二乙氧基乙醇对小鼠精子影响的实验研究

二乙氧基乙醇属醚类化合物,作为一种溶纤剂,在纺织、油漆、塑料制品等行业中广泛使用。近年来国内外临床、流行病学调查及动物实验资料表明,对雄性生殖系有明显的损伤作用,而对精子形态的影响未见明确报道。本实验目的是研究该物质对小鼠精子的影响,为制订卫生标准提...     

二乙氧基乙醇雄性大鼠生殖系统毒性研究

目的 观察研究二乙氧基乙醇(2-Ethoxyethanol,2-EE)染毒雄性大鼠睾丸和附睾毒性、精子毒性、以及性行为与妊娠率的改变,探讨各生殖毒性指标之间的关联性,为确定2-EE雄性生殖毒性健康监护指标和诊断指标,开展2-EE职业健康危险度评价提供科学依据.方法 选择清洁级雄性Wistar大鼠,分别给予剂量200、4...     

2-乙氧基乙醇急性染毒大鼠睾丸和血清某些生化指标的变化

目的观察2-乙氧基乙醇(2-ethoxythanol,EE)急性染毒大鼠睾丸某些酶活力及血清和睾丸中铜、锌含量变化,探讨EE致睾丸损伤的可能机制.方法将90只大鼠随机分为对照组、EE800、1600和3200mg/kg4组,每组20只.将EE用蒸馏水配制成溶液,采取一次性灌胃染毒.于灌胃后第12、24、48和72h,将各组动物随机处死5只,测定睾丸非特异性酯酶、芳基酯酶(ARE)活力及Cu、Zn含量;测定血清Cu、Zn含量及睾丸/体比值.结果染毒后72h,EE800、1600和3200mg/kg组睾丸重量/体重比值分别为0.92、0.87、0.80%,明显低于对照组0.94%(P＜0.05);染毒后12h,EE800、1600和3200mg/kg组睾丸及血清Zn含量分别为21.76、16.96、19.80μmoL/g和1.37、1.35、1.29mg/L,显著低于对照组的33.08μmol/g和1.46mg/L(P＜0.05);在染毒后24h,EE800、1600和3200mg/kg组睾丸Cu和Zn含量分别为1.91、1.91、2.14和22.60、23.75、25.65μg/g,显著高于对照组的1.31和14.μg/g(P＜0.01).结论EE染毒大鼠睾丸重量/体重比值、ARE酶活力及血清Zn含量显著降低而睾丸Zn含量明显升高.推测睾丸可能是EE的靶器官,EE具有明显的睾丸毒性.     

2—乙氧基乙醇对睾丸与附睾毒理病理研究

２－乙氧基乙醇对睾丸与附睾毒理病理研究高星１唐晓奈２刘建中１张希桥１２－乙氧基乙醇（２－Ｅｔｈｏｘｙｅｔｈａｎｏｌ，ＥＥ）在我国主要用于感光液生产溶剂。Ｍｏｒｉｓｅｙ等实验发现，ＥＥ可以引起睾丸重量下降与萎缩［１］。笔者对ＳＰ版生产男工精液和小鼠附睾...     

2—乙氧基乙醇染毒大鼠的睾丸苛些生化指标变化

目的 观察EE急性染毒大鼠睾丸某些酶活性和血清睾酮水平变化。探讨2-乙氧基乙醇（EE）致睾丸损伤的可能机理。方法 用EE800、1600和3200mg/Kg灌胃染毒,测定雄性Wister大鼠在染毒后6、12、24和48h血清睾酮含量和睾丸匀浆葡萄糖-6磷酸脱氢酶（G-6-PD）、山梨醇脱氢酶（SDH）及酸性磷酸酶（ACP）活性。结果 大鼠睾丸绝对重量、血清睾酮含量及睾丸匀浆G-6-PD、SDH及ACP活性均（极）显著下降。G-6-PD和SDH活性与血清睾酮含量呈（极）显著正相关。结论 推测EE的靶器官可能为睾丸,EE具有明显的雄性生殖毒性。     

