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Xinru Wang - One of the best experts on this subject based on the ideXlab platform.
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Exposure to Fenvalerate causes brain impairment during zebrafish development.
Toxicology letters, 2010Co-Authors: Xiangguo Shi, Shoulin Wang, Chen Yuan, Yong Zhou, Yan Long, Ling Song, Xinru WangAbstract:Compared with increasing evidence suggesting that Fenvalerate is neurotoxic to adults, further information regarding developmental toxicity of this compound attracts more attention. In this study, we used zebrafish as an environmental monitoring model to further explore the potential toxicity of Fenvalerate. Our results demonstrated that larvae exposed to Fenvalerate for 24-96 h displayed obvious morphological abnormalities, and the LC50 concentrations were 131.95 microg/L (LC50-24h), 107.18 microg/L (LC50-48 h), 21.76 microg/L (LC50-72 h), and 6.25 microg/L (LC50-96 h). To further investigate the effects of Fenvalerate on embryos and larvae, acridine orange staining was performed at a 50 microg/L concentration. Staining showed notable signs of apoptosis mainly in the brain. Further studies revealed that Fenvalerate induced alterations in SOD activity in larvae were concentration dependent and also related to the length of exposure. Fenvalerate also down-regulated the expression of ogg1 and dlx2 genes in a concentration dependent manner, which indicated that the oxidative-DNA repair system as well as neurogenesis were impaired. In this study, we investigated the toxicity of Fenvalerate using zebrafish, that provided new evidence of observable brain impairment during embryogenesis due to Fenvalerate exposure and discussed their implications for the development of Fenvalerate induced neurotoxicity.
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Fenvalerate inhibits the growth of primary cultured rat preantral ovarian follicles
Toxicology, 2010Co-Authors: Juan Fei, Jianfeng Chen, Shoulin Wang, Ling Song, Yankai Xia, Xinliang Ding, Kai Xue, Xinru WangAbstract:Abstract Fenvalerate is a widely used synthetic pyrethroid insecticide and is reported to disrupt reproductive function in humans and animals. However, little is known about its influence on follicular development. In this study, rat preantral follicles were primary cultured to investigate the effects of Fenvalerate on follicular survival rate, morphological change, steroid hormone levels and steroidogenesis related gene mRNA expression. Follicles were cultured with 0, 1, 5 and 25 μmol/L Fenvalerate for 72 h. And then the morphous was assessed by conventional light microscopy, steroid hormones were measured by RIA, and the expressions of steroidogenic acute regulatory protein (StAR) and cytochrome P450 side-chain cleavage enzyme (P450scc) were monitored by real-time quantitative PCR analysis. Results showed that Fenvalerate inhibited the augmentation of follicular diameters but did not have detectable effects on follicular survival rates. The level of steroid hormones, such as progesterone, testosterone and estradiol, was inhibited. The inhibition might be due to the decreased expression levels of StAR and P450scc. These results suggested that Fenvalerate restrained the follicular growth, and inhibited steroidogenesis by reducing StAR and P450scc gene expression, which might further contribute to the Fenvalerate-induced reproductive dysfunction.
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effects of Fenvalerate and cypermethrin on rat sperm motility patterns in vitro as measured by computer assisted sperm analysis
Journal of Toxicology and Environmental Health, 2008Co-Authors: Ling Song, Chen Yuan, Xia Hong, Yubang Wang, Hong Sun, Jianwei Zhou, Xinru WangAbstract:Fenvalerate and cypermethrin were reported to impair male reproductive function, inducing significant reductions in epididymal sperm count. Further, Fenvalerate was shown to reduce sperm motility. However, it is not clear whether Fenvalerate and cypermethrin might impact sperm motility directly or indirectly by affecting spermatogenesis via interaction with androgens or their receptors. In this study, sperm suspensions were treated with Fenvalerate and cypermethrin, respectively, at various concentrations (0, 1, 4, 16, or 64 μmol/L) for various times (1, 2, or 4 h). The motility parameters of sperm treated with these two insecticides were analyzed with a computer-assisted sperm analysis (CASA) system. The differential effects of Fenvalerate and cypermethrin on rat sperm motility patterns in vitro were also compared. Our study revealed that Fenvalerate and cypermethrin reduced sperm motility in vitro in a concentration- and time-dependent manner. Cypermethrin exerted a greater effect on sperm motility in c...
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Fenvalerate inhibits progesterone production through cAMP-dependent signal pathway.
