Acetamiprid has a wide range of influence on physiological functions in mammals.The objective of this study was to examine the effect of acetamiprid on the reproductive function of male mice,and to study the role of o...Acetamiprid has a wide range of influence on physiological functions in mammals.The objective of this study was to examine the effect of acetamiprid on the reproductive function of male mice,and to study the role of oxidative stress in acetamiprid-induced damage to the testes.Fifty adult Kunmin male mice （25-30 g） were divided into five groups （n=10 per group）,i.e.,control,blank,acetamiprid alone,acetamiprid and vitamin E,and vitamin E alone.All groups were treated for 35 d.The results showed that acetamiprid significantly decreased the body weight and the weight of testosterone-responsive organs,such as the testis,epididymis,seminal vesicle,and prostate.Furthermore,acetamiprid also significantly reduced the serum testosterone concentration,and decreased sperm count,viability,motility,and the intactness of the acrosome （P〈0.05 for each parameter）.The mice treated with acetamiprid had damaged seminiferous tubules and Leydig cells based on the histological structure of testes;there was degeneration of the mitochondria and endoplasmic reticulum of Leydig cells.These deleterious effects of acetamiprid may be mediated by increasing oxidative stress,as acetamiprid increased malondialdehyde and nitric oxide in the testes,reduced the activity of catalase,glutathione peroxidase,superoxide dismutase,and activated p38.The concentration of acetamiprid in the testes was lower than that in liver,so did the concentrations of liver function tests,including aspartate transaminase （AST）,alanine transaminase （ALT） and alkaline phosphatase （ALP）,which suggest that male reproductive function may be affected through the indirect action of its metabolites.Vitamin E significantly ameliorated the effects of acetamiprid.We conclude that acetamiprid damages male reproductive function through inducing oxidative stress in the testes.展开更多
Aim： To investigate the effect of formaldehyde （FA） on testes and the protective effect of vitamin E （VE） against oxidative damage by FA in the testes of adult rats. Methods： Thirty rats were randomly divided in...Aim： To investigate the effect of formaldehyde （FA） on testes and the protective effect of vitamin E （VE） against oxidative damage by FA in the testes of adult rats. Methods： Thirty rats were randomly divided into three groups： （1） control; （2） FA treatment group （FAt）; and （3） FAt ＋ VE group. FAt and FAt ＋ VE groups were exposed to FA by inhalation at a concentration of 10 mg/m^3 for 2 weeks. In addition, FAt ＋ VE group were orally administered VE during the 2-week FA treatment. After the treatment, the histopathological and biochemical changes in testes, as well as the quantity and quality of sperm, were observed. Results： The testicular weight, the quantity and quality of sperm, the activities of superoxide dismutase （SOD）, glutathione peroxidase （GSH-Px） and glutathione （GSH） were significantly decreased whereas the level of malondialdehyde （MDA） was significantly increased in testes of rats in FAt group compared with those in the control group. VE treatment restored these parameters in FAt ＋ VE group. In addition, microscopy with hematoxylin-eosin （HE） staining showed that seminiferous tubules atrophied, seminiferous epithelial cells disintegrated and shed in rats in FAt group and VE treatment significantly improved the testicular structure in FAt ＋ VE group. Conclusion： FA destroys the testicular structure and function in adult rats by inducing oxidative stress, and this damage could be partially reversed by VE.展开更多
Male reproductive health has deteriorated considerably in the last few decades. Nutritional, socioeconomic, lifestyle and environmental factors （among others） have been attributed to compromising male reproductive h...Male reproductive health has deteriorated considerably in the last few decades. Nutritional, socioeconomic, lifestyle and environmental factors （among others） have been attributed to compromising male reproductive health. In recent years, a large volume of evidence has accumulated that suggests that the trend of decreasing male fertility （in terms of sperm count, quality and other changes in male reproductive health） might be due to exposure to environmental toxicants. These environmental contaminants can mimic natural oestrogens and target testicular spermatogenesis, steroidogenesis, and the function of both Sertoli and Leydig cells. Most environmental toxicants have been shown to induce reactive oxygen species, thereby causing a state of oxidative stress in various compartments of the testes. However, the molecular mechanism（s） of action of the environmental toxicants on the testis have yet to be elucidated. This review discusses the effects of some of the more commonly used environmental contaminants on testicular function through the induction of oxidative stress and apoptosis.展开更多
