重金属生精细胞毒性研究进展

在生产和日常生活中,重金属污染物可通过皮肤、呼吸、消化道等多种途径进入人体,导致生殖器官和生精细胞受损,从而使得内分泌紊乱,引起生殖相关基因的异常表达,影响男(雄)性生精细胞凋亡的正常进行,导致精液质量降低,精子数量减少,精子畸形增多,甚至不育.笔者综述了铅、汞、镉、镍、锰、砷等重金属对生精细胞的毒性作用研究进展,为研...     

丙烯腈对雄性小鼠的生殖毒性作用

目的探讨丙烯腈的雄性生殖毒作用机制。方法以雄性小鼠为研究对象,腹腔注射染毒,流式细胞仪检测分析不同观察终点、不同染毒剂量对小鼠睾丸组织各倍体细胞、各时相生精上皮细胞的影响。结果丙烯腈影响次级精母细胞、精子细胞和精子的形成,主要作用于生精上皮细胞的有丝分裂期;丙烯腈诱导雄性小鼠生精细胞凋亡,随着染毒剂量的增加和时间的延长,凋亡发生率增高,第21天的各染毒组细胞凋亡最明显(P<0.05)。结论丙烯腈具有明显的雄性生殖毒性,干扰精子形成。     

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。     

胚胎期毒死蜱和氯氰菊酯混合暴露对仔代雄性大鼠生殖功能的影响

目的 观察低剂量毒死蜱和氯氰菊酯联合染毒对仔代雄性大鼠生殖功能的影响及其机理。方法 健康Wistar大鼠雌雄按2∶1合笼,孕鼠分为对照组、毒死蜱组、氯氰菊酯组、毒死蜱和氯氰菊酯联合染毒组等4组,每组8只,孕l至孕8天染毒孕鼠。给予雄性仔鼠普通饮食喂养至成年。股动脉放血法处死仔鼠,迅速分离脏器,计算脏器系数,附睾尾精子计数,计算精子活动率、精子畸形率。测定血清生殖激素和乙酰胆碱酯酶活力,观察睾丸组织病理改变、生殖细胞凋亡和生精细胞端粒酶的表达。〖HTH〗结果 联合染毒组雄性仔鼠睾丸、附睾的体重比值显著性降低(P<0.05),附睾尾精子总数显著低于对照组,血清FSH高于对照组,T低于对照组(P<0.05)。联合染毒组雄性仔鼠睾丸少量曲细精管生精上皮退化变性,生精细胞脱落,生精细胞凋亡指数明显高于对照组(P<0.05)。结论 胚胎期毒死蜱和氯氰菊酯混合染毒对仔代大鼠的生殖系统有明显的增毒作用;对睾丸的损伤及性激素水平(FSH、T)的协同影响,可能是产生联合生殖毒性的机理之一;提示对毒死蜱和氯氰菊酯进行环境健康风险评价时应考虑这种协同作用。     

甲基汞对小鼠睾丸细胞酶活性的影响

甲基汞是一类重要的环境污染物,可以引起以中枢神经系统为主的全身性损伤,并且能够通过胎盘作用于子代,产生胎儿性水俣病.甲基汞的生殖毒性不仅体现在它通过胎盘对胚胎发育及子代生长发育的影响,也体现在它对雄性生殖系统的损伤,能够影响生精过程使精子数量减少畸形率增高.因此,甲基汞对生殖系统的毒性作用越来越受到关注.为了进一步研究甲基汞对雄性生殖系统的毒作用,我们进行了甲基汞对小鼠睾丸细胞酶活性的研究.     

μ-cell法测定农药对男性精子机能影响的分析

目的研究农药对生育生殖的影响.方法采用μ-cell测定方法.结果暴露组精子的质量与数量都受到了影响,均呈下降趋势.结论长期暴露于农药污染,可能引起生育生殖功能的下降.     

丙烯腈对雄性小鼠生殖功能影响的研究

目的　研究丙烯腈对雄性小鼠生殖功能影响。方法　给雄性性成熟小鼠皮下注射 3 ,6 ,9,12mg·kg-1体重丙烯腈 5和 35天 ,观察睾丸细胞染色体畸变率、精子质量相关指标、雄鼠生育力。结果　染毒剂量达 6mg·kg-1即可致雄鼠活精率、雌鼠妊娠率下降 ,精子畸形率、死胎率、胎吸收率升高 ,与阴性对照组比较差异有显著性 (P <0 0 5 ) ;剂量达 9,12mg·kg-1时 ,除精子计数外 ,各观察指标均与阴性对照组差异有显著性或非常显著性 ,并呈现明显的剂量反应或剂量效应关系。结论　染毒丙烯腈6mg·kg-1及以上剂量可对雄性小鼠生殖功能产生损害作用。     

