补锌对三硝基甲苯所致大鼠睾丸损伤的拮抗作用

近年来,江泉观及其研究组开始注意三硝基甲苯(TNT)对雄(男)性生殖系统的影响,发现TNT可在大鼠睾丸内还原活化,睾丸锌含量下降并伴有睾丸绝对重量的改变;此外,TNT尚可导致大鼠睾丸某些酶(SDH,ACP,LDH,G6PD)活性改变,血清和睾丸内睾酮(T)含量     

三硝基甲苯对大鼠肾脏某些抗氧化酶活性的影响

本研究观察了三硝基甲苯（ＴＮＴ）不同剂量染毒和阳性对照安妥明处理对大鼠肾组织匀浆过氧化氢酶（ＣＡＴ）、谷胱甘肽过氧化物酶（ＧＳＨ－ＰＸ）、超氧化物歧化酶（ＳＯＤ）活性及肾组织蛋白含量的影响。结果表明,ＴＮＴ染毒组、阳性对照组大鼠肾匀浆ＣＡＴ与ＧＳＨ－ＰＸ活性显著高于对照组（Ｐ＜０．０５）,而肾蛋白含量显著降低（Ｐ＜０．０５）,表明ＴＮＴ染毒和安妥明处理均可诱导肾组织过氧化氢生成。推测ＴＮＴ可能具有诱发肾脏过氧化物小体增生作用     

睾酮对大鼠睾丸形态学的影响

本文研究了丙酸睾酮对大鼠睾丸形态超微结构的影响,结果发现：大剂量外源性丙酸睾酮可使睾丸出现抑制性超微结构的形态学改变。     

三硝基甲苯对大鼠胆固醇和甘油三酯影响的研究

不同剂量的三硝基甲苯(TNT)染毒大鼠,从染毒后第四周开始,各剂量组血清甘油三酯的含量显著下降;从染毒后第六周开始,各剂量组肝脏甘油三酯和胆固醇的含量明显低于对照组,血清胆固醇含量明显高于对照组;至染毒后第八周各指标均未见恢复。表明 TNT 对大鼠的脂代谢有一定的影响。     

镉对大鼠睾丸中某些酶活性及组织形态的影响

镉是环境中常见的有毒重金属之一,可引起多器官系统毒性,并且具有生殖系统（睾丸）毒性。我们研究了镉染毒后,大鼠睾丸组织中某些酶活性指标及组织形态的变化,探讨镉对生殖系统的毒性及其机制。材料与方法１．实验动物：成年雄性ＳＤ大鼠,由扬州大学动物实验中心提供...     

人和大鼠接触三硝基甲苯对血清铜蓝蛋白活性的影响

TNT是一种通过还原途径活化的毒物,其中毒机理已初步阐明为氧化性应激作用。我们通过现场调查和动物实验,进一步观察了TNT对接触工人和染毒大鼠血清铜蓝蛋白(CP)活性的影响。     

三硝基甲苯对人和小鼠体内环核苷酸影响的初步探讨

三硝基甲苯(TNT)对肝、眼、血液等损害研究较多,而对机体内环磷酸腺苷(cAMP)和环磷酸乌苷(cGMP)影响的报道罕见。本研究就TNT对体内CAMP和cGMP影响的规律进行了探讨.     

Reproductive toxicity of melamine against male mice and the related mechanism

Melamine is a nitrogen-containing heterocyclic organic compound with a triazine skeleton, which has been widely applied in industrial and chemical fields. Previous toxicity studies of melamine mainly focused on renal toxicity and hepatic pathological changes, but its toxicity against the reproductive system has seldom been assessed. We investigated the effects of melamine on the reproductive system of male mice. Forty healthy male Kunming mice were randomly divided into a normal saline negative control group, a low-dose melamine group, a medium-dose melamine group and a high-dose melamine group (n?=?10). The mice were administered for five consecutive days and killed on the 35th day after first administration. In melamine administration groups, seminiferous tubules had disordered, loose arrangement, and spermatogenic cells at all levels obviously decreased. The sperm count and motility decreased significantly, and the sperm deformity rate increased significantly. Melamine induced apoptosis of testicular spermatogenic cells. To further explore the mechanism, we detected metabolism-related enzymes sorbitol dehydrogenase (SDH) and lactate dehydrogenase (LDH) as well as oxidative stress indices superoxide dismutase (SOD) and malondialdehyde (MDA). The activities of SDH, LDH and SOD in melamine treatment groups decreased significantly, and the MDA level increased obviously. The expressions of apoptosis-related proteins Bcl-2, Bax and caspase-3 were detected by immunohistochemistry. The expression of Bcl-2 significantly increased, but those of Bax and caspase-3 significantly reduced (p?相似文献   