睾丸精子和附睾精子冷冻保存研究

目的 探讨以0.25ml麦管为载体,Irvine为精子冷冻保护剂的方法在睾丸精子和附睾精子冷冻复苏中的应用.方法 收集2019年7月至2020年12月期间诊断性睾丸/附睾穿刺术后剩余的睾丸精子悬液样本10份和附睾精子悬液样本20份,以0.25ml麦管为载体,Irvine为精子冷冻保护剂进行冷冻复苏,评估冷冻复苏效果.结...     

二甲苯对小鼠睾丸毒性作用的研究

二甲苯(Xylene)对人体神经系统的危害已得到公认,但对睾丸毒性作用的研究甚少。本实验采用睾丸组织酶检测、光镜及电镜检查等方法,研究了二甲苯对小鼠睾丸毒性作用。 材料与方法 1.受试物:二甲苯是齐鲁石化公司研究院试剂厂的产品,分析纯。 2.动物分组及染毒:雄性昆明种小鼠,8周龄,体重25～28g,由山东省医学科学院动物房提供。动物随机分为3个染毒组(二甲苯1.25、2.5和8.5g/     

N-乙酰半胱氨酸对急性乙醇暴露致小鼠睾丸损伤的保护作用

目的在成功建立乙醇诱导小鼠睾丸损伤模型的基础上,该研究主要探讨N-乙酰半胱氨酸(NAC)对急性乙醇暴露致小鼠睾丸损伤的保护作用。方法该研究由2个实验组成。实验1:28只雄性小鼠被随机分成4组,对照组和乙醇(1、3、6 g·kg-1)处理组;实验2:24只雄性小鼠被随机分成4组,对照组、乙醇组、NAC组和NAC+乙醇组。2个实验均于乙醇处理后24h剖杀小鼠,取睾丸称重,各组小鼠睾丸用MDF液固定,制作石蜡切片,以备后续睾丸HE染色和免疫组织化学检测。结果 3和6 g·kg-1乙醇暴露明显引起小鼠睾丸内多核巨细胞并向管腔内生殖细胞脱落等组织病理学改变;1和3 g·kg-1乙醇暴露明显抑制小鼠睾丸生殖细胞增殖;NAC明显保护3 g·kg-1乙醇暴露所致小鼠睾丸病理学损伤,显著减轻3 g·kg-1乙醇暴露对小鼠睾丸细胞增殖的抑制作用。结论 NAC明显保护乙醇急性暴露对小鼠睾丸组织病理学损伤。     

丙酮缩二乙醇液相裂解制备2—乙氧基丙烯

丙酮和原甲酸三乙酯以氯化铵为催化剂反应制得丙酮缩二乙醇,再在硅油中高温裂解制得2－乙氧基丙烯,总收率64．8％。     

Ethambutol induces testicular damage and decreases the sperm functional competence in Swiss albino mice

The present study reports the effect of ethambutol (EMB) on testicular function. Prepubertal and adult male Swiss albino mice were treated with 40, 80, 160 mg/kg body weight of EMB, intraperitoneally, every alternate day for 4 weeks. After 2 weeks gap, mice were sacrificed to collect caudal spermatozoa. EMB treatment resulted in a dose-dependent decrease in the testicular weight, sperm count and motility while the percentage of sperm with head abnormalities, immature chromatin (P < 0.001) and DNA damage increased (P < 0.01). In addition, EMB treatment resulted in significant depletion of glutathione (P < 0.05–P < 0.01) and histopathological abnormalities such as large cells, vacuolation of tubules and isolated colonies of spermatogenic cells were observed. Oct4, 17β-Hsd and c-Kit mRNA was marginally elevated in EMB treated testes at the highest dose studied. In conclusion, the result of the present study indicates that EMB has adverse effect on testicular function and impairs the sperm functional competence.     