酒精对雄性大鼠生殖系统的影响

目的了解酒精对雄性大鼠睾丸生精功能及血清睾酮(T)、黄体生成素(LH)、卵泡刺激素(FSH)的影响,探讨酒精对生殖系统的毒性作用。方法将30只雄性大鼠随机分成2组,酒精组用人类饮用白酒经口灌胃,2mL/d,每天1次;对照组用蒸馏水以同样方法灌胃,连续28d。末次灌胃24h后处死取材。结果酒精组雄性大鼠体重明显低于对照组(P<0.05)。酒精组雄性大鼠血清中T、LH及FSH水平均较对照组低(P<0.05);酒精组雄性大鼠精子数量、活动率、精子活力均低于对照组(P<0.05),精子畸形率高于对照组(P<0.05);组织学观察显示酒精组曲精小管萎缩变细,精细胞排列紊乱疏松,生精细胞变性、坏死、脱落。结论酒精对雄性大鼠生殖系统有明显的毒性作用,一方面直接作用于睾丸,抑制精子发生和睾酮合成,另一方面还使下丘脑-垂体轴生殖内分泌功能受损。减少饮酒对优生有重要意义。     

酒精对雄性大鼠生殖系统的影响

目的了解酒精对雄性大鼠睾丸生精功能及血清睾酮(T)、黄体生成素(LH)、卵泡刺激素(FSH)的影响,探讨酒精对生殖系统的毒性作用。方法将30只雄性大鼠随机分成2组,酒精组用人类饮用白酒经口灌胃,2mL/d,每天1次;对照组用蒸馏水以同样方法灌胃,连续28d。末次灌胃24h后处死取材。结果酒精组雄性大鼠体重明显低于对照组(P0.05)。酒精组雄性大鼠血清中T、LH及FSH水平均较对照组低(P0.05);酒精组雄性大鼠精子数量、活动率、精子活力均低于对照组(P0.05),精子畸形率高于对照组(P0.05);组织学观察显示酒精组曲精小管萎缩变细,精细胞排列紊乱疏松,生精细胞变性、坏死、脱落。结论酒精对雄性大鼠生殖系统有明显的毒性作用,一方面直接作用于睾丸,抑制精子发生和睾酮合成,另一方面还使下丘脑-垂体轴生殖内分泌功能受损。减少饮酒对优生有重要意义。     

J江C市段有机提取物对雄性大鼠的生殖毒性研究

目的探讨J江C市段江水有机提取物对雄性大鼠的生殖毒性。方法固相萃取法提取江水中有机物,以不同剂量给予雄性大鼠亚慢性(90d)染毒(隔天灌胃剂量分别相当源水2L、12L、72L/kg.bw),观察了睾丸与附睾病理改变,睾丸组织自由基损伤水平,并进行了精子畸形率检测和生殖细胞DNA流式细胞仪分析。结果在72L/kg染毒剂量下,大鼠睾丸可出现以支持细胞空泡变性和生精细胞脱落为特征的病理损伤;睾丸组织中总超氧化物歧化酶(T-SOD)活力显著降低(P<0.05),谷胱甘肽S转移酶(GST)活力显著升高(P<0.05);精子畸形率显著增高(P<0.05);FCM分析提示圆形精子向长形精子的转化过程明显加强(P<0.01)。结论在高剂量时,J江C市段有机提取物具有一定的雄性生殖毒性,主要表现为睾丸的氧化性损伤和对精子质量的影响。     

Influence of pesticides on male fertility

Several studies have shown a decline in human semen quality and increased risks of male subfertility. This paper provides an overview of the mechanisms of pesticide-induced reproductive toxicity and the effects on male fertility since exposure to pesticides may be one of the causes of these disorders. Pesticides may directly damage spermatozoa, alter Sertoli cell or Leydig cell function, or disrupt the endocrine function in any stage of hormonal regulation (hormone synthesis, release, storage, transport, and clearance; receptor recognition and binding; thyroid function; and the central nervous system). These mechanisms are described with respect to the effects of pesticide exposure in vitro and in vivo. In epidemiologic studies, effects on sperm quality and time to pregnancy are reviewed. Clear effects on male fertility have been demonstrated for some pesticides [eg, dibromochloropropane, ethylene dibromide]. But results from more recent studies are inconsistent, and no uniform conclusion can be drawn about the effects of pesticides on male reproduction.     

