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Gonzalo Martinezrodriguez - One of the best experts on this subject based on the ideXlab platform.
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Testicular Development and plasma sex steroid levels in cultured male senegalese sole solea senegalensis kaup
General and Comparative Endocrinology, 2006Co-Authors: Angel Garcialopez, V Fernandezpasquier, E Couto, Adelino V M Canario, Carmen Sarasquete, Gonzalo MartinezrodriguezAbstract:Testicular Development and plasma levels of sex steroids (11-ketotestosterone (11-KT), testosterone (T) and 17,20beta-dihydroxy-4-pregnen-3-one (17,20beta-P)) were investigated for the first time in cultured male Senegalese sole Solea senegalensis. The germ cell dynamics and gonadosomatic index (IG) were monitored. Based on the relative abundance of the different types of germ cells present, the spermatogenetic cycle was divided into five stages: early (I; spermatogonia (SPG)), mid (II; SPG, spermatocytes (SPC) and spermatids (SPD)), and late spermatogenesis (III; SPC, SPD, and spermatozoa (SPZ)), functional maturation (IV; SPD and SPZ), and recovery (V; SPD, SPZ, and SPG). During summer, fish had stage I and V testes and the lowest values in plasma levels of sex steroids and IG. Testicular recrudescence seemed to begin in autumn, as denoted by the first increase in IG and in the levels of 11-KT and T, and the appearance of testes at stage II and III. During winter, the levels of 11-KT and T peaked and soon began to decrease, the IG slightly declined and the proportion of running males (RM) gradually increased. In spring, levels of 11-KT and T continued to decline, the IG slightly increased and the proportion of RM peaked concomitantly with the occurrence of stage IV testes. Plasma levels of 17,20beta-P did not change significantly throughout Testicular Development. Transformation of SPD into SPZ followed a group-synchronous fashion, a phenomenon which parallels asynchronous oocyte Development reported in females. This mechanism would be consistent with the observed small quantity of sperm that can be manually stripped at any one time and other aspects of S. senegalensis reproductive biology.
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Testicular Development and plasma sex steroid levels in cultured male senegalese sole solea senegalensis kaup
General and Comparative Endocrinology, 2006Co-Authors: Angel Garcialopez, V Fernandezpasquier, E Couto, Adelino V M Canario, Carmen Sarasquete, Gonzalo MartinezrodriguezAbstract:Abstract Testicular Development and plasma levels of sex steroids (11-ketotestosterone (11-KT), testosterone (T) and 17,20β-dihydroxy-4-pregnen-3-one (17,20β-P)) were investigated for the first time in cultured male Senegalese sole Solea senegalensis . The germ cell dynamics and gonadosomatic index ( I G ) were monitored. Based on the relative abundance of the different types of germ cells present, the spermatogenetic cycle was divided into five stages: early (I; spermatogonia (SPG)), mid (II; SPG, spermatocytes (SPC) and spermatids (SPD)), and late spermatogenesis (III; SPC, SPD, and spermatozoa (SPZ)), functional maturation (IV; SPD and SPZ), and recovery (V; SPD, SPZ, and SPG). During summer, fish had stage I and V testes and the lowest values in plasma levels of sex steroids and I G . Testicular recrudescence seemed to begin in autumn, as denoted by the first increase in I G and in the levels of 11-KT and T, and the appearance of testes at stage II and III. During winter, the levels of 11-KT and T peaked and soon began to decrease, the I G slightly declined and the proportion of running males (RM) gradually increased. In spring, levels of 11-KT and T continued to decline, the I G slightly increased and the proportion of RM peaked concomitantly with the occurrence of stage IV testes. Plasma levels of 17,20β-P did not change significantly throughout Testicular Development. Transformation of SPD into SPZ followed a group-synchronous fashion, a phenomenon which parallels asynchronous oocyte Development reported in females. This mechanism would be consistent with the observed small quantity of sperm that can be manually stripped at any one time and other aspects of S. senegalensis reproductive biology.
Hua Wang - One of the best experts on this subject based on the ideXlab platform.
