锰对小鼠睾丸中微量元素含量及某些生化指标的影响

给雄性小鼠亚急性染毒，腹腔注射硫酸锰３０、６０ｍｇ／ｋｇ。以观察锰对雄性小鼠生殖系统的影响。结果表明，锰可致早期精细细胞微核率升高，精子数和活动精子率减少，畸形精子率增加。睾丸组织微量元素铜、锌、钙有所改变，乳酸脱氢酶（ＬＤＨ）、碱性磷酸酶（ＡＬＰ）和胆固醇（ＣＨＯ）含量减少。血清睾酮含量减少，黄体生成素（ＬＨ）含量增高。结果提示，锰可对雄性小鼠产生毒性作用。     

空气污染物对哺乳动物生殖和胚胎发育的影响

日益严重的空气污染已对人们的生命健康构成巨大的危害。大量的流行病学研究表明,严重的空气污染对生殖系统有着多重负面影响。对男性而言,可导致睾丸体积减小和质量减轻,精子数量、浓度降低,运动力与形态学改变,并可引起精子染色体畸变、DNA断裂,最终表现为男性生殖功能的下降,导致不育。而对女性,空气污染与卵巢结构与功能受损、生殖细胞发育异常、排卵率下降以及雌激素分泌异常等显著相关。另外,长期暴露于空气污染的环境中,孕妇的流产率明显增高,且更易造成胎儿畸形的发生。综述多种主要空气污染物对男、女生殖器官(系统)、生殖细胞、生殖功能及胚胎发育影响的最新研究进展。     

锰对雄性小鼠生殖毒性的研究

采用一组试验方法研究了硫酸锰对雄性小鼠生殖系统的影响。实验结果表明，硫酸锰能引起早期精细胞和骨髓嗜多染红细胞微核发生率增加，精子数量减少，活动精子率下降，精子畸形率增高，精子尾部低渗肿胀率下降，血清睾酮含量下降，ＬＨ升高。本研究提示硫酸锰对哺乳动物雄性生殖细胞和体细胞有遗传损伤效应，对小鼠精子有毒性作用，并对血中性激素有影响．     

丙烯腈对雄性小鼠性成熟的影响

目的探讨丙烯腈对未成年雄性小鼠性成熟过程的影响。方法以未成年雄性小鼠为研究对象,采用连续5 d腹腔注射染毒,观察35 d后剖杀,进行睾丸组织病理、精子形态观察以及睾丸生殖细胞流式细胞仪检测分析,综合判断丙烯腈对雄性性成熟的影响。结果丙烯腈对未成年雄性小鼠睾丸组织的影响,表现为曲细精管基膜断裂,曲细精管内生殖细胞的数量减少,管腔内成熟精子减少,中、高剂量组曲细精管管腔内成熟精子百分比仅为阴性对照组的1/3和1/6(P<0.01);精子形态结构异常增加,其中高剂量组精子畸形率为阴性对照组的2.6倍(P<0.05);睾丸组织中多种精子细胞成熟障碍,各染毒组精细胞凋亡增加,其中高剂量组精细胞凋亡率为阴性对照组的1.75倍(P<0.05)。结论丙烯腈影响雄性小鼠的性成熟过程,是雄性生殖毒性作用机制之一。     

全氟类化合物在人体与动物体内的生殖毒性

全氟类化合物（polyfluorinated chemicals，PFCs）是一类来自工业生产，存在于人们日常生活环境中内分泌干扰物（endocrine disruptors，EDCs）。研究表明，PFCs可以聚集在生物体内，并通过影响甾体激素合成、诱导生殖系统细胞凋亡、拮抗激素受体等机制，在生殖系统表现出毒性作用。在男性中，这类物质被证明与精子的质量与数量的下降及异常精子比率的上调有关，干扰男性性激素水平（如睾酮）；而在女性中也发现血液或卵泡液中PFCs水平的升高，往往伴随着性激素及促性腺激素（如雌孕激素，卵泡刺激素等）水平的异常以及生育力的下降，这类物质在孕期的暴露甚至有影响至下一代的可能。此外，已有动物实验从分子层面对这类物质的毒性机制进行了证实，因此PFCs的生殖毒性值得关注。     