Toxicology letters, 2007Co-Authors: Xia Hong, Jianfeng Chen, Shoulin Wang, Ling Song, Yubang Wang, Hong Sun, Xinru WangAbstract:Fenvalerate is a widely used synthetic pyrethroid insecticide and is known to impede the male reproductive function. However, the mechanisms remain to be elucidated. In this study, mouse Leydig tumor cells (MLTC-1) were used to investigate the effects of Fenvalerate on progesterone production. Fenvalerate treatment inhibited progesterone secretion induced by human chorionic gonadotropin (hCG), cholera toxin (CT) or forskolin and decreased cAMP levels induced by hCG, but not by CT or forskolin, which suggested a repaired site on the upstream components of G protein or G protein per se by Fenvalerate in the cAMP-mediated signal pathway. Furthermore, the addition of cAMP analog, 8-Br-cAMP, could not reverse Fenvalerate-suppressed progesterone synthesis, indicating that Fenvalerate interfered with the downstream molecules of cAMP. In addition, Fenvalerate decreased steroidogenic acute regulatory protein (StAR) mRNA and protein levels, and also profoundly inhibited the activity of P450 side chain cleavage enzyme (P450scc) which was consistent with the decreased expression of P450scc mRNA and protein in MLTC-1 cells. These results suggested that Fenvalerate might inhibit progesterone production by attenuating cAMP generation and inhibiting StAR expression and P450scc activity.
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Fenvalerate-induced alterations in calcium homeostasis in rat ovary.
Biomedical and environmental sciences : BES, 2006Co-Authors: Jianfeng Chen, Ru Liu, Lin Song, Hebron C Chang, Xinru WangAbstract:Objective To observe the effects of Fenvalerate on calcium homeostasis in rat ovary. Methods Female SpragueDawley rats were orally given Fenvalerate at daily doses of 0.00, 1.91, 9.55, and 31.80 mg/kg for four weeks. The ovary ultrastucture was observed by electron microscopy. Serum free calcium concentration was measured by atomic absorption spectrophotometry. The activities of phosphorylase a in rat ovary were evaluated by the chromatometry. The total content of calmodulin in ovary was estimated by ELISA at each stage of estrous cycle. Radioimmunoassay (RIA) was used to evaluate the level of serum progesterone. Results Histopathologically, damages of ovarian corpus luteum cells were observed. An increase in serum free calcium concentration was observed in rats treated with 31.80mg/kg Fenvalerate. The activities of phosphorylase a enhanced in all treated groups, and Fenvalerate increased the total content of calmodulin significantly in estrus period. Serum progesterone levels declined in Fenvalerate exposed rats in diestrus. Conclusion Fenvalerate interferes with calcium homeostasis in rat ovary. Also, the inhibitory effects of Fenvalerate on serum progesterone levels may be mediated partly through calcium signals.
Ping Liu - One of the best experts on this subject based on the ideXlab platform.
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gender specific impairments on cognitive and behavioral development in mice exposed to Fenvalerate during puberty
Toxicology Letters, 2011Co-Authors: Xiu Hong Meng, Hua Wang, Xian-feng Zhao, Ping Liu, Guihai ChenAbstract:In human and rodent models, endocrine disrupting chemicals (EDCs) interfere with the development of cognition and behaviors. Fenvalerate is a potential EDC. The purpose of this study was to examine whether pubertal Fenvalerate exposure altered behavioral development. Mice were orally administered with either vehicle or Fenvalerate (7.5 or 30 mg/kg/day) from postnatal day (PND) 28 to PND56. Learning and memory were assessed by Morris Water Maze. Aggressive performance was evaluated by aggressive behavior test. Anxiety-related activities were detected by three tests: open-field, plus-maze and black-white alley. Sensorimotor function was analyzed using beam walking and tightrope. Results found that the impairment for spatial learning and memory was more severe in Fenvalerate-exposed female mice than in male mice. In addition, pubertal Fenvalerate exposure inhibited aggressive behavior in males. Moreover, pubertal Fenvalerate exposure increased anxiety activities in females. Altogether, these results suggest that pubertal Fenvalerate exposure impairs spatial cognition and behavioral development in a gender-dependent manner. These findings identify Fenvalerate as candidate environmental risk factors for cognitive and behavioral development, especially in the critical period of development.
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effects of pubertal Fenvalerate exposure on testosterone and estradiol synthesis and the expression of androgen and estrogen receptors in the developing brain
Toxicology Letters, 2011Co-Authors: Ping Liu, Hua Wang, Yuan Hua Chen, Xiu Hong Meng, Xian-feng Zhao, Mei Zhao, Cheng ZhangAbstract:Fenvalerate is a potential endocrine disruptor. Several studies have demonstrated that Fenvalerate dis- rupts testosterone (T) synthesis in testes. T and estradiol (E2) are de novo synthesized in the developing brain. Thus, the aim of the present study was to investigate the effects of pubertal Fenvalerate exposure on the synthesis of T and E2 and the expression of androgen receptor (AR) and estrogen receptors (ERs) in cerebral cortex. CD-1 mice were orally administered daily with either vehicle or Fenvalerate (7.5 or 30 mg/kg) from postnatal day (PND) 28 to PND56. The level of T and E2 in cerebral cortex was signifi- cantly decreased in males exposed to Fenvalerate. In agreement with the decrease in T and E2 syntheses, the expression of 17-HSD, a key enzyme for T synthesis, was significantly reduced in cerebral cortex of Fenvalerate-exposed males. Conversely, in females, the expression of 17-HSD in cerebral cortex was mildly up-regulated by Fenvalerate and the level of T and E2 was mildly increased. Pubertal Fenvalerate exposure had no effect on the expression of StAR, P45017 and P450scc, the key enzymes for T synthesis, and P450 aromatase, the key enzyme for E2 synthesis, in cerebral cortex of males and females. Inter- estingly, the expression of AR in cerebral cortex was up-regulated in male and female mice exposed to Fenvalerate, whereas pubertal Fenvalerate exposure did not affect the level of ER and ER in cerebral cortex. Taken together, these results suggest that pubertal Fenvalerate exposure disrupts T and E2 syn- thesis and the expression of AR in cerebral cortex. These changes of steroid status in the developing brain might be deleterious for neurobehavioral development.
