmol/L下降为 (1.70± 0 .31)mmol/L(P <0 .0 5 ) ,且乳酸含量与细胞凋亡呈正相关(P <0 .0 5 )。　结论 :单侧隐睾症对侧睾丸损伤可能与其神经传导反射性血流减少引起生精细胞凋亡有关     

睾丸生精细胞增殖发育中SCF/c-kit系统的研究进展

干细胞因子与其受体原癌基因受体(c-k itR)相互作用,对各阶段生精细胞的增殖、分化、减数分裂和细胞凋亡等产生重要的旁分泌调控作用,一直以来都是生殖领域研究的热点。本文就SCF/c-k it系统对生精细胞发育的调控作用、机制以及影响因素的研究进展作简要的综述。     

睾丸扭转后生精细胞凋亡与iNOS基因表达

本文研究了睾丸扭转复位后生精细胞凋亡与iNOS基因表达的关系。采用大鼠建立左侧睾丸扭转复位模型(720,2h)。用TUNEL法和免疫组化SP法分别检测扭转复位后第五天生精细胞凋亡和iNOS基因表达。研究发现凋亡主要见于染色质降解的生精细胞(初级精母细胞和圆形精子细胞)。问质细胞和支持细胞未见凋亡发生。iNOS表达见于各级生精细胞,在染色质降解的生精细胞(即凋亡细胞)强表达。本研究表明睾丸扭转复位后生精细胞凋亡增加与iNOS基因表达密切相关。睾丸局部NO生成异常可能是生精细胞凋亡增加的原因之一。     

睾丸扭转后生精细胞凋亡与iBOS基因表达

本文研究了睾丸扭转复位后生精细胞凋亡与iBOS基因表达的关系。采用大鼠建立左侧睾丸扭转复位模型（720,2h)。用TUNEL法和免疫组化SP法分别检测扭转复位后第五天生精细胞凋亡和iBOS基因表达。研究发现凋亡主要见于染色质降解的生精细胞（初级精母细胞和圆形精子细胞）。间质细胞和支持细胞未见凋亡发生。iBOS表达见于各级生精细胞,在染色质降解的生精细胞（即凋亡细胞）强表达。本文研究表明睾丸扭转复位后生精细胞凋亡增加与iBOS基因表达密切相关。睾丸局部NO生成异常可能是生精细胞凋亡增加的原因之一。     

睾丸支持细胞与生精细胞凋亡的关系

生精细胞处于支持细胞构造的环境中 ,激素、生长因子和温度以及它们与支持细胞的联系调控着生精细胞的分化与成熟 ;细胞之间的旁分泌信号转导亦调节着生精细胞凋亡的过程。在睾丸生精细胞发生的自发性凋亡和诱发性凋亡中 ,支持细胞表达和分泌的产物扮演重要角色。     

精索静脉曲张致睾丸生精功能障碍的机制研究进展

精索静脉曲张(Varicocele,VC)是男性生殖系统常见病之一,随着男性不育发病率越来越高,对VC与男性生殖关系的研究成为生殖医学的热点问题之一。近年来,对VC影响睾丸生精功能障碍机制的研究,主要着眼于睾丸温度升高、缺氧、氧化应激、返流、细胞凋亡等诸多环节,但对其确切的机制尚未阐明。探讨VC致睾丸生精功能障碍的机制对临床应用具有重要意义,本文对国内外VC致睾丸生精功能障碍的相关文献进行综述,以期为临床应用提供参考。     

环境内分泌干扰物对男性生殖健康影响的研究进展

近年来,环境内分泌干扰物(EDCs)对人类的生物学效应日益引起关注,大量实验及流行病学资料表明EDCs具有生殖和发育毒性,能导致男性精子质量下降、生殖系统发育异常及肿瘤,其作用机制非常复杂。深入研究EDCs与男性生殖健康的关系,是关系到人类繁衍的重大问题。     

精索静脉曲张大鼠生精细胞凋亡的实验研究

目的 :探讨外科所致的精索静脉曲张对大鼠生精细胞凋亡的影响。　方法 :采用成年雄性Wistar大鼠复制左精索静脉曲张模型 ;用原位末端脱氧核苷酸转移酶标记法 (TUNEL)检测睾丸生精细胞凋亡。　结果 :实验组的细胞凋亡率显著高于假手术对照组 (P <0 .0 5 )。　结论 :外科所致的精索静脉曲张大鼠睾丸生长减缓 ,生精细胞凋亡增加 ,这可能是其影响生育能力的机制之一。     

Endocrine Disruptors and the Breast: Early Life Effects and Later Life Disease

Breast cancer risk has both heritable and environment/lifestyle components. The heritable component is a small contribution (5–27 %), leaving the majority of risk to environment (e.g., applied chemicals, food residues, occupational hazards, pharmaceuticals, stress) and lifestyle (e.g., physical activity, cosmetics, water source, alcohol, smoking). However, these factors are not well-defined, primarily due to the enormous number of factors to be considered. In both humans and rodent models, environmental factors that act as endocrine disrupting compounds (EDCs) have been shown to disrupt normal mammary development and lead to adverse lifelong consequences, especially when exposures occur during early life. EDCs can act directly or indirectly on mammary tissue to increase sensitivity to chemical carcinogens or enhance development of hyperplasia, beaded ducts, or tumors. Protective effects have also been reported. The mechanisms for these changes are not well understood. Environmental agents may also act as carcinogens in adult rodent models, directly causing or promoting tumor development, typically in more than one organ. Many of the environmental agents that act as EDCs and are known to affect the breast are discussed. Understanding the mechanism(s) of action for these compounds will be critical to prevent their effects on the breast in the future.     

