久效磷对雄性孔雀鱼生殖毒性研究

采用静态亚急性毒性试验方法,用1.0 mg/L久效磷暴露孔雀鱼40 d,统计孔雀鱼的繁殖情况,同时每隔10 d取精巢进行组织切片观察,研究了久效磷对雄性孔雀鱼生殖的影响.结果表明,1.0 mg/L久效磷暴露的雌鱼繁殖次数、产仔鱼数量以及仔鱼存活数与对照组相比明显降低.雄鱼体色逐渐变浅,由鲜艳的橘红色转变为黯淡的橘黄色.精巢组织损伤主要表现为对精母细胞和谢尔托立氏细胞的影响,并且随暴露时间的延长精巢组织损伤逐渐加剧.精母细胞出现核膜溶解、染色质溢出现象; 基膜部分溶解、局部融合的精小囊数量增多; 部分小囊里的精子细胞发育出现不同步现象; 精巢的精小囊数量逐渐减少; 精巢出现多个空泡; 输精小管基膜溶解.谢尔托立氏细胞出现提前膨大并大量增生,局部解体的精子束数量增多,游离精子现象加剧.久效磷对精巢结构的损伤,抑制了精巢内的正常精子发生过程,降低了精子的密度和数量,导致孔雀鱼繁殖次数和仔鱼数量减少.     

Oxidative stress and biochemical perturbations induced by insecticides mixture in rat testes

The joint action of pyrethroids, lambda-cyhalothrin (LC) in combination with organophosphates, fenitrothione (FNT) on antioxidant defense system and lipid peroxidation biomarkers in rat testes was studied. The results suggest that incubation of testes homogenate with different concentrations of insecticide mixture for different time intervals significantly decreased the activity of antioxidant enzymes, like glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT), and the level of reduced glutathione (GSH). In addition, a significant inhibition in transaminases (AST, ALT), phosphatases (AcP, AlP) activity and protein content were observed. On the other hand, FNT plus LC increased the cellular lipid peroxidation (LPO) level and the activity of lactate dehydrogenase (LDH). In conclusion, the use of insecticides mixture might cause marked oxidative damage in a concentration and time-dependent manner.     

3-甲基-4-硝基酚对公鸡睾丸早期发育的影响

研究环境内分泌干扰物3-甲基-4-硝基酚(3-methyl-4-nitrophenol,PNMC)对公鸡睾丸早期发育的影响。48只1 d龄白羽公鸡随机分成3个组,分别为对照组、10和100 mg·L-1PNMC处理组,连续饮水42 d。检测公鸡的生长性能、睾丸重量和指数、睾丸的结构变化、血清激素水平和睾丸中CYP17A1及其相关基因的表达情况。结果显示:与对照组相比,10 mg·L-1PNMC处理组显著降低公鸡的生长性能;睾丸重量和睾丸指数均无显著性变化;睾丸细精管生精细胞均有不同程度的空泡兼或脱落;血清孕酮和雌二醇水平均无显著性差异,睾酮水平随饮水中PNMC浓度的升高呈递减的趋势;公鸡睾丸中CYP17A1、HSD3B2和CYP19A1有升高的趋势,HSD17B4在10 mg·L-1PNMC组呈降低的趋势,在100 mg·L-1PNMC组呈升高的趋势。结果表明:饮水中添加10 mg·L-1PNMC显著影响了公鸡的生长性能;饮水中添加100 mg·L-1PNMC引起公鸡睾丸细精管生精细胞变性、坏死,造成结构病理损伤,从而对生殖系统造成损伤。     

低剂量长期铅暴露对雄性黑斑蛙精巢组织关键酶活性的影响

在实验条件下,将健康的性成熟雄性黑斑蛙暴露于0.1、0.2、0.4、0.8和1.6mg·L-1的Pb2+溶液中30d,以Ca2+-ATP酶、Na+-K+-ATP酶、Ca2+-Mg2+-ATP酶、β-葡萄糖醛酸苷酶(β-DG)、乳酸脱氢酶(LDH)和酸性磷酸酶(ACP)活性为指标,进行了长期铅暴露对雄性黑斑蛙生殖毒性的研究.结果表明:随着铅染毒剂量的增加,Ca2+-ATP酶和Na+-K+-ATP酶活性被诱导,Ca2+-Mg2+-ATP酶活性被抑制,当Ca2+-Mg2+-ATP酶的抑制程度超过Ca2+-ATP酶和Na+-K+-ATP酶的代偿机制时,会抑制精子的发生,进而导致雄性生殖毒性;在1.6mg·L-1Pb2+处理下,ACP酶被显著抑制,提示支持细胞受损,精子总数受到影响;在0.4mg·L-1Pb2+处理下,LDH酶被显著抑制,提示生精细胞受损,精子质量受到影响.     