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Fenvalerate induces germ cell apoptosis in mouse testes through the fas fasl signaling pathway
Archives of Toxicology, 2011Co-Authors: Xian-feng Zhao, Hua Wang, Cheng Zhang, Qun Wang, Ping Liu, Ying ZhangAbstract:Fenvalerate has a potentially adverse effect on male reproduction and spermatogenesis, whereas the precise mechanism remains obscure. The present study investigated the effects of Fenvalerate on germ cell apoptosis in testes. Adult male mice were administered with Fenvalerate (15 or 60 mg/kg) by gavage for 28 days. Germ cell apoptosis was determined by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL). The number of TUNEL+ germ cells per tubule and the percentage of tubules with TUNEL+ germ cells were significantly increased in testes of mice treated with Fenvalerate in a dose-dependent manner. TUNEL+ germ cells were observed mainly in stages VII–VIII and also stages IX–XII seminiferous tubules in testes. Additional experiments showed that Fenvalerate increased the level of active caspase-8 and caspase-3 in testes. In addition, Fenvalerate upregulated the expression of Fas and FasL in testes. No significant difference on the expression of Bcl-2 and Bax in testes was observed between Fenvalerate-treated mice and controls. Fenvalerate did not affect the leakage of cytochrome c from mitochondria into cytoplasm. In addition, Fenvalerate did not cause the activation of caspase-9 in testes. Taken together, these results suggest that Fenvalerate induces germ cell apoptosis in testes through the Fas/FasL signaling pathway.
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maternal Fenvalerate exposure during pregnancy persistently impairs testicular development and spermatogenesis in male offspring
Food and Chemical Toxicology, 2010Co-Authors: Heng Zhang, Hua Wang, Cheng Zhang, Qun Wang, Xian-feng Zhao, Huan Ning, Ying Zhang, Ping LiuAbstract:Abstract Fenvalerate, a widely used pyrethroid insecticide, has been associated with poor semen quality. As yet, little is known about the effects of prenatal Fenvalerate exposure on testicular development. The present study investigated the effects of prenatal Fenvalerate exposure on testicular development and spermatogenesis. The pregnant mice were administered Fenvalerate (30 mg/kg) by gavage daily from gestational day (gd) 13 to gd 18. The weights of testes and epididymides were significantly decreased in mice whose mothers were exposed to Fenvalerate during pregnancy. Importantly, maternal Fenvalerate exposure during pregnancy markedly decreased the number of mature seminiferous tubules (stages VII and VIII) in testes of adult male offspring. In addition, maternal Fenvalerate exposure during pregnancy significantly reduced the number of epididymal spermatozoa in adult male offspring. Additional experiments showed that the level of serum testosterone (T) was significantly decreased in male fetuses whose mothers were exposed to Fenvalerate during pregnancy. Correspondingly, mRNA and protein levels of P450 17α , a T synthetic enzyme, were significantly decreased in fetal testes. Moreover, the disruptive effect of prenatal Fenvalerate exposure on testicular T synthesis was irreversible. In conclusion, prenatal Fenvalerate exposure irreversibly impairs testicular development and spermatogenesis at least into early adulthood.
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Pubertal and early adult exposure to Fenvalerate disrupts steroidogenesis and spermatogenesis in mice at adulthood.
Journal of applied toxicology : JAT, 2010Co-Authors: Heng Zhang, Hua Wang, Cheng Zhang, Qun Wang, Xian-feng Zhao, Ping Liu, Huan Ning, Ying ZhangAbstract:Fenvalerate, a pyrethroid insecticide used worldwide, has been shown to have a potentially adverse effect on male reproduction. Our earlier study showed that maternal Fenvalerate exposure during lactation impaired testicular development in male offspring. In this study, we investigated the effects of pubertal and early adult exposure to Fenvalerate on steroidogenesis and spermatogenesis in mice. Male mice were administered Fenvalerate (60 mg/kg) by gavage daily from postnatal day 35 (PND35) to PND63. Results showed that sperm count was significantly decreased in Fenvalerate-treated mice. In addition, Fenvalerate markedly decreased the layers of spermatogenic cells, disturbed the array of spermatogenic cells and increased the number of apoptotic cells in testes. The adverse effects of Fenvalerate on male reproduction seemed to be associated with a decrease in serum and testicular testosterone (T). Although pubertal and early adult exposure to Fenvalerate had little effect on the number of Leydig cells in testes, mRNA and protein levels of testicular T biosynthetic enzymes including P45017α and P450scc were significantly downregulated in Fenvalerate-treated mice. In conclusion, pubertal and early adult Fenvalerate exposure induces a deleterious effect on steroidogenesis and spermatogenesis in adulthood. The decreased testicular T synthesis partially contributes to Fenvalerate-induced impairment on spermatogenesis. Copyright © 2010 John Wiley & Sons, Ltd.