缺锌对雄性大鼠生殖系统影响的实验研究

:参照国外配方 ,制成缺锌饲料建立缺锌大鼠模型 ,研究缺锌对雄性大鼠生殖系统生长发育及其与精子质量的关系。结果表明 :缺锌组大鼠血清锌与睾酮显著低于其他各组 ,精囊腺、包皮腺、提肛肌的脏器指数、精子密度、活率、穿透力等均较其他组低。睾丸形态学观察发现 :睾丸间质细胞及各级生精细胞形态异常。提示缺锌可对雄性大鼠生殖系统产生不利的影响     

运动对男性生殖影响的研究进展

运动对男性生殖的作用具有双重性，即合理运动有益于生殖内分泌，超负荷运动却常会损害男性的生育力。合理运动量的体能锻炼，卵泡刺激素（FSH）水平相比锻炼前上升，黄体生成激素（LH）和睾酮（T）水平显著上升；改善睾丸局部微环境，还改变生殖细胞的表观遗传修饰，有利于后代健康。超负荷运动则使睾丸微环境的温度显著上升，热应激可损伤精子的结构和功能并最终导致男性生育力下降；超负荷运动还抑制促性腺激素释放激素（GnRH）神经元和垂体功能，干扰生殖激素分泌。此外，运动还使精子DNA CpG岛相关基因发生明显的去甲基化，影响微小RNA（miRNA）表达水平，影响表观遗传。综述运动对男性生殖的影响及其机制。     

活性氧与弱精子症

弱精子症病因错综复杂,近年来发现生殖系统中活性氧（ROS）产生过多蚓起弱精子症的重要病因之一。综述ROS引起弱精子症的病理作用机制及清除ROS、治疗ROS引的弱精子症的药物和方法。     

镉对雄（男）性生殖系统毒性的研究进展

镉（Cadmium）是有毒重金属,其对肝、肾、肺、骨骼、生殖系统及血液系统均有毒性,雄性生殖系统对镉的毒性更加敏感。镉进入机体后抑制类固醇激素合成急性调节蛋白（steroidogenic acute regulatory protein,StAR）、胆固醇侧链裂解酶（P450scc）、3β-羟类固醇脱氢酶（3β-HSD）以及17β-HSD等睾酮合成关键酶活性,使睾酮合成受到抑制,血浆睾酮水平下降。镉可诱导生殖细胞凋亡,引起睾丸细胞和细胞器的超微结构变化,最终损害雄性生殖系统的功能。内分泌紊乱、氧化应激失衡和凋亡通路的激活在镉毒性机制中发挥着重要作用,某些抗氧化剂和抗凋亡药物可在一定程度上拮抗镉的生殖毒性。综述镉对雄（男）性生殖能力的影响和毒性机制。     

精子氧化损伤及抗氧化剂的研究

随着对男性生殖健康的关注,人们开展了许多关于精子氧化损伤和抗氧化剂在男性生殖系统中的应用研究.在正常的生理条件下,精子产生微量的活性氧(reactive oxygen species,ROS),这对于受精、顶体反应和获能是必需的.然而,如果产生的ROS增加超过自身清除能力的增加,就会导致精子质膜的过氧化损伤和DNA完整性的丢失,最终导致精子细胞死亡、降低受精率.目前,实验室和临床已经有许多研究关注抗氧化剂在氧化损伤引起的男性生殖问题中的作用,主要通过抑制ROS的产生或者消除过多的ROS来保护精子免受氧化损伤的影响,特别是在缺乏精浆的体外处理中尤为重要.     

The controversial efficacy of vitamin E for human male infertility

Vitamin E (VE) is major lipophilic chain-breaking antioxidant which protects tissue polyunsaturated fatty acids (PUFA) against peroxidation, a property that could be beneficial in the male reproductive physiology because the membranes of germ cells and spermatozoa are very sensitive to oxidation because of their high content of PUFA. Some of the available data on the efficacy of VE as an oral drug for male infertility or as an additive during in vitro manipulations of spermatozoa were reviewed here, observing that they are often contradictory, possibly because: (1) antioxidant therapy could be ineffective in certain studies not concentrated on men in whom oxidative stress is implicated as an infertility factor, and (2) the VE antioxidant therapy is a double-edged sword strictly depending on the dosage or the in vitro concentration of the vitamin. Thus, further laboratory and clinical studies with better-defined experimental conditions should be performed to establish the in vitro and in vivo efficacy of VE for human male infertility.     