Evaluation of reproductive and developmental toxicity of cypermethrin in male albino rats

The ever-increasing use of pesticides in the agricultural and public health has become a major cause of sterility in human and various other animals particularly in males. This study was sought to screen the toxic impacts of cypermethrin (synthetic pyrethroid) on reproduction and development. Twenty-four Wistar male rats divided into four groups were orally administered cypermethrin of daily doses 50, 75, or 100 mg?kg^?1 bwt per day for 45 days; and for developmental toxicity, 12 female rats were separated into two groups. Maternal rats (experimental) were administered cypermethrin (100?mg?kg^?1) by gavage daily from 6th to 17th day of gestation, and the control group was dosed only vehicle (olive oil). The body weights, fertility index, biochemical, enzymatic, hormonal, and histopathological parameters were the criteria used to evaluate the toxicity of cypermethrin. Study showed significant decline in the weight of testes, epididymises, seminal vesicles, and ventral prostate, and reduction in sperm counts both in epididymises and testes in chemical-treated animals. Pre- and post- fertility test showed 50%, 80%, and 100% negative results after treatment. A significant degenerative reduction in testicular glycogen and sialic acid was also noted. In contrast, protein and cholesterol levels of testes were significantly increased. In addition, acid phosphatase activity was significantly increased, while alkaline phosphatase, testosterone, leutinizing hormone (LH), and follicle stimulating hormone (FSH) levels were diminished. Histology of testes showed degenerative changes in seminiferous tubules. Cypermethrin exposure during gestation produced adverse effects markedly in females and fetuses.     

DNA damage in mouse organs and in human sperm cells by bisphenol A

Abstract

The in vivo genotoxic potential of bisphenol A using the comet assay in mice and in human sperm cells in vitro without metabolizing enzymes was studied. Male mice were exposed by oral gavage to the following doses of bisphenol A (0 125, 250 and 500?mg/kg body weight). DNA damage was investigated in liver, kidney, testes, urinary bladder, colon and lungs cells. In testicular cells, a significant increase in DNA strand breaks was observed in the lowest, but not in the medium or highest dose groups. Histopathological investigation of the testicular samples did not show any treatment dose-related effects. No DNA strand breaks were observed in any of the other investigated tissues. In human sperm cells in vitro, bisphenol A did not induce DNA strand breaks.     

Metal Interactions in carcinogenesis†

Mixed exposures to a number of metallic compounds may give rise to a carcinogenic response in humans.

An interaction between occupational exposure to arsenic and cigarette smoking has been documented epidemiologically. A multiplicative effect was indicated concerning the occurrence of lung cancer when both of the exposures were present. Several experimental studies have been reported in the literature concerning interactions between benzo(a)pyrene and Fe₂O₃ as well as some other metallic compounds like Ni₃S₂, PbO, MgO and TiO₂ in relation to respiratory carcinogenicity. There is also limited evidence of a positive interaction between arsenic trioxide and benzo(a)pyrene. Particles containing V and Ni were obtained from the flue gases of power plants burning heavy fuel oil. Such particles were not carcinogenic themselves but enhanced the carcinogenicity of benzo(a)pyrene even more efficiently than Fe₂O₃.

Increased dietary selenium intakes can decrease the carcinogenicity of several organic carcinogens in animals and dietary zinc can effectuate both enhancement and inhibition of carcinogenicity depending on dietary concentration.     

镉对黑斑蛙精巢细胞色素P450酶及谷胱甘肽转移酶活性的影响

细胞色素P450酶(CYP450)和谷胱甘肽转移酶(GST)是动物体内主要的解毒酶,在外源毒物的转化和代谢过程中具有重要作用.本文在实验条件下, 将健康性成熟黑斑蛙(Rana nigromaculata)暴露于浓度分别为0.005、0.01、0.05、0.1、0.5和1.0 mg·L^-1的Cd溶液中30 d, 采用荧光分光光度法和紫外分光光度法测定精巢组织乙氧基异酚恶唑脱乙基酶(EROD)、红霉素N-脱甲基酶 (ERND)、氨基比林-N-脱甲基醇酶(APND)和谷胱甘肽转移酶(GST)活性,探讨Cd在精巢的可能代谢过程和毒性机理.结果表明, 与对照组比较, EROD和GST酶活性在0.5和1.0 mg·L^-1 Cd处理组被显著抑制; ERND酶活性在0.01~1.0 mg·L^-1 Cd处理组均被显著抑制;而APND酶活性在各处理组响应变化不明显.结果显示, 精巢EROD、ERND和GST对Cd胁迫的敏感性高于APND, 黑斑蛙精巢中EROD、ERND和GST酶活性的响应可用来评价环境中低水平Cd的污染效应.     

碲化镉量子点对小鼠睾丸组织的氧化损伤（Effects of CdTe Quantum Dots on the Antioxidant Enzymes Activity and Lipid Peroxidation in Testes of Mice）

为探讨碲化镉量子点(CdTeQDs)对小鼠睾丸的急性氧化损伤作用,将20只雄性ICR小鼠随机分成4组:对照组、1d、3d、7d(3个不同时间组),采用尾静脉注射进行一次性染毒2.5μmol·kg-1CdTeQDs,对照组注射等体积生理盐水.染毒后对睾丸的脏器系数以及组织中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)活性,丙二醛(MDA)含量分别进行测定,从而检测CdTeQDs对睾丸组织的急性氧化损伤作用.结果显示,与对照组相比,随染毒时间的延长,睾丸脏器系数无显著性变化(p>0.05);GSH-Px和SOD活性随染毒时间的延长呈逐渐升高趋势;而CAT活性呈逐渐降低趋势,且与对照组差异显著(p<0.01);MDA含量显著高于对照(p<0.01),且随时间变化不大.CdTeQDs染毒可导致小鼠睾丸组织氧化损伤,其损伤程度与染毒时间之间具有一定的时间-效应关系.