Ying Zhang - One of the best experts on this subject based on the ideXlab platform.
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Fenvalerate induces germ cell apoptosis in mouse testes through the fas fasl signaling pathway
Archives of Toxicology, 2011Co-Authors: Xian-feng Zhao, Hua Wang, Cheng Zhang, Qun Wang, Ping Liu, Ying ZhangAbstract:Fenvalerate has a potentially adverse effect on male reproduction and spermatogenesis, whereas the precise mechanism remains obscure. The present study investigated the effects of Fenvalerate on germ cell apoptosis in testes. Adult male mice were administered with Fenvalerate (15 or 60 mg/kg) by gavage for 28 days. Germ cell apoptosis was determined by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL). The number of TUNEL+ germ cells per tubule and the percentage of tubules with TUNEL+ germ cells were significantly increased in testes of mice treated with Fenvalerate in a dose-dependent manner. TUNEL+ germ cells were observed mainly in stages VII–VIII and also stages IX–XII seminiferous tubules in testes. Additional experiments showed that Fenvalerate increased the level of active caspase-8 and caspase-3 in testes. In addition, Fenvalerate upregulated the expression of Fas and FasL in testes. No significant difference on the expression of Bcl-2 and Bax in testes was observed between Fenvalerate-treated mice and controls. Fenvalerate did not affect the leakage of cytochrome c from mitochondria into cytoplasm. In addition, Fenvalerate did not cause the activation of caspase-9 in testes. Taken together, these results suggest that Fenvalerate induces germ cell apoptosis in testes through the Fas/FasL signaling pathway.
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maternal Fenvalerate exposure during pregnancy persistently impairs testicular development and spermatogenesis in male offspring
Food and Chemical Toxicology, 2010Co-Authors: Heng Zhang, Hua Wang, Cheng Zhang, Qun Wang, Xian-feng Zhao, Huan Ning, Ying Zhang, Ping LiuAbstract:Abstract Fenvalerate, a widely used pyrethroid insecticide, has been associated with poor semen quality. As yet, little is known about the effects of prenatal Fenvalerate exposure on testicular development. The present study investigated the effects of prenatal Fenvalerate exposure on testicular development and spermatogenesis. The pregnant mice were administered Fenvalerate (30 mg/kg) by gavage daily from gestational day (gd) 13 to gd 18. The weights of testes and epididymides were significantly decreased in mice whose mothers were exposed to Fenvalerate during pregnancy. Importantly, maternal Fenvalerate exposure during pregnancy markedly decreased the number of mature seminiferous tubules (stages VII and VIII) in testes of adult male offspring. In addition, maternal Fenvalerate exposure during pregnancy significantly reduced the number of epididymal spermatozoa in adult male offspring. Additional experiments showed that the level of serum testosterone (T) was significantly decreased in male fetuses whose mothers were exposed to Fenvalerate during pregnancy. Correspondingly, mRNA and protein levels of P450 17α , a T synthetic enzyme, were significantly decreased in fetal testes. Moreover, the disruptive effect of prenatal Fenvalerate exposure on testicular T synthesis was irreversible. In conclusion, prenatal Fenvalerate exposure irreversibly impairs testicular development and spermatogenesis at least into early adulthood.
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Pubertal and early adult exposure to Fenvalerate disrupts steroidogenesis and spermatogenesis in mice at adulthood.
Journal of applied toxicology : JAT, 2010Co-Authors: Heng Zhang, Hua Wang, Cheng Zhang, Qun Wang, Xian-feng Zhao, Ping Liu, Huan Ning, Ying ZhangAbstract:Fenvalerate, a pyrethroid insecticide used worldwide, has been shown to have a potentially adverse effect on male reproduction. Our earlier study showed that maternal Fenvalerate exposure during lactation impaired testicular development in male offspring. In this study, we investigated the effects of pubertal and early adult exposure to Fenvalerate on steroidogenesis and spermatogenesis in mice. Male mice were administered Fenvalerate (60 mg/kg) by gavage daily from postnatal day 35 (PND35) to PND63. Results showed that sperm count was significantly decreased in Fenvalerate-treated mice. In addition, Fenvalerate markedly decreased the layers of spermatogenic cells, disturbed the array of spermatogenic cells and increased the number of apoptotic cells in testes. The adverse effects of Fenvalerate on male reproduction seemed to be associated with a decrease in serum and testicular testosterone (T). Although pubertal and early adult exposure to Fenvalerate had little effect on the number of Leydig cells in testes, mRNA and protein levels of testicular T biosynthetic enzymes including P45017α and P450scc were significantly downregulated in Fenvalerate-treated mice. In conclusion, pubertal and early adult Fenvalerate exposure induces a deleterious effect on steroidogenesis and spermatogenesis in adulthood. The decreased testicular T synthesis partially contributes to Fenvalerate-induced impairment on spermatogenesis. Copyright © 2010 John Wiley & Sons, Ltd.
