丙烯酰胺的雄性生殖毒性

丙烯酰胺在工业和科研实验中广泛应用，是一种较为常见的化工原料。近年来证实，丙烯酰胺还存在于高温加热的淀粉类食品中。丙烯酰胺具有多种毒性效应，近年研究发现丙烯酰胺具有生殖毒性，表现为对雄性生殖行为、雄性生殖内分泌功能和精子生成的影响等几个方面，其可能的机制包括丙烯酰胺作用于睾丸间质细胞，与马达蛋白、染色体和DNA形成烷化物以及通过氧化损伤来影响雄性生殖。     

多氯联苯的雄性生殖毒性研究进展

多氯联苯(PCBs)是一类环境中广泛存在的具有雌激素样效应的持久性有机污染物,它对男性生殖的损害正越来越受到关注。研究表明睾丸组织中多种不同类型的细胞暴露于PCBs能产生不同的毒性效应。本文就近年来PCBs暴露对睾丸生精细胞、支持细胞、间质细胞以及母体暴露后雄性子代的毒性效应研究进行综述。建议根据目前男性生殖流行病学的调查结果进行深入的机制研究,同时睾丸支持细胞的胞间连接可作为PCBs睾丸毒性研究的突破方向之一。     

赭曲霉毒素A的毒理学特征及损害雄性生殖健康的研究进展

赭曲霉毒素A(OTA)对人类和动物具有肾毒性、致畸毒性、神经毒性和免疫毒性等,最近十几年不断被证明还具有生殖毒性。因此,人们已经开始重视OTA对人类生殖健康的危害,并对其损害生殖健康的发生途径和分子机制进行了研究。研究证明,OTA可作为机体内的一种内分泌干扰物影响生殖系统的功能。对雄性动物和男性来说,OTA是一种睾丸毒素,可降低精子质量,还可能诱发睾丸癌变。基于上述内容,本文阐述了OTA的毒理学特征及毒代动力学过程,集中讨论了OTA引发的各种毒害作用的机制及研究进展。总之,OTA对雄性生殖健康的危害不容小觑,本文旨在引起人们对OTA危害雄性生殖健康的重视。     

机动车尾气雄性生殖毒性的研究进展

本文主要从机动车尾气对动物、动物后代的生殖毒性及人群流行病学研究以及人类对机动车尾气生殖毒性的保护性研究等方面，就机动车尾气对雄性生殖毒性的研究最新进展进行了综述，旨在对机动车尾气的生殖毒性有更全面的认识。     

外源性毒素对雄性动物生殖的影响

外源性毒素 (如砷、二英等 )可通过各种途径进入动物体内并不断蓄积 ,对机体产生毒性作用 ,并可能对雄性动物的生殖产生不良影响。现就常见的矿物性毒素和外源性雌激素对雄性生殖的影响及其作用机制作一综述     

环境雌激素致雄性生殖系统发育异常途径的研究进展

大量动物实验表明环境雌激素(EEs)具有生殖和(或)发育毒性,其致雄性生殖系统发育畸形的机制复杂,尤其作用途径目前仍很不明了。本文从EEs干扰睾丸发育、影响睾丸激素产生、代谢并进而致雄性生殖系统发育畸形的可能途径介绍近年来国内外取得的进展。     

拟除虫菊酯类农药的男(雄)性生殖毒性研究进展

拟除虫菊酯作为一种新型农药,由于其高效、低毒而替代有机氯类农药被广泛应用。近年来,越来越多的证据表明,拟除虫菊酯类农药能够降低精子密度和活力,诱导精子头部畸形,增加畸形精子数量,损伤精子DNA以及诱导精子DNA的非整倍性,并影响生殖激素水平,具有生殖毒性。本文从动物实验和人群研究两个方面,就几种近年来使用较广泛和研究较多的拟除虫菊酯类农药杀虫剂对男(雄)性生殖毒性的研究最新进展进行了综述,以探讨拟除虫菊酯类农药杀虫剂对男(雄)性生殖毒性的作用机制。     