An exploratory analysis of the effect of pesticide exposure on the risk of spontaneous abortion in an Ontario farm population

The toxicity of pesticides on human reproduction is largely unknown--particularly how mixtures of pesticide products might affect fetal toxicity. The Ontario Farm Family Health Study collected data by questionnaire on the identity and timing of pesticide use on the farm, lifestyle factors, and a complete reproductive history from the farm operator and eligible couples living on the farm. A total of 2,110 women provided information on 3,936 pregnancies, including 395 spontaneous abortions. To explore critical windows of exposure and target sites for toxicity, we examined exposures separately for preconception (3 months before and up to month of conception) and postconception (first trimester) windows and for early (< 12 weeks) and late (12-19 weeks) spontaneous abortions. We observed moderate increases in risk of early abortions for preconception exposures to phenoxy acetic acid herbicides [odds ratio (OR) = 1.5; 95% confidence interval (CI), 1.1-2.1], triazines (OR = 1.4; 95% CI, 1.0-2.0), and any herbicide (OR = 1.4; 95% CI, 1.1-1.9). For late abortions, preconception exposure to glyphosate (OR = 1.7; 95% CI, 1.0-2.9), thiocarbamates (OR = 1.8; 95% CI, 1.1-3.0), and the miscellaneous class of pesticides (OR = 1.5; 95% CI, 1.0-2.4) was associated with elevated risks. Postconception exposures were generally associated with late spontaneous abortions. Older maternal age (> 34 years of age) was the strongest risk factor for spontaneous abortions, and we observed several interactions between pesticides in the older age group using Classification and Regression Tree analysis. This study shows that timing of exposure and restricting analyses to more homogeneous endpoints are important in characterizing the reproductive toxicity of pesticides.     

氯化饮用水有机提取物对睾丸支持细胞的毒性效应研究

目的：探讨氯化饮用水有机污染物对人类生殖健康的潜在危害。方法：采用固相萃取技术富集水中有机物,应用大鼠睾丸支持细胞与生精细胞共培养系统对某市氯化饮用水有机提取物的生殖毒性进行了研究。结果：有机提取物对生精细胞脱落率未产生明显影响,但可刺激支持细胞分泌乳酸,结论：氯化饮用水有机提取物具有潜在的生殖毒性效应。     

有机氯农药雄性生殖毒性中MAPK信号转导途径的作用机制

促有丝分裂原活化蛋白激酶(MAPK)信号传导途径与细胞生长、分化、凋亡等密切相关,在介导细胞凋亡过程中起着重要作用。近年研究发现MAPK途径在调控有机氯农药诱导雄性生殖毒性中发挥了极为重要的作用,并且发现活性氧的大量生成是介导有机氯农药作用于MAPK途径的关键性物质。探讨有机氯农药诱导细胞凋亡的发生发展与MAPK信号途径关系,有助于从分子水平上深入的阐明有机氯农药诱导雄性生殖障碍的作用机制。     

快杀灵对雄性小鼠生殖毒性的病理学观察

[目的]探讨快杀灵的雄性生殖毒性.[方法]用不同总剂量（9.1、18.2、36.4 mg/kg）低浓度快杀灵给小鼠经口连续灌胃染毒10d,染毒后35 d处死小鼠取材,应用光镜和电镜技术对睾丸、附睾进行组织病理学观察.[结果]光镜观察：36.4mg/kg组曲细精管萎缩,生精细胞数量减少,排列紊乱.电镜观察可见,生精细胞线粒体肿胀,溶酶体增多;支持细胞线粒体扩张甚至空泡化,溶酶体增多,与生精细胞间的连接破坏,裂隙明显增宽.[结论]快杀灵具有明显的生殖毒性,睾丸是其作用的靶器官,靶细胞为生殖细胞和支持细胞.     

Pesticide use by persons who reported a high pesticide exposure event in the agricultural health study

Almost 16% of the pesticide applicators in the Agricultural Health Study (AHS) cohort (a cohort that includes 52,629 private applicators) reported having a high pesticide exposure event (i.e., an incident or experience while using a pesticide that caused an unusually high personal exposure). Pesticides involved in these events were compared to the frequency with which specific pesticides were ever used by the AHS cohort. Generally, pesticides with greater acute toxicity were more frequently involved with the high pesticide exposure event than were other pesticides. Whereas it is clear that the use of acutely toxic pesticides may be related to more frequent visits to health care facilities, the reason that the spills and immersions of the high pesticide exposure events are associated with the acute toxicity of the pesticide is not intuitively clear. This analysis suggests that current practices directed at minimizing pesticide exposures may not be sufficient for acutely toxic or irritating chemicals.     