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Lactational Fenvalerate exposure permanently impairs testicular development and spermatogenesis in mice
Toxicology letters, 2009Co-Authors: Heng Zhang, Hua Wang, Cheng Zhang, Qun Wang, Xian-feng Zhao, Huan Ning, Ying Zhang, Ping LiuAbstract:Fenvalerate, a widely used synthetic pyrethroid insecticide, has been associated with poor semen quality in human being. However, little is known about the effects of lactational Fenvalerate exposure on testicular development and spermatogenesis. The purpose of the present study was to investigate the effects of maternal Fenvalerate exposure during lactation on testicular development and spermatogenesis in male offspring. Maternal mice were administered with Fenvalerate (60 mg/kg) by gavage daily from postnatal day (PND) 0 to PND21. Lactational Fenvalerate exposure markedly decreased the absolute and relative weights of testes and increased the number of apoptotic cells in testes of pups at weaning. Histological examinations showed abnormal seminiferous tubules with large vacuoles or complete spermatogenic failure in testes of Fenvalerate-treated mice at weaning. Additional experiment showed that lactational Fenvalerate exposure markedly reduced mRNA and protein levels of testicular P450scc, a testosterone (T) synthesis enzyme. Consistent with down-regulation of testicular P450scc, the level of serum and testicular T at weaning was significantly decreased in pups whose mothers were exposed to Fenvalerate during lactation. Although the expression of testicular P450scc and serum and testicular T in adulthood restored to control level, the decreased weight of testes and histological changes were irreversible. Importantly, the percentage of mature seminiferous tubules (stages VII and VIII) and the number of spermatozoa were obviously decreased in adult male mice whose mothers were exposed to Fenvalerate during lactation. Taken together, these results suggest that lactational Fenvalerate exposure permanently impairs testicular development and spermatogenesis.
Hua Wang - One of the best experts on this subject based on the ideXlab platform.
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maternal Fenvalerate exposure induces fetal intrauterine growth restriction through disrupting placental thyroid hormone receptor signaling
Toxicological Sciences, 2017Co-Authors: Bo Wang, Ji Jie Liu, Yan Wang, Ru Shen, Hua Wang, Yuan Hua Chen, Cheng Zhang, Xiu Hong MengAbstract:Fenvalerate is an environmental endocrine disruptor that disrupts testosterone and estradiol synthesis. Nevertheless, whether Fenvalerate disturbs placental TR signaling remains unclear. The aim of this study was to investigate whether maternal Fenvalerate exposure causes fetal intrauterine growth restriction (IUGR) and to explore the role of placental thyroid hormone receptor (TR) signaling. Pregnant mice except controls were orally administered to Fenvalerate (0.2, 2.0, or 20 mg/kg) daily throughout pregnancy. As expected, fetal weight was lowered in dams that were administered with 20.0 mg/kg of Fenvalerate. Moreover, the rate of IUGR was elevated not only in male fetuses but also in female fetuses of dams exposed to 20.0 mg/kg of Fenvalerate. Histopathology showed that the internal space of blood vessels in the labyrinth layer was smaller in placentas of mice exposed to Fenvalerate. Mechanistic study found no significant difference on TT4 level in maternal serum, although TT3 level in maternal serum was slightly reduced in dams exposed to 2.0 mg/kg of Fenvalerate. Interestingly, placental TRα1 and TRβ1 mRNAs were reduced in mice exposed to Fenvalerate. Moreover, nuclear translocation of placental TRβ1 was suppressed in Fenvalerate-exposed mice. Further analysis showed that placental Vegfα and Igf2, several target genes of TR signaling, were down-regulated in Fenvalerate-exposed mice. In addition, mRNA level of placental CD36, Snat1, and Snat2, 3 nutrient transporters, were reduced in Fenvalerate-exposed mice. These results suggest that maternal Fenvalerate exposure induces fetal IUGR through disrupting placental TR signaling. These results provide a novel mechanistic explanation for Fenvalerate-induced fetal IUGR.