Ambient air pollution exposure and damage to male gametes: human studies and in situ 'sentinel' animal experiments

Globally there is concern that adverse reproductive outcomes and fertility impairment in humans may be caused by exposure to environmental contaminants. Air pollution in particular has been linked to DNA damage, abnormal sperm morphology, and reduced sperm performance in men. Experimental studies using model species (mice and rats) exposed in situ provide evidence that ambient air pollution can cause damage to the respiratory system and other tissues or organs. This can take the form of DNA damage and other genetic changes throughout the body, including induced mutations, DNA strand breaks, and altered methylation patterns in male germ cells. Human and animal studies together provide strong evidence that air pollution, especially airborne particulate matter, at commonly occurring ambient levels is genotoxic to male germ cells. The mechanistic link between air pollution exposure and induced genetic changes in male germ cells is currently unclear. 'Sentinel' animal experiments explicitly examining air pollution affects on sperm quality in laboratory rodents have not been conducted and would provide a critical link to observations in humans. The importance of air pollution compared to other factors affecting fertility and reproductive outcomes in humans is not clear and warrants further investigation.     

Oxidative stress, male infertility and the role of carnitines

Oxidative stress has been shown to be a major cause of male infertility; a large proportion of infertile men have elevated levels of seminal reactive oxygen species (ROS). High concentrations of ROS cause sperm pathology such as ATP depletion leading to insufficient axonemal phosphorylation, lipid peroxidation and loss of motility and viability. L-carnitine, a naturally occurring enzymatic antioxidant, is a necessary factor in the utilization of long chain fatty acids to produce energy. Furthermore, it plays a pivotal role in the maturation of spermatozoa within the male reproductive tract. Epididymal plasma contains the highest levels of L-carnitine found in the human body, and initiation of sperm motility occurs in parallel to L-carnitine increase in the epididymal lumen. It is known that L-carnitine prevents the formation of ROS, scavenges free radicals and protects cells from peroxidative stress. Moreover, it plays a key role in sperm metabolism by providing readily available energy for use by spermatozoa, which positively affects sperm motility, maturation and the spermatogenic process. L-carnitine and its derivatives have been proposed recently for treatment of male infertility, and a number of controlled and uncontrolled human and animal studies have been conducted to indicate their possible application. As a result, antioxidant therapy with carnitines may represent a new nonhormonal option within a broader therapeutic strategy in men with ROS-mediated infertility.     

Oxidative stress

Oxidative stress is defined by an imbalance between increased levels of reactive oxygen species (ROS) and a low activity of antioxidant mechanisms. An increased oxidative stress can induce damage to the cellular structure and potentially destroy tissues. However, ROS are needed for adequate cell function, including the production of energy by the mitochondria. Increased oxidative stress has been incriminated in physiological conditions, such as aging and exercise, and in several pathological conditions, including cancer, neurodegenerative diseases, cardiovascular diseases, diabetes, inflammatory diseases, and intoxications. However, prevention by antioxidants has been mostly inefficient. Therefore, a rigorous scientific evaluation in well-defined conditions is mandatory to define the appropriate place for manipulations of the oxidative pathways in human medicine.     

Ambient air pollution exposure and damage to male gametes: human studies and in situ ‘sentinel’ animal experiments

Globally there is concern that adverse reproductive outcomes and fertility impairment in humans may be caused by exposure to environmental contaminants. Air pollution in particular has been linked to DNA damage, abnormal sperm morphology, and reduced sperm performance in men. Experimental studies using model species (mice and rats) exposed in situ provide evidence that ambient air pollution can cause damage to the respiratory system and other tissues or organs. This can take the form of DNA damage and other genetic changes throughout the body, including induced mutations, DNA strand breaks, and altered methylation patterns in male germ cells. Human and animal studies together provide strong evidence that air pollution, especially airborne particulate matter, at commonly occurring ambient levels is genotoxic to male germ cells. The mechanistic link between air pollution exposure and induced genetic changes in male germ cells is currently unclear. ‘Sentinel’ animal experiments explicitly examining air pollution affects on sperm quality in laboratory rodents have not been conducted and would provide a critical link to observations in humans. The importance of air pollution compared to other factors affecting fertility and reproductive outcomes in humans is not clear and warrants further investigation.     