口服丙烯酰胺对雄性大鼠生长发育及生殖机能的影响

目的:研究丙烯酰胺对雄性大鼠的生殖毒性作用。方法:30只21日龄断奶未成熟雄性大鼠随机分为3组,实验组Ⅰ和实验组Ⅱ分别通过自由饮水方式口服5 mg/kg.d和10 mg/kg.d的丙烯酰胺溶液8周,对照组饮用自来水。分两批(第4周和第8周时)对体重、脏器重等指标进行检测,并做睾丸和附睾的组织形态学观察;第8周时,同时检查附睾尾精子密度和精子形态。结果:两实验组大鼠体重增加显著低于对照组(P<0.05),至实验8周时,睾丸、附睾性器官发育已受到影响,实验组Ⅱ大鼠附睾尾部精子密度明显低于对照组(P<0.05),实验组Ⅰ与对照组差异不显著(P>0.05)。睾丸出现不同程度的病理变化,发生调亡的生精小管周围间质细胞显著增多(P<0.05)。结论:丙烯酰胺会对生精小管产生毒性作用而导致雄性大鼠精子生成减少。     

农药杀虫剂的男(雄)性生殖毒性研究进展

本文从动物实验和人群研究两个方面就几类近年来使用较广泛和研究较多的农药杀虫剂对男 (雄 )性生殖毒性的研究进展作一综述 ,探讨农药杀虫剂对男 (雄 )性生殖毒性作用的机制 ,并提出目前评价人类生殖危害仍存在的问题。     

骨桥蛋白在雄性哺乳动物生殖系统中的作用

骨桥蛋白(OPN)为一种多功能的细胞外基质蛋白,在多种组织及体液中广泛表达,参与各项生理及病理过程。同时,OPN也表达于女性及男性的生殖系统,参与了胚胎的着床、生长发育及分化等生殖过程。近年来研究表明,OPN普遍存在于雄性哺乳动物的生殖系统中,并与雄性动物的生育力有着密切的关系,可能影响精子的质量及其受精过程等。对OPN相关功能的研究将有助于解释男性不育的机制,提高辅助生殖技术的成功率。     

化妆品中丙烯酰胺及其检测的研究进展

丙烯酰胺是生产聚丙烯酰胺的原料,在化妆品中存在的微量丙烯酰胺是生产过程中添加聚丙烯酰胺引入的。由于丙烯酰胺具有神经毒性和潜在致癌性,已被列为化妆品中的限制使用成分,加强化妆品中丙烯酰胺的监测具有重要意义。本文综述了丙烯酰胺的来源、用途和危害性,总结了目前化妆品中丙烯酰胺测定的所用的样品前处理方法,以及丙烯酰胺气相色谱法、液相色谱法、液相色谱-串联质谱法等各种检测方法的最新研究进展,同时对化妆品样品中丙烯酰胺检测技术的发展趋势进行了展望,表明采用串联质谱技术（如GC-MS/MS、LC-MS/MS）对进行复杂样品中丙烯酰胺进行检测是未来的发展趋势。     

奥美定注入小香猪体内后生殖毒性的观察

目的　观察奥美定注入小香猪体内后的生殖毒性。方法　注入奥美定后观察小香猪母代及子代的生长、健康情况 ,抽出奥美定检测丙烯酰胺单体含量以及抽血查染色体及微核试验观察。结果　 6只母代小香猪健康 ,2只与公猪交配 ,4个月及 5个月后生出 9只及 4只子代小猪 ,健康情况亦良好。在半年及 1年后分别抽出奥美定检测丙烯酰胺单体没有增加 ,共检测 9只小香猪的染色体包括母代及子代 ,均未发现数目畸变及结构畸变 ,微核试验有细微的变化 ,并初步反映出与用药量大小呈正相关 ,但超量注射的一只动物 (18.5ml/kg)变化的千分值仍在正常范围内。结论　从目前几项观察与检测指标看 ,实验量奥美定注入小香猪体内尚不具生殖遗传毒性     

Protective effects of vitamin E on sodium arsenite‐induced toxicity,testicular measurements and histopathological studies of testes in Teddy goat bucks

The objective of this study was to investigate the toxic effects of arsenic on testicular measurements and histology of adult Teddy goats bucks and to examine whether these toxic effects are scavenged by vitamin E. Twelve adult Teddy goat bucks were divided randomly into three groups, A, B and C. Group A was kept as control, the B was given sodium arsenite 5 mg/kg BW per day, and group C was fed with vitamin E 200 mg/kg BW per day + arsenic 5 mg/kg BW per day. This treatment was continued for 84 days. Analysis of data revealed that the testicular measurements (scrotal circumference, width, length and weight) were significantly reduced in arsenic‐treated animals, whereas there were ameliorating effects of vitamin E on these parameters. The major histopathological changes were present in the form of loss of germinal epithelium, atrophy of Leydig cells and vacuolations. Vitamin E in combination with sodium arsenite increased the active spermatogenesis as well as restoration of germinal epithelium. It can be concluded from the present findings that sodium arsenite causes toxicity in the male reproductive system of Teddy goat bucks with major changes in parenchyma of testes. Supplementation of vitamin E has protective effects on the toxicity of sodium arsenite on the reproductive system of male Teddy goat bucks.     