Effects of endocrine disruptors on obesity

Environmental chemicals with hormone-like activity can disrupt the programming of endocrine signalling pathways that are established during perinatal life and result in adverse consequences that may not be apparent until much later in life. Increasing evidence implicates developmental exposure to environmental hormone mimics with a growing list of adverse health consequences in both males and females. Most recently, obesity has been proposed to be yet another adverse health effect of exposure to endocrine disrupting chemicals (EDCs) during critical stages of development. Obesity is quickly becoming a significant human health crisis because it is reaching epidemic proportions worldwide, and is associated with chronic illnesses such as diabetes and cardiovascular disease. In this review, we summarize the literature reporting an association of EDCs and the development of obesity, and further describe an animal model of exposure to diethylstilbestrol that has proven useful in studying mechanisms involved in abnormal programming of various oestrogen target tissues during differentiation. Together, these data suggest new targets (i.e. adipocyte differentiation and mechanisms involved in weight homeostasis) of abnormal programming by EDCs, and provide evidence that support the scientific term 'the developmental origins of adult disease'. The emerging idea of an association of EDCs and obesity expands the focus on obesity from intervention and treatment to include prevention and avoidance of these chemical modifiers.     

沙眼衣原体感染与生精细胞凋亡

目的 :探讨沙眼衣原体 (Ct)感染与生精细胞凋亡的关系。　方法 :采用瑞 姬染色和末端脱氧核苷酸转移酶 (TdT)介导的脱氧核苷酸原位末端标记法 (TUNEL)检测凋亡生精细胞。　结果 :Ct感染组中生精细胞凋亡率明显高于正常对照组 (P <0 .0 1 )。　结论 :Ct感染可引起生精细胞凋亡 ,为阐明Ct感染引起男性不育的机制提供了客观依据     

In vivo analysis of germ cell apoptosis reveals the existence of stage-specific `social' control of germ cell death in the seminiferous epithelium

It has become clear in recent years that programmed cell death is regulated during development by signals from other cells. Nevertheless, compared to the `social' control of cell proliferation, relatively little is known about the `social' control of cell death in other systems. Since in a previous study we showed that induced germ cell apoptosis occurs at specific stages of the spermatogenic cycle, in this study we aimed to ascertain the existence of supracellular control of germ cell death during spermatogenesis. Therefore, the TUNEL technique has been used to analyse whether all of the different germ cell types are induced to die at these specific stages in animals injected intratesticularly with one of several inducers of apoptosis. Our findings suggest that all of the investigated agents trigger apoptosis in all the diverse progenies of germ cells existing at stages I, XII or XIV of the spermatogenic cycle. In contrast, at most other stages the number of apoptotic cells was similar to that found in control animals. These data are consistent with the existence of an intercellular control of germ cell death during spermatogenesis. We conclude that the seminiferous epithelium provides a suitable in vivo model to study the mechanisms underlying the `social' control of apoptosis.     

内分泌干扰物对精液质量的影响

内分泌干扰化合物(endocrine disrupting chemicals,EDCs)是指外源性的能干扰人类或动物内分泌系统诸环节并导致异常效应,或使其后代内分泌功能发生改变的化学物质。EDCs种类繁多,广泛存在于土壤、水、甚至食物中。本文从农药、塑料增塑剂和洗涤剂这3类常见EDCs着手,从流行病学和生物学角度阐述了其对人类及动物精液质量的影响。     

LM23基因沉默引起大鼠睾丸生精细胞凋亡

目的 研究LM23基因敲低后生精细胞的凋亡状况及与凋亡相关基因表达改变.方法 用TUNEL方法检测睾丸细胞的凋亡情况,用大鼠全基因组表达谱芯片检测LM23基因敲低后凋亡相关基因的表达改变.结果 TUNEL结果显示,LM23基因敲低侧大鼠睾丸生精小管内大量生精细胞发生凋亡.大鼠全基因组表达谱芯片分析结果显示,许多促凋亡基因如Bcl-2家族的促凋亡基因表达上调,而抗凋亡基因如Faf1和Zfp91基因的表达明显下调.结论 敲低大鼠的LM23基因,启动了Bcl-2家族介导的线粒体凋亡途径,引发了生精细胞发生大量凋亡.     

肉碱与男性生殖

肉碱是机体内重要的条件必需营养素,具有广泛的生理作用。男性附睾与精子中含有体内最高浓度的肉碱,肉碱不仅在启动精子运动、促进精子成熟和提高精子受精能力等方面具有重要作用,而且在调节Sertoli细胞功能、保护精子对抗氧化损伤、减少生精细胞凋亡、抑制精子聚集等方面具有重要意义。本文就肉碱在男性生殖中的作用做一综述。