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gender specific impairments on cognitive and behavioral development in mice exposed to Fenvalerate during puberty
Toxicology Letters, 2011Co-Authors: Xiu Hong Meng, Hua Wang, Xian-feng Zhao, Ping Liu, Guihai ChenAbstract:In human and rodent models, endocrine disrupting chemicals (EDCs) interfere with the development of cognition and behaviors. Fenvalerate is a potential EDC. The purpose of this study was to examine whether pubertal Fenvalerate exposure altered behavioral development. Mice were orally administered with either vehicle or Fenvalerate (7.5 or 30 mg/kg/day) from postnatal day (PND) 28 to PND56. Learning and memory were assessed by Morris Water Maze. Aggressive performance was evaluated by aggressive behavior test. Anxiety-related activities were detected by three tests: open-field, plus-maze and black-white alley. Sensorimotor function was analyzed using beam walking and tightrope. Results found that the impairment for spatial learning and memory was more severe in Fenvalerate-exposed female mice than in male mice. In addition, pubertal Fenvalerate exposure inhibited aggressive behavior in males. Moreover, pubertal Fenvalerate exposure increased anxiety activities in females. Altogether, these results suggest that pubertal Fenvalerate exposure impairs spatial cognition and behavioral development in a gender-dependent manner. These findings identify Fenvalerate as candidate environmental risk factors for cognitive and behavioral development, especially in the critical period of development.
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effects of pubertal Fenvalerate exposure on testosterone and estradiol synthesis and the expression of androgen and estrogen receptors in the developing brain
Toxicology Letters, 2011Co-Authors: Ping Liu, Hua Wang, Yuan Hua Chen, Xiu Hong Meng, Xian-feng Zhao, Mei Zhao, Cheng ZhangAbstract:Fenvalerate is a potential endocrine disruptor. Several studies have demonstrated that Fenvalerate dis- rupts testosterone (T) synthesis in testes. T and estradiol (E2) are de novo synthesized in the developing brain. Thus, the aim of the present study was to investigate the effects of pubertal Fenvalerate exposure on the synthesis of T and E2 and the expression of androgen receptor (AR) and estrogen receptors (ERs) in cerebral cortex. CD-1 mice were orally administered daily with either vehicle or Fenvalerate (7.5 or 30 mg/kg) from postnatal day (PND) 28 to PND56. The level of T and E2 in cerebral cortex was signifi- cantly decreased in males exposed to Fenvalerate. In agreement with the decrease in T and E2 syntheses, the expression of 17-HSD, a key enzyme for T synthesis, was significantly reduced in cerebral cortex of Fenvalerate-exposed males. Conversely, in females, the expression of 17-HSD in cerebral cortex was mildly up-regulated by Fenvalerate and the level of T and E2 was mildly increased. Pubertal Fenvalerate exposure had no effect on the expression of StAR, P45017 and P450scc, the key enzymes for T synthesis, and P450 aromatase, the key enzyme for E2 synthesis, in cerebral cortex of males and females. Inter- estingly, the expression of AR in cerebral cortex was up-regulated in male and female mice exposed to Fenvalerate, whereas pubertal Fenvalerate exposure did not affect the level of ER and ER in cerebral cortex. Taken together, these results suggest that pubertal Fenvalerate exposure disrupts T and E2 syn- thesis and the expression of AR in cerebral cortex. These changes of steroid status in the developing brain might be deleterious for neurobehavioral development.
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Fenvalerate induces germ cell apoptosis in mouse testes through the fas fasl signaling pathway
Archives of Toxicology, 2011Co-Authors: Xian-feng Zhao, Hua Wang, Cheng Zhang, Qun Wang, Ping Liu, Ying ZhangAbstract:Fenvalerate has a potentially adverse effect on male reproduction and spermatogenesis, whereas the precise mechanism remains obscure. The present study investigated the effects of Fenvalerate on germ cell apoptosis in testes. Adult male mice were administered with Fenvalerate (15 or 60 mg/kg) by gavage for 28 days. Germ cell apoptosis was determined by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL). The number of TUNEL+ germ cells per tubule and the percentage of tubules with TUNEL+ germ cells were significantly increased in testes of mice treated with Fenvalerate in a dose-dependent manner. TUNEL+ germ cells were observed mainly in stages VII–VIII and also stages IX–XII seminiferous tubules in testes. Additional experiments showed that Fenvalerate increased the level of active caspase-8 and caspase-3 in testes. In addition, Fenvalerate upregulated the expression of Fas and FasL in testes. No significant difference on the expression of Bcl-2 and Bax in testes was observed between Fenvalerate-treated mice and controls. Fenvalerate did not affect the leakage of cytochrome c from mitochondria into cytoplasm. In addition, Fenvalerate did not cause the activation of caspase-9 in testes. Taken together, these results suggest that Fenvalerate induces germ cell apoptosis in testes through the Fas/FasL signaling pathway.