Fish oil,contained in eicosapentaenoic acid and docosahexaenoic acid,attenuates testicular and spermatological damage induced by cisplatin in rats

The aim of this study was to investigate the beneficial effects of the fish oil (FO) supplementation on oxidative stress, sperm characteristics and histological alterations in the male reproductive system of rats against cisplatin (CP) toxicity. The rats were divided randomly into 4 equal groups (control, FO, CP and FO + CP). FO was orally administered at the dose of 1 softgel per rat per day for 14 days and CP was intraperitoneally given at the dose of 7 mg kg^?1 with a single injection. In CP + FO group, they were applicated at the same doses and times. The results showed that CP caused a significant oxidative damage via induction of lipid peroxidation and reduction in the antioxidant defence system potency in the testis tissue. In addition, sperm motility and sperm concentration significantly decreased but the abnormal sperm rate and histopathological testicular damage increased with CP treatment. On the other hand, FO treatment prevented oxidative, histopathological and spermatological effects of CP and reversed side effects of CP. In conclusion, FO supplementation had significant beneficial effects against CP toxicity on male reproductive system and toxic effects of CP can be prevented by FO treatment. Therefore, it appears that fish oil may be useful for the prevention and treatment of cisplatin‐induced reproductive system toxicity.     

Protocatechuic acid prevents reproductive damage caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in male rats

In this study, it was aimed to determinate beneficial effects of protocatechuic acid (PCA) against reproductive toxicity caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environmental contaminant. For this purpose, 28 rats were equally divided into four groups (control, TCDD 2 μg kg(-1) per week, PCA 100 mg kg(-1) per day and TCDD + PCA group), and compounds were orally administered for 45 days. The results indicated that TCDD induced oxidative stress via an increase in thiobarbituric acid-reactive substances levels and a decrease in reduced glutathione, catalase, glutathione peroxidise and SOD levels in male rats. In contrast, PCA treatment prevented toxic effects of TCDD in terms of oxidative stress. Additionally, sperm motility, sperm concentration and serum testosterone levels significantly decreased, and pathologic testicular damage increased with TCDD exposure. However, these effects of TCDD on sperm characteristics, histopathological changes and hormone levels were reversed by PCA treatment. In conclusion, it was found that TCDD exposure induced reproductive toxicity (oxidative, hormonal, histopathological and spermatological alternations) in male rats and PCA treatment could prevent toxic effects of TCDD. Thus, PCA may be useful for the prevention and treatment of reproductive toxicity caused by TCDD.     

The effects of acrylamide and Vitamin E administration during pregnancy on adult rats testis

Thirty rats, with confirmed pregnancies by vaginal smear, were divided into five groups, each including six rats, as the Control, Corn Oil, Vitamin E, Acrylamide, Vitamin E + Acrylamide groups. The births were monitored on the 21st day to select the male rats, and the selected male rats were decapitated at the end of the 8th week. Oxidant–antioxidant parameters, serum hormone levels and histopathological examinations were performed on testis tissues of the rats. It was found that acrylamide (AA) negatively affected the serum hormone levels (Total Testosterone, Progesterone, FSH, LH, Estradiol), oxidant–antioxidant parameters in the tissues (MDA, GSH, NO, SOD, CAT, TAS, TOS) (p < 0.05) and the histological findings (the Johnson's score, seminiferous tubule diameter, histopathological images), and Vitamin E administration resulted with an increase in the total testosterone, progesterone, FSH, LH, GSH, TAS, NO, SOD, CAT levels (p < 0.05) and an improvement in histopathological findings. Currently, it is almost inevitable to be exposed to food‐induced AA toxicity and such toxicity is likely to cause lifelong damage. It was concluded that Vitamin E was able to present a protective effect in the testis tissue against AA toxicity; however, further studies are necessary.     