氧化应激与妊娠

氧化应激是指活性氧生成与抗氧化防御系统之间的不平衡状态。氧化应激可在活性氧生成超过抗氧化防御系统时或者在抗氧化剂活性降低时发生。近年来,氧化应激作为多种疾病的发病原因而备受关注。在产科,许多研究表明氧化应激和妊娠有关。     

槟榔碱对生殖与泌尿系统的影响

近年来,对槟榔的研究已不局限其对口腔的危害及对癌症的诱发,而逐渐扩展到其对人体其他主要器官及系统的影响。研究表明,槟榔果的主要成分槟榔碱可对男（雄）性的泌尿生殖系统以及女（雌）性泌尿生殖系统和妊娠造成损伤。对男（雄）性生殖系统,槟榔碱可导致活性氧簇增高并引起氧化应激反应。槟榔碱还可上调肿瘤坏死因子α水平及诱导环氧合酶2（COX-2）高表达,影响免疫系统进而对精子造成损伤。另外,槟榔碱通过多种途径刺激睾丸Leydig细胞分泌合成过量睾酮。对女（雌）性泌尿生殖系统及妊娠,槟榔碱可造成卵细胞损伤。孕妇长期咀嚼槟榔会影响新生儿出生结局,如低出生体质量和婴幼儿死亡。动物胚胎模型研究结果显示,槟榔碱可产生胚胎毒性,影响胚胎发育。对两性泌尿系统,槟榔碱诱导慢性肾病（CKD）的发生并致使膀胱癌进一步恶化。阐述槟榔碱对生殖和泌尿系统的损伤作用可进一步了解此类生物成分的危害,并能及时且有效地建立疾病的预防机制。     

精子DNA损伤的研究进展

随着男性不育症发病率的升高,精液常规检测已不足以精确评估男性生育力。近年来,精子DNA损伤检测作为一项评估精子质量及男性生育力更精准的指标,逐步成为生殖医学领域的研究热点。精子DNA损伤的机制包括精子发生异常、氧化应激损伤、精子凋亡异常等。目前,精子染色质结构分析法(SCSA)已经成为检测精子DNA完整性的金标准。精子DNA损伤可能与男性不育、辅助生殖结局及后代生长、发育相关。笔者拟就精子DNA损伤的机制、检测方法、对男性生育力的影响及其与辅助生殖技术的关系进行综述,旨在为男性不育症的临床诊断提供依据。     

Effects of Cinnamon (C. zeylanicum) Bark Oil Against Taxanes-Induced Damages in Sperm Quality,Testicular and Epididymal Oxidant/Antioxidant Balance,Testicular Apoptosis,and Sperm DNA Integrity

The aim of this study was to investigate whether cinnamon bark oil (CBO) has protective effect on taxanes-induced adverse changes in sperm quality, testicular and epididymal oxidant/antioxidant balance, testicular apoptosis, and sperm DNA integrity. For this purpose, 88 adult male rats were equally divided into 8 groups: control, CBO, docetaxel (DTX), paclitaxel (PTX), DTX+PTX, DTX+CBO, PTX+CBO, and DTX+PTX+CBO. CBO was given by gavage daily for 10 weeks at the dose of 100 mg/kg. DTX and PTX were administered by intraperitoneal injection at the doses of 5 and 4 mg/kg/week, respectively, for 10 weeks. DTX+PTX and DTX+PTX+CBO groups were treated with DTX during first 5 weeks and PTX during next 5 weeks. DTX, PTX, and their mixed administrations caused significant decreases in absolute and relative weights of all reproductive organs, testosterone level, sperm motility, concentration, glutathione level, and catalase activity in testicular and epididymal tissues. They also significantly increased abnormal sperm rate, testicular and epididymal malondialdehyde level, apoptotic germ cell number, and sperm DNA fragmentation and significantly damaged the histological structure of testes. CBO consumption by DTX-, PTX-, and DTX+PTX-treated rats provided significant ameliorations in decreased relative weights of reproductive organs, decreased testosterone, decreased sperm quality, imbalanced oxidant/antioxidant system, increased apoptotic germ cell number, rate of sperm with fragmented DNA, and severity of testicular histopathological lesions induced by taxanes. In conclusion, taxanes cause impairments in sperm quality, testicular and epididymal oxidant/antioxidant balance, testicular histopathological structure, and sperm DNA integrity, and long-term CBO consumption protects male reproductive system of rats.