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maternal Fenvalerate exposure during pregnancy persistently impairs testicular development and spermatogenesis in male offspring
Food and Chemical Toxicology, 2010Co-Authors: Heng Zhang, Hua Wang, Cheng Zhang, Qun Wang, Xian-feng Zhao, Huan Ning, Ying Zhang, Ping LiuAbstract:Abstract Fenvalerate, a widely used pyrethroid insecticide, has been associated with poor semen quality. As yet, little is known about the effects of prenatal Fenvalerate exposure on testicular development. The present study investigated the effects of prenatal Fenvalerate exposure on testicular development and spermatogenesis. The pregnant mice were administered Fenvalerate (30 mg/kg) by gavage daily from gestational day (gd) 13 to gd 18. The weights of testes and epididymides were significantly decreased in mice whose mothers were exposed to Fenvalerate during pregnancy. Importantly, maternal Fenvalerate exposure during pregnancy markedly decreased the number of mature seminiferous tubules (stages VII and VIII) in testes of adult male offspring. In addition, maternal Fenvalerate exposure during pregnancy significantly reduced the number of epididymal spermatozoa in adult male offspring. Additional experiments showed that the level of serum testosterone (T) was significantly decreased in male fetuses whose mothers were exposed to Fenvalerate during pregnancy. Correspondingly, mRNA and protein levels of P450 17α , a T synthetic enzyme, were significantly decreased in fetal testes. Moreover, the disruptive effect of prenatal Fenvalerate exposure on testicular T synthesis was irreversible. In conclusion, prenatal Fenvalerate exposure irreversibly impairs testicular development and spermatogenesis at least into early adulthood.
Cheng Zhang - One of the best experts on this subject based on the ideXlab platform.
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maternal Fenvalerate exposure induces fetal intrauterine growth restriction through disrupting placental thyroid hormone receptor signaling
Toxicological Sciences, 2017Co-Authors: Bo Wang, Ji Jie Liu, Yan Wang, Ru Shen, Hua Wang, Yuan Hua Chen, Cheng Zhang, Xiu Hong MengAbstract:Fenvalerate is an environmental endocrine disruptor that disrupts testosterone and estradiol synthesis. Nevertheless, whether Fenvalerate disturbs placental TR signaling remains unclear. The aim of this study was to investigate whether maternal Fenvalerate exposure causes fetal intrauterine growth restriction (IUGR) and to explore the role of placental thyroid hormone receptor (TR) signaling. Pregnant mice except controls were orally administered to Fenvalerate (0.2, 2.0, or 20 mg/kg) daily throughout pregnancy. As expected, fetal weight was lowered in dams that were administered with 20.0 mg/kg of Fenvalerate. Moreover, the rate of IUGR was elevated not only in male fetuses but also in female fetuses of dams exposed to 20.0 mg/kg of Fenvalerate. Histopathology showed that the internal space of blood vessels in the labyrinth layer was smaller in placentas of mice exposed to Fenvalerate. Mechanistic study found no significant difference on TT4 level in maternal serum, although TT3 level in maternal serum was slightly reduced in dams exposed to 2.0 mg/kg of Fenvalerate. Interestingly, placental TRα1 and TRβ1 mRNAs were reduced in mice exposed to Fenvalerate. Moreover, nuclear translocation of placental TRβ1 was suppressed in Fenvalerate-exposed mice. Further analysis showed that placental Vegfα and Igf2, several target genes of TR signaling, were down-regulated in Fenvalerate-exposed mice. In addition, mRNA level of placental CD36, Snat1, and Snat2, 3 nutrient transporters, were reduced in Fenvalerate-exposed mice. These results suggest that maternal Fenvalerate exposure induces fetal IUGR through disrupting placental TR signaling. These results provide a novel mechanistic explanation for Fenvalerate-induced fetal IUGR.
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effects of pubertal Fenvalerate exposure on testosterone and estradiol synthesis and the expression of androgen and estrogen receptors in the developing brain
Toxicology Letters, 2011Co-Authors: Ping Liu, Hua Wang, Yuan Hua Chen, Xiu Hong Meng, Xian-feng Zhao, Mei Zhao, Cheng ZhangAbstract:Fenvalerate is a potential endocrine disruptor. Several studies have demonstrated that Fenvalerate dis- rupts testosterone (T) synthesis in testes. T and estradiol (E2) are de novo synthesized in the developing brain. Thus, the aim of the present study was to investigate the effects of pubertal Fenvalerate exposure on the synthesis of T and E2 and the expression of androgen receptor (AR) and estrogen receptors (ERs) in cerebral cortex. CD-1 mice were orally administered daily with either vehicle or Fenvalerate (7.5 or 30 mg/kg) from postnatal day (PND) 28 to PND56. The level of T and E2 in cerebral cortex was signifi- cantly decreased in males exposed to Fenvalerate. In agreement with the decrease in T and E2 syntheses, the expression of 17-HSD, a key enzyme for T synthesis, was significantly reduced in cerebral cortex of Fenvalerate-exposed males. Conversely, in females, the expression of 17-HSD in cerebral cortex was mildly up-regulated by Fenvalerate and the level of T and E2 was mildly increased. Pubertal Fenvalerate exposure had no effect on the expression of StAR, P45017 and P450scc, the key enzymes for T synthesis, and P450 aromatase, the key enzyme for E2 synthesis, in cerebral cortex of males and females. Inter- estingly, the expression of AR in cerebral cortex was up-regulated in male and female mice exposed to Fenvalerate, whereas pubertal Fenvalerate exposure did not affect the level of ER and ER in cerebral cortex. Taken together, these results suggest that pubertal Fenvalerate exposure disrupts T and E2 syn- thesis and the expression of AR in cerebral cortex. These changes of steroid status in the developing brain might be deleterious for neurobehavioral development.