A mixture of seven antiandrogens induces reproductive malformations in rats

To date, regulatory agencies have not considered conducting cumulative risk assessments for mixtures of chemicals with diverse mechanisms of toxicity because it is assumed that the chemicals will act independently and the individual chemical doses are not additive. However, this assumption is not supported by new research addressing the joint effects of chemicals that disrupt reproductive tract development in the male rat by disrupting the androgen signalling pathway via diverse mechanisms of toxicity [i.e. androgen receptor (AR) antagonism in the reproductive tract vs. inhibition of androgen synthesis in the foetal testis]. In this study, pregnant rats were exposed to four dilutions of a mixture containing vinclozolin, procymidone, linuron, prochloraz, benzyl butyl phthalate, dibutyl phthalate and diethylhexyl phthalate during the period of sexual differentiation and male offspring were assessed for effects on hormone sensitive endpoints including: anogenital distance, infant areolae retention and reproductive tract tissue weights and malformations. The ratio of the chemicals in the mixture was based upon each chemical's ED(50) for inducing reproductive tract malformations (hypospadias or epididymal agenesis). The observed responses from the mixture were compared with predicted responses generated with a toxic equivalency approach and models of dose addition, response addition or integrated addition. As hypothesized, we found that the mixture of chemicals that alter the androgen signalling pathway via diverse mechanisms disrupted male rat reproductive tract differentiation and induced malformations in a cumulative, dose-additive manner. The toxic equivalency and dose addition models provided the best fit to observed responses even though the chemicals do not act via a common cellular mechanism of action. The current regulatory framework for conducting cumulative risk assessments needs to consider the results, including those presented herein, which indicate that chemicals that disrupt foetal tissues during sexual differentiation act in a cumulative, dose-additive manner irrespective of the specific cellular mechanism of toxicity.     

Endocrine disruptors and estrogenic effects on male reproductive axis

Endocrine disruptors （e.g., polychlorinated biphenyls [PCBs], dichlorodiphenyl-trichloroethane [DDT], dioxin, and some pesticides） are estrogen-like and anti-androgenic chemicals in the environment. They mimic natural hormones, inhibit the action of hormones, or alter the normal regulatory function of the endocrine system and have potential hazardous effects on male reproductive axis causing infertility. Although testicular and prostate cancers, abnormal sexual development, undescended testis, chronic inflammation, Sertoli-cell-only pattern, hypospadias, altered pituitary and thyroid gland functions are also observed, the available data are insufficient to deduce worldwide conclusions. The development of intra-cytoplasmic sperm injection （ICSI） is beyond doubt the most important recent breakthrough in the treatment of male infertility, but it does not necessarily treat the cause and may inadvertently pass on adverse genetic consequences. Many well-controlled clinical studies and basic scientific discoveries in the physiology, biochemistry, and molecular and cellular biology of the male reproductive system have helped in the identification of greater numbers of men with male factor problems. Newer tools for the detection of Y-chromosome deletions have further strengthened the hypothesis that the decline in male reproductive health and fertility may be related to the presence of certain toxic chemicals in the environment. Thus the etiology, diagnosis, and treatment of male factor infertility remain a real challenge. Clinicians should always attempt to identify the etiology of a possible testicular toxicity, assess the degree of risk to the patient being evaluated for infertility, and initiate a plan to control and prevent exposure to others once an association between occupation/toxicant and infertility has been established.     

The effect of p-nonylphenol, an environmental toxicant with oestrogenic properties, on fertility potential in adult male rats

Infertility is a sad reality and it is now evident that several aspects of male reproductive health have changed for the worse over the past 30–50  years. para -nonylphenol (p-NP), an environmental toxicant with oestrogenic properties, was tested for its effect on male fertility potential. When adult male rats were exposed to 100  mg  kg⁻¹ p-NP the histological parameters of the seminiferous tubules were adversely affected. Although spermatogenesis was already established in these males at the time exposure commenced, p-NP still had an effect on the histology of the seminiferous tubules. Increasing the level to 250  mg  kg⁻¹ additionally resulted in a smaller weight gain and signs of epididymal toxicity, while 400  mg  kg⁻¹ also impaired testicular mass and sperm count. In the last two groups spermatogenesis was also affected in some animals. Because p-NP had an effect on established spermatogenesis in the rat, one could speculate that the same effects might also occur in humans. It would appear that p-NP had toxic effects on both the testis and epididymis and both structures might be important in impairing male fertility. Bio-accumulation may enhance the negative effects at even lower p-NP concentrations over longer exposure periods than reported here.