Effects of chlorpyrifos on reproductive toxicology of male rats

The aim of this study is to investigate the effects of subchronic exposure to chlorpyrifos on reproductive toxicology of male rats. Forty healthy male rats were divided into four groups: three exposure groups and a control group. Chlorpyrifos was administered orally to male rats at 0, 2.7, 5.4, and 12.8mg/kg for 90 days to evaluate the toxic alterations in testicular histology, testicular marker enzyme activities and related genes expression levels, sperm dynamics, and testosterone levels. The body weight and the testis weight of animals did not show any significant changes. Chlorpyrifos brought about marked reduction in testicular sperm counts, sperm motility, and significant growth of sperm malformation rate in exposed males. Histopathological examination of testes showed mild to severe degenerative changes in seminiferous tubules at various dose levels. The levels of testosterone (T) showed a decreasing tendency, and there was a statistical difference between the 5.4, 12.8 mg/kg groups, and the control group. The levels of follicle stimulating hormone (FSH) were significantly increased in 5.4 and 12.8 mg/kg groups, but there were no obvious effects on the levels of luteinizing hormone (LH) and estradiol (E₂). A significant increase in the activities of LDH and LDH‐x was observed in chlorpyrifos exposed rats in 5.4 and12.8 mg/kg groups, but the expression levels of related genes had no significant differences between chlorpyrifos exposure groups and the control group. These results suggest that chlorpyrifos has adverse effects on reproductive system of male rats. © 2013 Wiley Periodicals, Inc. Environ Toxicol 29: 1083–1088, 2014.     

三硝基甲苯对雄性生殖毒性的研究

急性、亚急性和亚慢性TNT染毒大鼠睾丸铜锌含量和多种酶活性皆有所变化;睾丸和血清睾酮含量下降。大鼠辜丸游离间质细胞与TNT共同孵育时,睾酮形成量明显下降;间质细胞与TNT孵育后,活性氧与脂质过氧化阳性物质含量明显增加。补锌在一定程度上能拮抗TNT对大鼠的生殖毒性。横断面调查表明,TNT接触男工自觉性功能降低者增加,血清睾酮含量下降,精液常规检查有阳性所见。     

Impact of boric acid exposure at different concentrations on testicular DNA and male rats fertility

Abstract

The aim of this study was to investigate the consequences of exposure to three levels of boric acid (BA) on male rats reproduction, fertility and progeny outcome, with emphasis on testicular DNA level and quality. Adult male rats (12 weeks old) were treated orally with 125, 250 and 500?mg/kg?bwt/d of BA for 60?d. The results indicated that BA administration at 125?mg/kg?bwt had no adverse effects on fertility, sperm characteristics or prenatal development of the impregnated females. However, at dose 250?mg, BA treatment significantly increased serum nitric oxide, testosterone, estradiol levels and testicular boron and calcium levels and also significantly reduced serum arginase activity, sperm quality and testicular DNA content with minor DNA fragmentation. The impact of BA exposure at dose 250?mg on male rats fertility was translated into increases in pre-implantation loss with a resulting decrease in the number of live fetuses/litter. In addition to the significant alteration of biochemical measurements, observed at dose 250?mg, administration of BA at 500?mg caused testicular atrophy, severe damage of spermatogenesis, spermiation failure and significant reduction of Mg and Zn testicular levels. None of the male rats, treated with 500?mg/kg?bwt, could impregnate untreated females, suggesting the occurrence of definitive loss of fertility. In conclusion, BA impaired fertility, in a dose-dependant manner, by targeting the highly proliferative cells, the germ cells, through decreasing DNA synthetic rate rather than the induction of DNA damage.     

Effects of opioid (tramadol) treatment on testicular functions in adult male rats: The role of nitric oxide and oxidative stress

相似文献   

Microcystin (-LR) affects hormones level of male mice by damaging hypothalamic-pituitary system

Microcystin (-LR) (MC-LR) is a broad distributed hepatotoxic microcystin produced by common freshwater phytoplankton species. Recently, its toxic effects on male reproductive system drew great attention. To investigate its reproductive toxicity and the underlying mechanism, BALB/c mice were exposed to MC-LR by intraperitoneal injection with different injection duration (1, 4, 7 and 14 days) and injection concentration (3.75, 7.5, 15 and 30 μg kg b.w.⁻¹ day⁻¹) as an in vivo test. For in vitro test, isolated mice Leydig cells were exposed to MC-LR at doses of 1, 10, 100, 250, 500 750 and 1000 nmol/L for 24 h. MC-LR did not induce significant changes in Kiss-1, GPR54, Gnrhr, Fshr or Lhr expression. It decreased the Gnrh expression in a dose- and duration-dependent manner. It increased and subsequently decreased the expressions of FSH, LH and testosterone. In in vivo test, MC-LR was not able to enter Leydig cells and had no cytotoxicity on Leydig cells. The results showed that MC-LR affected male mice serum hormones and mRNA expressions by damaging the hypothalamic-pituitary systems.     