梗阻性无精子症附睾精子与睾丸精子行ICSI治疗结局比较

目的 比较梗阻性无精子症应用附睾精子与睾丸精子行卵胞浆内单精子注射技术（ICSI）的临床结局.方法 回顾分析2011年及2012年梗阻性无精子症患者于我中心ICSI助孕110周期,根据精子来源,分为附睾精子组（PESA组）及睾丸精子组（TESA组）,比较两组间的2PN受精率、卵裂率、可移植胚胎率、临床妊娠率、流产率等.结果 2PN受精率TESA组（77.8％）明显低于PESA组（84.5％）（P＜0.05）.TESA组与PESA组的卵裂率（97.1％、97.6％）、可移植胚胎率（74.4％、70.7％）、临床妊娠率（78.6％、67.1％）、流产率（4.6％、7.3％）,两组比较差异均无统计学意义（P＞0.05）.结论 TESA精子用于ICSI治疗2PN受精率比PESA精子低,TESA精子与PESA精子妊娠结局无显著差异.     

Protective effects of ursodeoxycholic acid against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced testicular damage in mice

The protective effect of ursodeoxycholic acid (UDCA), a biliary component found in bears, on 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced testicular damage in mice was investigated. Fifty C57BL/6J mice were equally divided into five groups. The mice in the control group received the vehicle and standard chow. The single TCDD treatment group received 27.5 microg/kg of TCDD subcutaneously. The UDCA-included treatment group received pulverized chow containing 0.125%, 0.25% and 0.5% UDCA, respectively, for 70 days starting 10 days before TCDD injections. The body and testicular weights were shown to be decreased in the single TCDD treatment group, while the decrease was prevented by UDCA added to the chow. In addition, the decrease in the serum-luteinizing hormone (LH) or the follicle stimulating hormone (FSH) secondary to a TCDD injection was not observed in the UDCA-included treatment group. Contrary to the single TCDD treatment group, the germinal epithelium and intercellular space were relatively well preserved in the UDCA-included treatment group. Adding UDCA also normalized TCDD-induced irregular ultrastructural changes such as development of phagolysosomes, inflated smooth endoplasmic reticulum (SER), dilated and altered mitochondria, necrosis and completely damaged seminiferous tubules. Moreover, in the experiment for Arnt expression, UDCA added to the chow suppressed the TCDD-induced relocation of Arnt from the cytoplasm to the nuclei. In conclusion, TCDD-induced testicular toxicity was effectively protected by UDCA. There was almost complete recovery of the testes in the UDCA-included treatment group. Thus, UDCA may be useful for the prevention and treatment of TCDD-induced testicular damage.     

邻苯二甲酸二-2-乙基已酯对雄性大鼠的生殖毒性

邻苯二甲酸二－２－乙基乙酯（ＤＥＨＰ）染毒期间,大鼠睾丸和附睾严重萎缩;附睾尾精子数量显著减少,精子死亡率和畸形率明显增高;血清和睾丸内睾酮明显下降;睾丸乳酸脱氢酶（ＬＤＨ）和葡萄糖－６－磷酸脱氢酶（Ｇ６ＰＤＨ）活性显著升高;存在剂量－反应和时间－效应关系。恢复期,除Ｇ６ＰＤＨ外,其它观察指标均恢复到对照组水平。提示短期暴露ＤＥＨＰ引起的雄性生殖毒性为可逆性损伤     