Ocular toxicity from pesticide exposure: A recent review

Toxic effects on eyes result from exposure to pesticides via inhalation, ingestion, dermal contact and ocular exposure. Exposure of unprotected eyes to pesticides results in the absorption in ocular tissue and potential ocular toxicity. Recent literature on the risks of ocular toxicity from pesticide exposure is limited. Ocular toxicity from pesticide exposure, including the dose-response relationship, has been studied in different animal species. Cholinesterase enzymes have been detected in animal ocular tissue, with evidence of organophosphate-induced inhibition. Pathological effects of pesticides have been observed in conjunctiva, cornea, lens, retina and the optic nerve. Pesticide exposure has been associated with retinopathy in agricultural workers and wives of farmers who used pesticides. Saku disease, an optico-autonomic peripheral neuropathy, has been described in Japan in people living in an area where organophosphates were used. Pesticide exposure is also associated with abnormal ocular movements. Progressive toxic ocular effects leading to defective vision are a serious health concern. Agricultural workers are at high risk of exposure to pesticides and associated ocular toxicity. Primary prevention is the appropriate method of protecting eyes from pesticide-related damage. This includes improved eye safety and care in workplaces, and effective pesticide regulation for maintenance of public eye health.     

The toxicology of 1,2-dibromo-3-chloropropane (DBCP): a brief review.

The accumulating data demonstrating the reproductive toxicity of 1, 2-dibromo-3-chloropropane (DBCP) are reviewed. The sentinel event was the discovery of infertility in male pesticide manufacturing workers. In spite of early evidence of testicular damage, first in laboratory animals and later in humans, DBCP has been widely used as a nematocide in the United States and is still used in other countries. The spermatogenic effects of DBCP are usually irreversible, and there is also evidence of toxicity to the female reproductive system. DBCP is also a CNS depressant, a liver and kidney toxin, and a skin, eye, and respiratory irritant, and is probably carcinogenic. Environmental contamination of air and water may be an additional source of exposure. Materials often used to protect workers from toxic chemicals are not being deployed for use by exposed workers, and in any case are relatively ineffective.     

Assessment of the potential reproductive toxicity of long-term exposure of adult male rats to low-dose formaldehyde

Formaldehyde (FA), a ubiquitous environmental pollutant, is extensively used in hospitals, laboratories and many industrial settings. Previous studies have showed that short-term, high-dose FA exposure is toxic to male reproduction of mammals. In this paper, we evaluated the male reproductive toxicity of long-term, low-dose formaldehyde exposure in rats, and explored the potential mechanisms. A total of 30 Sprague-Dawley male rats were randomly allotted to three groups, rats were exposed to FA at a dose of 0 (control), 0.5, 2.46 mg/m3 respectively by inhalation for consecutive 60 days. The results indicated that the reproductive toxicity of FA is dose-dependent. Testicular, epididymal structure and function in rats of 0.5 mg/m3 FA exposure group showed no obvious difference compared with those in control group. However, sperm quantity and quality, testicular seminiferous tubular diameter, the activities of superoxide dismutase and glutathione peroxidase was significantly decreased whereas the level of malondialdehyde was significantly increased in rats of 2.46 mg/m3 FA exposure group compared with those in control group. Moreover, histopathological results showed atrophy of seminiferous tubules, decreases of spermatogenic cells and the lumina were oligozoospermic in testes of 2.46 mg/m3 FA exposure rats. In conclusion, the level of 0.5 mg/m3 can be considered as a safe level for FA exposure, but long-term FA exposure at a dose of 2.46 mg/m3 has a harmful effect on male reproduction by inducing oxidative stress in male rats.     

Toxicity of pesticides to aquatic microorganisms: a review

Microorganisms contribute significantly to primary production, nutrient cycling, and decomposition in estuarine eco-systems; therefore, detrimental effects of pesticides on microbial species may have subsequent impacts on higher trophic levels. Pesticides may affect estuarine microorganisms via spills, runoff, and drift. Both the structure and the function of microbial communities may be impaired by pesticide toxicity. Pesticides may also be metabolized or bioaccumulated by microorganisms. Mechanisms of toxicity vary, depending on the type of pesticide and the microbial species exposed. Herbicides are generally most toxic to phototrophic microorganisms, exhibiting toxicity by disrupting photosynthesis. Atrazine is the most widely used and most extensively studied herbicide. Toxic effects of organophosphate and organochlorine insecticides on microbial species have also been demonstrated, although their mechanisms of toxicity in such nontarget species remain unclear. There is a great deal of variability in the toxicity of even a single pesticide among microbial species. When attempting to predict the toxicity of pesticides in estuarine ecosystems, effects of pesticide mixtures and interactions with nutrients should be considered. The toxicity of pesticides to aquatic microorganisms, especially bacteria and protozoa, is an area of research requiring further study.