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maternal lps exposure during pregnancy impairs Testicular Development steroidogenesis and spermatogenesis in male offspring
PLOS ONE, 2014Co-Authors: Hua Wang, Cheng Zhang, Lulu Yang, Biwei Wang, Yinyin Huang, Yuanhua ChenAbstract:Lipopolysaccharide (LPS) is associated with adverse Developmental outcomes including embryonic resorption, fetal death, congenital teratogenesis and fetal growth retardation. Here, we explored the effects of maternal LPS exposure during pregnancy on Testicular Development, steroidogenesis and spermatogenesis in male offspring. The pregnant mice were intraperitoneally injected with LPS (50 µg/kg) daily from gestational day (GD) 13 to GD 17. At fetal period, a significant decrease in body weight and abnormal Leydig cell aggregations were observed in males whose mothers were exposed to LPS during pregnancy. At postnatal day (PND) 26, anogenital distance (AGD), a sensitive index of altered androgen action, was markedly reduced in male pups whose mothers were exposed to LPS daily from GD13 to GD 17. At PND35, the weight of testes, prostates and seminal vesicles, and serum testosterone (T) level were significantly decreased in LPS-treated male pups. At adulthood, the number of sperm was significantly decreased in male offspring whose mothers were exposed to LPS on GD 13–17. Maternal LPS exposure during gestation obviously diminished the percent of seminiferous tubules in stages I–VI, increased the percent of seminiferous tubules in stages IX–XII, and caused massive sloughing of germ cells in seminiferous tubules in mouse testes. Moreover, maternal LPS exposure significantly reduced serum T level in male mice whose mothers were exposed to LPS challenge during pregnancy. Taken together, these results suggest that maternal LPS exposure during pregnancy disrupts T production. The decreased T synthesis might be associated with LPS-induced impairments for spermatogenesis in male offspring.
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maternal cypermethrin exposure during lactation impairs Testicular Development and spermatogenesis in male mouse offspring
Environmental Toxicology, 2011Co-Authors: Hua Wang, Cheng Zhang, Qun Wang, Xian-feng Zhao, Ping Liu, Huan Ning, Ying Zhang, Sufang Wang, Xiuhong MengAbstract:Within the last decade, numerous epidemiological studies have demonstrated that endocrine disruptors are a possible cause for a decline in semen quality. Cypermethrin is a widely used pyrethroid insecticide, but little is known about its potentially adverse effects on male reproduction. In the present study, we investigated the effects of maternal cypermethrin exposure during lactation on Testicular Development and spermatogenesis in male offspring. Maternal mice were administered with cypermethrin (25 mg/kg) by gavage daily from postnatal day 0 (PND0) to PND21. Results showed that the weight of testes at PND21 was significantly decreased in pups whose mothers were exposed to cypermethrin during lactation. Maternal cypermethrin exposure during lactation markedly decreased the layers of spermatogenic cells, increased the inside diameter of seminiferous tubules, and disturbed the array of spermatogenic cells in testes of pups at PND21. In addition, maternal cypermethrin exposure during lactation markedly reduced mRNA and protein levels of Testicular P450scc, a testosterone (T) synthetic enzyme. Correspondingly, the level of serum and Testicular T at weaning was significantly decreased in pups whose mothers were exposed to cypermethrin during lactation. Although the expression of Testicular T synthetic enzymes and serum and Testicular T in adulthood had restored to control level, the decreased Testicular weight and histological changes were irreversible. Importantly, the number of spermatozoa was significantly decreased in adult male offspring whose mothers were exposed to cypermethrin during lactation. In conclusion, maternal cypermethrin exposure during lactation permanently impairs Testicular Development and spermatogenesis in male offspring, whereas cypermethrin-induced endocrine disruption is reversible.
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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 cadmium exposure impairs Testicular Development and spermatogenesis via disrupting Testicular testosterone synthesis in adult mice
Reproductive Toxicology, 2010Co-Authors: Hua Wang, Cheng Zhang, Heng Zhang, Qun Wang, Xian-feng Zhao, Ping Liu, Xiuhong Meng, Ying ZhangAbstract:Abstract Cadmium (Cd) is a well-known Testicular toxicant. However, the effects of pubertal Cd exposure on Testicular Development and spermatogenesis remained to be elucidated. The present study investigated the effects of pubertal Cd exposure on Testicular Development and spermatogenesis. Male CD-1 mice were intraperitoneally injected with CdCl 2 (1 mg/kg) daily from postnatal day 35 (PND35) to PND70. As expected, pubertal Cd exposure significantly decreased the number of spermatozoa in epididymides. In addition, pubertal Cd exposure markedly reduced the weights of testes, epididymides and prostate and seminal vesicle in adult mice. A significant decrease in serum and Testicular testosterone (T) was observed in mice exposed to Cd during puberty. Moreover, pubertal Cd exposure markedly reduced mRNA and protein levels of Testicular StAR, P450scc, P450 17α and 17β-HSD. Taken together, these results suggest that the decreased Testicular T synthesis might partially contribute to pubertal Cd-induced impairment on Testicular Development and spermatogenesis in mice.
Angel Garcialopez - One of the best experts on this subject based on the ideXlab platform.