萘普替尼对雄性大鼠睾丸形态结构和附睾精子质量的影响

目的 探究萘普替尼对雄性大鼠睾丸形态结构及附睾精子质量的影响。方法 将30只雄性SD大鼠随机分为30和70 d两组,每组又分为对照组和萘普替尼低、高剂量组（0.75、3.00 mg/kg）,ig给药,每天给药1次,给药体积10 mL/kg。每天进行1次症状观察,每周称量一次体质量,大鼠分别于给药35和70 d后次日处死,肉眼检查各脏器有无异常,检测双侧睾丸质量和横径、附睾尾精子数量和活力,睾丸固定进行组织病理学检查。结果 萘普替尼高剂量组动物均从给药第14天开始,出现腹泻、脱毛、口鼻眼处有红色分泌物,随着给药天数的增加,症状加重;给药70 d组其中1只动物于给药60 d开始出现血尿症状。给药35 d组大鼠从给药21 d开始,给药70 d组从14 d开始,高剂量大鼠体质量明显低于同期对照组（P<0.01）。与对照组比较,给药组雄鼠的双侧睾丸绝对质量和脏器指数、睾丸横径、附睾尾精子数量和活力及睾丸组织病理学检查并未随给药剂量的增加和给药时间的延长而出现明显变化。结论 萘普替尼对雄性大鼠的睾丸组织及精子质量无明显影响。     

Molecular mechanism on the testicular toxicity of 1,3-dinitrobenzene in Sprague-Dawley rats: preliminary study

The present study was conducted to elucidate the possible molecular mechanism of germinal cell apoptosis induced by Sertoli cell damage after 1,3-dinitrobenzene (1,3-DNB), a testicular toxicant, was administered to laboratory male rats. In this study, male Sprague-Dawley rats were administered with a single oral dose of 1,3-DNB (25 mg/kg body weight). Histopathological examinations and TUNEL methods revealed a marked increase in the number of apoptotic pachytene spermatocytes in seminiferous tubules showing stages VII–VIII and IX–XI of the spermatogenic cycle at 24 h after 1,3-DNB treatment. In immunohistochemical analysis, the cytoplasm and nuclei of pachytene spermatocytes were sometimes stained with antibodies to Bax and cleaved caspase-3 at 24 h after treatment. RT-PCR analysis for apoptosis-related gene expression showed that the expression of Bax,Bcl-2, Bcl-xL, and Bcl-xs genes, which are implicated in mitochondrial pathway, was significantly upregulated in the testes of the treated rats. These results suggest that the mitochondrial pathway is mainly involved in the testicular germinal cell apoptosis in rats induced by 1,3-DNB.     

Repeated exposure to iron oxide nanoparticles causes testicular toxicity in mice

The aim of this study was to determine whether repeated exposure to iron oxide nanoparticles (Fe₂O₃‐NPs) could be toxic to mice testis. Fe₂O₃‐NPs (25 and 50 mg/kg) were intraperitoneally administered into mice once a week for 4 weeks. Our study showed that Fe₂O₃‐NPs have the ability to cross the blood‐testis barrier to get into the testis. The findings showed that exposure resulted in the accumulation of Fe₂O₃‐NPs which was evidenced from the iron content and accumulation in the testis. Furthermore, 25 and 50 mg/kg Fe₂O₃‐NPs administration increased the reactive oxygen species, lipid peroxidation, protein carbonyl content, glutathione peroxidase activity, and nitric oxide levels with a concomitant decrease in the levels of antioxidants—superoxide dismutase, catalase, glutathione, and vitamin C. Increased expression of Bax, cleaved‐caspase‐3, and cleaved‐PARP confirms apoptosis. Serum testosterone levels increased with increased concentration of Fe₂O₃‐NPs exposure. In addition, the histopathological lesions like vacuolization, detachment, and sloughing of germ cells were also observed in response to Fe₂O₃‐NPs treatment. The data from our study entailed that testicular toxicity caused by Fe₂O₃‐NPs exposure may be associated with Fe₂O₃‐NPs accumulation leading to oxidative stress and apoptosis. Therefore, precautions should be taken in the safe use of Fe₂O₃‐NPs to avoid complications in the fertility of males. Further research will unravel the possible molecular mechanisms on testicular toxicity of Fe₂O₃‐NPs. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 594–608, 2017.     