Use of the Adverse Outcome Pathway (AOP) framework to evaluate species concordance and human relevance of Dibutyl phthalate (DBP)-induced male reproductive toxicity

Dibutyl phthalate (DBP) is a phthalate ester used as a plasticizer, and solvent. Studies using rats consistently report that DBP exposure disrupts normal development of the male reproductive system in part via inhibition of androgen synthesis. However, studies using xenograft models report that in human fetal testis DBP exposure is unlikely to impair testosterone synthesis. These results question the validity of the rat model for assessment of male reproductive effects caused by DBP. The Adverse Outcome Pathway (AOP) framework was used to evaluate the available evidence for DBP-induced toxicity to the male reproductive system. Three relevant biological elements were identified: 1) fetal rats are more sensitive than other rodents and human fetal xenografts to DBP-induced anti-androgenic effects, 2) DBP-induced androgen-independent adverse outcomes are conserved amongst different mammalian models and human fetal testis xenografts, and 3) DBP-induced anti-androgenic effects are conserved in different mammalian species when exposure occurs during postnatal life stages.     

Dose-dependent alterations in androgen-regulated male reproductive development in rats exposed to Di(n-butyl) phthalate during late gestation.

Di(n-butyl) phthalate (DBP) is a commercially important plasticizer and ubiquitous environmental contaminant. Since previous, limited dose-response studies with DBP that reported alterations in male reproductive development and function failed to establish a NOAEL (no-observed-adverse-effect level), an extensive dose-response study was conducted. Pregnant CD rats were given DBP by gavage at 0, 0.5, 5, 50, or 100 mg/kg/day (n = 19-20) or 500 mg/kg/day (n = 11) from gestation day 12 to 21. In male offspring, anogenital distance was decreased at 500 mg DBP/kg/day. Retained areolas or nipples were present in 31 and 90% of male pups at 100 and 500 mg/kg/day, respectively. Preputial separation was not delayed by DBP treatment in males with normal external genitalia, but cleft penis (hypospadias) was observed in 5/58 rats (4/11 litters) at 500 mg/kg/day. Absent or partially developed epididymis (23/58 rats in 9/11 litters), vas deferens (16/58 animals in 9/11 litters), seminal vesicles (4/58 rats in 4/11 litters), and ventral prostate (1/58 animals) occurred at 500 mg/kg/day. In 110-day-old F(1) males, the weights of the testis, epididymis, dorsolateral and ventral prostates, seminal vesicles, and levator ani-bulbocavernosus muscle were decreased at 500 mg/kg/day. At 500 mg/kg/day, widespread seminiferous tubule degeneration was seen in 25/58 rats (in 9/11 litters), focal interstitial cell hyperplasia in 14/58 rats (in 5/11 litters), and interstitial cell adenoma in 1/58 rats (in 1/11 litters). For this 10-day prenatal (embryonic and fetal) exposure to DBP, the NOAEL and LOAEL (lowest-observed-adverse-effect level) were 50 and 100 mg/kg/day, respectively. This is currently the lowest NOAEL described for the toxicity of DBP.     

Intracranial cycloheximide: effect on male mouse sexual behavior and plasma testosterone.

Cycloheximide (Cyclo), an inhibitor of protein synthesis, infused bilaterally into the preoptic area (POA) of intact B6D2F male mice significantly inhibited male sexual behavior when the males were presented with receptive females 12 hr after treatment. The few males that ejaculated appeared to copulate normally. This finding suggests that Cyclo acts primarily by inhibiting sexual arousal rather than sexual performance. The inhibition of sexual behavior was not observed when the males were tested 84 hr after treatment. After exposure to an estrous female, plasma testosterone levels were measured in males with POA infusions of Cyclo or saline vehicle. No significant difference was found, but both groups had significantly higher levels of plasma testosterone than males not exposed to estrous females. It is suggested that the interference with sexual behavior by Cyclo was not due to interference with the neuroendocrine mechanisms controlling blood andorgen levels, but due to Cyclo acting directly on the neural circuits controlling sexual responsiveness.     

吸入麻醉药对男(雄)性生殖的影响

近年来,吸入麻醉药对男性生殖方面的影响被人们所关注,本文主要就吸入麻醉药对男(雄)性精子发生、运动、获能、顶体反应以及受精能力等生殖方面的影响加以总结.