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Testicular Development and plasma sex steroid levels in cultured male senegalese sole solea senegalensis kaup
General and Comparative Endocrinology, 2006Co-Authors: Angel Garcialopez, V Fernandezpasquier, E Couto, Adelino V M Canario, Carmen Sarasquete, Gonzalo MartinezrodriguezAbstract:Testicular Development and plasma levels of sex steroids (11-ketotestosterone (11-KT), testosterone (T) and 17,20beta-dihydroxy-4-pregnen-3-one (17,20beta-P)) were investigated for the first time in cultured male Senegalese sole Solea senegalensis. The germ cell dynamics and gonadosomatic index (IG) were monitored. Based on the relative abundance of the different types of germ cells present, the spermatogenetic cycle was divided into five stages: early (I; spermatogonia (SPG)), mid (II; SPG, spermatocytes (SPC) and spermatids (SPD)), and late spermatogenesis (III; SPC, SPD, and spermatozoa (SPZ)), functional maturation (IV; SPD and SPZ), and recovery (V; SPD, SPZ, and SPG). During summer, fish had stage I and V testes and the lowest values in plasma levels of sex steroids and IG. Testicular recrudescence seemed to begin in autumn, as denoted by the first increase in IG and in the levels of 11-KT and T, and the appearance of testes at stage II and III. During winter, the levels of 11-KT and T peaked and soon began to decrease, the IG slightly declined and the proportion of running males (RM) gradually increased. In spring, levels of 11-KT and T continued to decline, the IG slightly increased and the proportion of RM peaked concomitantly with the occurrence of stage IV testes. Plasma levels of 17,20beta-P did not change significantly throughout Testicular Development. Transformation of SPD into SPZ followed a group-synchronous fashion, a phenomenon which parallels asynchronous oocyte Development reported in females. This mechanism would be consistent with the observed small quantity of sperm that can be manually stripped at any one time and other aspects of S. senegalensis reproductive biology.
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Testicular Development and plasma sex steroid levels in cultured male senegalese sole solea senegalensis kaup
General and Comparative Endocrinology, 2006Co-Authors: Angel Garcialopez, V Fernandezpasquier, E Couto, Adelino V M Canario, Carmen Sarasquete, Gonzalo MartinezrodriguezAbstract:Abstract Testicular Development and plasma levels of sex steroids (11-ketotestosterone (11-KT), testosterone (T) and 17,20β-dihydroxy-4-pregnen-3-one (17,20β-P)) were investigated for the first time in cultured male Senegalese sole Solea senegalensis . The germ cell dynamics and gonadosomatic index ( I G ) were monitored. Based on the relative abundance of the different types of germ cells present, the spermatogenetic cycle was divided into five stages: early (I; spermatogonia (SPG)), mid (II; SPG, spermatocytes (SPC) and spermatids (SPD)), and late spermatogenesis (III; SPC, SPD, and spermatozoa (SPZ)), functional maturation (IV; SPD and SPZ), and recovery (V; SPD, SPZ, and SPG). During summer, fish had stage I and V testes and the lowest values in plasma levels of sex steroids and I G . Testicular recrudescence seemed to begin in autumn, as denoted by the first increase in I G and in the levels of 11-KT and T, and the appearance of testes at stage II and III. During winter, the levels of 11-KT and T peaked and soon began to decrease, the I G slightly declined and the proportion of running males (RM) gradually increased. In spring, levels of 11-KT and T continued to decline, the I G slightly increased and the proportion of RM peaked concomitantly with the occurrence of stage IV testes. Plasma levels of 17,20β-P did not change significantly throughout Testicular Development. Transformation of SPD into SPZ followed a group-synchronous fashion, a phenomenon which parallels asynchronous oocyte Development reported in females. This mechanism would be consistent with the observed small quantity of sperm that can be manually stripped at any one time and other aspects of S. senegalensis reproductive biology.
Xiuhong Meng - One of the best experts on this subject based on the ideXlab platform.