Development of a category approach to predict the testicular toxicity of chemical substances structurally related to ethylene glycol methyl ether

We propose a category approach to assessing the testicular toxicity of chemicals with a similar structure to ethylene glycol methyl ether (EGME). Based on toxicity information for EGME and related chemicals and accompanied by adverse outcome pathway information on the testicular toxicity of EGME, this category was defined as chemicals that are metabolized to methoxy- or ethoxyacetic acid, a substance responsible for testicular toxicity. A Japanese chemical inventory was screened using the Hazard Evaluation Support System, which we have developed to support a category approach for predicting the repeated-dose toxicity of chemical substances. Quantitative metabolic information on the related chemicals was then considered, and seventeen chemicals were finally obtained from the inventory as a shortlist for the category. Available data in the literature shows that chemicals for which information is available on the metabolic formation of EGME, ethylene glycol ethyl ether, methoxy- or ethoxyacetic acid do in fact possess testicular toxicity, suggesting that testicular toxicity is a concern, due to metabolic activation, for the remaining chemicals. Our results clearly demonstrate practical utility of AOP-based category approach for predicting repeated-dose toxicity of chemicals.     

Triclosan exhibits a tendency to accumulate in the epididymis and shows sperm toxicity in male sprague‐dawley rats

Triclosan (TCS) is considered a potent endocrine disruptor that causes reproductive toxicity in non‐mammals, but it is still unclear exactly whether TCS has adverse effects on the sperm or reproductive organs in mammals. In this study, we aimed to evaluate the distribution status of TCS in male reproductive organs of rats, and seek the correlation with the TCS‐induced sperm toxicity or reproductive organ damage. Male rats were intragastrically administered with TCS at a dose of 50 mg/kg, the kinetics of TCS in the plasma and reproductive organs were investigated. TCS in testes and prostates both showed a lower‐level distritbution compared to that in the plasma, which indicates it has no tendency to accumulate in those organs. However, TCS in the epididymides showed a longer elimination half‐life (t_1/2z), a longer the mean retention time (MRT), and a lower clearance (CL_Z/F) compared with those in the plasma. Besides, the ratios of mean area under the concentration‐time curve (AUC)_{0–96h(epididymides/plasma)} and AUC_{0–∞(epididymides/plasma)} were 1.13 and 1.51, respectively. These kinetic parameters suggest TCS has an accumulation tendency in the epididymides. Based on this, we investigated the TCS‐induced sperm toxicity and histopathological changes of reproductive organs in rats. TCS was given intragastrically at doses of 10, 50, and 200 mg/kg for 8 weeks. Rats treated with the high dose (200 mg/kg) of TCS showed a significant decrease in daily sperm production (DSP), changes in sperm morphology and epididymal histopathology. Considering the histopathological change in the epididymides, TCS may induce the epididymal damage due to the epididymal accumulation of that. © 2013 Wiley Periodicals, Inc. Environ Toxicol 30: 83–91, 2015.     

Altered sperm chromatin structure in mice exposed to sodium fluoride through drinking water

This study investigated the effects of sodium fluoride (NaF) on sperm abnormality, sperm chromatin structure, protamine 1 and protamine 2 (P1 and P2) mRNA expression, and histones expression in sperm in male mice. NaF was orally administrated to male mice at 30, 70, and 150 mg/l for 49 days (more than one spermatogenic cycle). Sperm head and tail abnormalities were significantly enhanced at middle and high doses. Similarly, sperm chromatin structure was also adversely affected by NaF exposure, indicating DNA integrity damage. Furthermore, middle and high NaF significantly reduced the mRNA expressions of P1 and P2, and P1/P2 ratio, whereas the sperm histones level was increased, suggesting the abnormal histone‐protamine replacement. Therefore, we concluded that the mechanism by which F induced mice sperm abnormality and DNA integrity damage may involved in the alterations in P1, P2, and histones expression in sperm of mice. © 2012 Wiley Periodicals, Inc. Environ Toxicol 29: 690–696, 2014.