基金supported by the Natural Science Foundation Project of CQ CSTC,China(2010BB1138)the National Innovation Experiment Program for Undergraduate,China (091063530)
文摘Acetamiprid has a wide range of influence on physiological functions in mammals.The objective of this study was to examine the effect of acetamiprid on the reproductive function of male mice,and to study the role of oxidative stress in acetamiprid-induced damage to the testes.Fifty adult Kunmin male mice （25-30 g） were divided into five groups （n=10 per group）,i.e.,control,blank,acetamiprid alone,acetamiprid and vitamin E,and vitamin E alone.All groups were treated for 35 d.The results showed that acetamiprid significantly decreased the body weight and the weight of testosterone-responsive organs,such as the testis,epididymis,seminal vesicle,and prostate.Furthermore,acetamiprid also significantly reduced the serum testosterone concentration,and decreased sperm count,viability,motility,and the intactness of the acrosome （P〈0.05 for each parameter）.The mice treated with acetamiprid had damaged seminiferous tubules and Leydig cells based on the histological structure of testes;there was degeneration of the mitochondria and endoplasmic reticulum of Leydig cells.These deleterious effects of acetamiprid may be mediated by increasing oxidative stress,as acetamiprid increased malondialdehyde and nitric oxide in the testes,reduced the activity of catalase,glutathione peroxidase,superoxide dismutase,and activated p38.The concentration of acetamiprid in the testes was lower than that in liver,so did the concentrations of liver function tests,including aspartate transaminase （AST）,alanine transaminase （ALT） and alkaline phosphatase （ALP）,which suggest that male reproductive function may be affected through the indirect action of its metabolites.Vitamin E significantly ameliorated the effects of acetamiprid.We conclude that acetamiprid damages male reproductive function through inducing oxidative stress in the testes.
基金grants from the SciTechnical Development Project of Shaanxi Province, China （2005K15-G2） Traditional Chinese Project of Shaanxi Province, China （2005024） Natural Science Foundation of Xi＇ an Jiaotong University （573026）.
文摘Aim： To investigate the effect of formaldehyde （FA） on testes and the protective effect of vitamin E （VE） against oxidative damage by FA in the testes of adult rats. Methods： Thirty rats were randomly divided into three groups： （1） control; （2） FA treatment group （FAt）; and （3） FAt ＋ VE group. FAt and FAt ＋ VE groups were exposed to FA by inhalation at a concentration of 10 mg/m^3 for 2 weeks. In addition, FAt ＋ VE group were orally administered VE during the 2-week FA treatment. After the treatment, the histopathological and biochemical changes in testes, as well as the quantity and quality of sperm, were observed. Results： The testicular weight, the quantity and quality of sperm, the activities of superoxide dismutase （SOD）, glutathione peroxidase （GSH-Px） and glutathione （GSH） were significantly decreased whereas the level of malondialdehyde （MDA） was significantly increased in testes of rats in FAt group compared with those in the control group. VE treatment restored these parameters in FAt ＋ VE group. In addition, microscopy with hematoxylin-eosin （HE） staining showed that seminiferous tubules atrophied, seminiferous epithelial cells disintegrated and shed in rats in FAt group and VE treatment significantly improved the testicular structure in FAt ＋ VE group. Conclusion： FA destroys the testicular structure and function in adult rats by inducing oxidative stress, and this damage could be partially reversed by VE.
文摘Male reproductive health has deteriorated considerably in the last few decades. Nutritional, socioeconomic, lifestyle and environmental factors （among others） have been attributed to compromising male reproductive health. In recent years, a large volume of evidence has accumulated that suggests that the trend of decreasing male fertility （in terms of sperm count, quality and other changes in male reproductive health） might be due to exposure to environmental toxicants. These environmental contaminants can mimic natural oestrogens and target testicular spermatogenesis, steroidogenesis, and the function of both Sertoli and Leydig cells. Most environmental toxicants have been shown to induce reactive oxygen species, thereby causing a state of oxidative stress in various compartments of the testes. However, the molecular mechanism（s） of action of the environmental toxicants on the testis have yet to be elucidated. This review discusses the effects of some of the more commonly used environmental contaminants on testicular function through the induction of oxidative stress and apoptosis.