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Fenvalerate induces germ cell apoptosis in mouse testes through the fas fasl signaling pathway
Archives of Toxicology, 2011Co-Authors: Xian-feng Zhao, Hua Wang, Cheng Zhang, Qun Wang, Ping Liu, Ying ZhangAbstract:Fenvalerate has a potentially adverse effect on male reproduction and spermatogenesis, whereas the precise mechanism remains obscure. The present study investigated the effects of Fenvalerate on germ cell apoptosis in testes. Adult male mice were administered with Fenvalerate (15 or 60 mg/kg) by gavage for 28 days. Germ cell apoptosis was determined by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL). The number of TUNEL+ germ cells per tubule and the percentage of tubules with TUNEL+ germ cells were significantly increased in testes of mice treated with Fenvalerate in a dose-dependent manner. TUNEL+ germ cells were observed mainly in stages VII–VIII and also stages IX–XII seminiferous tubules in testes. Additional experiments showed that Fenvalerate increased the level of active caspase-8 and caspase-3 in testes. In addition, Fenvalerate upregulated the expression of Fas and FasL in testes. No significant difference on the expression of Bcl-2 and Bax in testes was observed between Fenvalerate-treated mice and controls. Fenvalerate did not affect the leakage of cytochrome c from mitochondria into cytoplasm. In addition, Fenvalerate did not cause the activation of caspase-9 in testes. Taken together, these results suggest that Fenvalerate induces germ cell apoptosis in testes through the Fas/FasL signaling pathway.
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maternal Fenvalerate exposure during pregnancy persistently impairs testicular development and spermatogenesis in male offspring
Food and Chemical Toxicology, 2010Co-Authors: Heng Zhang, Hua Wang, Cheng Zhang, Qun Wang, Xian-feng Zhao, Huan Ning, Ying Zhang, Ping LiuAbstract:Abstract Fenvalerate, a widely used pyrethroid insecticide, has been associated with poor semen quality. As yet, little is known about the effects of prenatal Fenvalerate exposure on testicular development. The present study investigated the effects of prenatal Fenvalerate exposure on testicular development and spermatogenesis. The pregnant mice were administered Fenvalerate (30 mg/kg) by gavage daily from gestational day (gd) 13 to gd 18. The weights of testes and epididymides were significantly decreased in mice whose mothers were exposed to Fenvalerate during pregnancy. Importantly, maternal Fenvalerate exposure during pregnancy markedly decreased the number of mature seminiferous tubules (stages VII and VIII) in testes of adult male offspring. In addition, maternal Fenvalerate exposure during pregnancy significantly reduced the number of epididymal spermatozoa in adult male offspring. Additional experiments showed that the level of serum testosterone (T) was significantly decreased in male fetuses whose mothers were exposed to Fenvalerate during pregnancy. Correspondingly, mRNA and protein levels of P450 17α , a T synthetic enzyme, were significantly decreased in fetal testes. Moreover, the disruptive effect of prenatal Fenvalerate exposure on testicular T synthesis was irreversible. In conclusion, prenatal Fenvalerate exposure irreversibly impairs testicular development and spermatogenesis at least into early adulthood.
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Pubertal and early adult exposure to Fenvalerate disrupts steroidogenesis and spermatogenesis in mice at adulthood.
Journal of applied toxicology : JAT, 2010Co-Authors: Heng Zhang, Hua Wang, Cheng Zhang, Qun Wang, Xian-feng Zhao, Ping Liu, Huan Ning, Ying ZhangAbstract:Fenvalerate, a pyrethroid insecticide used worldwide, has been shown to have a potentially adverse effect on male reproduction. Our earlier study showed that maternal Fenvalerate exposure during lactation impaired testicular development in male offspring. In this study, we investigated the effects of pubertal and early adult exposure to Fenvalerate on steroidogenesis and spermatogenesis in mice. Male mice were administered Fenvalerate (60 mg/kg) by gavage daily from postnatal day 35 (PND35) to PND63. Results showed that sperm count was significantly decreased in Fenvalerate-treated mice. In addition, Fenvalerate markedly decreased the layers of spermatogenic cells, disturbed the array of spermatogenic cells and increased the number of apoptotic cells in testes. The adverse effects of Fenvalerate on male reproduction seemed to be associated with a decrease in serum and testicular testosterone (T). Although pubertal and early adult exposure to Fenvalerate had little effect on the number of Leydig cells in testes, mRNA and protein levels of testicular T biosynthetic enzymes including P45017α and P450scc were significantly downregulated in Fenvalerate-treated mice. In conclusion, pubertal and early adult Fenvalerate exposure induces a deleterious effect on steroidogenesis and spermatogenesis in adulthood. The decreased testicular T synthesis partially contributes to Fenvalerate-induced impairment on spermatogenesis. Copyright © 2010 John Wiley & Sons, Ltd.