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maternal cypermethrin exposure during lactation impairs Testicular Development and spermatogenesis in male mouse offspring
Environmental Toxicology, 2011Co-Authors: Hua Wang, Cheng Zhang, Qun Wang, Xian-feng Zhao, Ping Liu, Huan Ning, Ying Zhang, Sufang Wang, Xiuhong MengAbstract:Within the last decade, numerous epidemiological studies have demonstrated that endocrine disruptors are a possible cause for a decline in semen quality. Cypermethrin is a widely used pyrethroid insecticide, but little is known about its potentially adverse effects on male reproduction. In the present study, we investigated the effects of maternal cypermethrin exposure during lactation on Testicular Development and spermatogenesis in male offspring. Maternal mice were administered with cypermethrin (25 mg/kg) by gavage daily from postnatal day 0 (PND0) to PND21. Results showed that the weight of testes at PND21 was significantly decreased in pups whose mothers were exposed to cypermethrin during lactation. Maternal cypermethrin exposure during lactation markedly decreased the layers of spermatogenic cells, increased the inside diameter of seminiferous tubules, and disturbed the array of spermatogenic cells in testes of pups at PND21. In addition, maternal cypermethrin exposure during lactation markedly reduced mRNA and protein levels of Testicular P450scc, a testosterone (T) synthetic enzyme. Correspondingly, the level of serum and Testicular T at weaning was significantly decreased in pups whose mothers were exposed to cypermethrin during lactation. Although the expression of Testicular T synthetic enzymes and serum and Testicular T in adulthood had restored to control level, the decreased Testicular weight and histological changes were irreversible. Importantly, the number of spermatozoa was significantly decreased in adult male offspring whose mothers were exposed to cypermethrin during lactation. In conclusion, maternal cypermethrin exposure during lactation permanently impairs Testicular Development and spermatogenesis in male offspring, whereas cypermethrin-induced endocrine disruption is reversible.
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pubertal cadmium exposure impairs Testicular Development and spermatogenesis via disrupting Testicular testosterone synthesis in adult mice
Reproductive Toxicology, 2010Co-Authors: Hua Wang, Cheng Zhang, Heng Zhang, Qun Wang, Xian-feng Zhao, Ping Liu, Xiuhong Meng, Ying ZhangAbstract:Abstract Cadmium (Cd) is a well-known Testicular toxicant. However, the effects of pubertal Cd exposure on Testicular Development and spermatogenesis remained to be elucidated. The present study investigated the effects of pubertal Cd exposure on Testicular Development and spermatogenesis. Male CD-1 mice were intraperitoneally injected with CdCl 2 (1 mg/kg) daily from postnatal day 35 (PND35) to PND70. As expected, pubertal Cd exposure significantly decreased the number of spermatozoa in epididymides. In addition, pubertal Cd exposure markedly reduced the weights of testes, epididymides and prostate and seminal vesicle in adult mice. A significant decrease in serum and Testicular testosterone (T) was observed in mice exposed to Cd during puberty. Moreover, pubertal Cd exposure markedly reduced mRNA and protein levels of Testicular StAR, P450scc, P450 17α and 17β-HSD. Taken together, these results suggest that the decreased Testicular T synthesis might partially contribute to pubertal Cd-induced impairment on Testicular Development and spermatogenesis in mice.
Francis J P Ebling - One of the best experts on this subject based on the ideXlab platform.
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the hypogonadal hpg mouse as a model to investigate the estrogenic regulation of spermatogenesis
Human Fertility, 2006Co-Authors: Francis J P Ebling, Margaret O Nwagwu, Helen Baines, Michelle Myers, J B KerrAbstract:The hypogonadal (hpg) mouse is an excellent animal model in which to investigate the mechanism of action of estrogens on spermatogenesis because it has arrested reproductive Development without the need for surgical, endocrine, pharmacological or immunological intervention. Hpg mice are hypogonadotrophic and fail to show normal postnatal Testicular Development due to the congenital inability to synthesize gonadotropin-releasing hormone in the hypothalamus. The hpg testis remains responsive to gonadotropins and androgens in that fertility can be induced by treatment with these hormones. Surprisingly, chronic treatment with low concentrations of estradiol alone induces qualitatively normal spermatogenesis. The induction of Testicular Development by estradiol in hpg mice is accompanied by a paradoxical increase in FSH production. The actions of estradiol in hpg mice appear to be via genomic estrogen receptors, as concurrent treatment with estrogen-receptor antagonist ICI182,780 completely blocks these pituit...
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estrogenic induction of spermatogenesis in the hypogonadal hpg mouse role of androgens
Reproduction, 2005Co-Authors: Helen Baines, Margaret O Nwagwu, J B Kerr, Edwina Furneaux, Jane M Stewart, T M Mayhew, Francis J P EblingAbstract:Testicular Development is arrested in the hypogonadal (hpg) mouse due to a congenital deficiency of hypothalamic gonadotropin-releasing hormone synthesis. Previous studies have demonstrated that chronic treatment of these mice with estradiol induces Testicular maturation and qualitatively normal spermatogenesis, but it is not known whether these are direct effects via estrogen receptors expressed in the testis, or indirect actions via the pituitary gland. The aim of the current studies was to determine whether the actions of estradiol require the presence of androgens. Sensitive assays revealed that chronic estradiol treatment produced time-dependent increases in pituitary FSH production but no increases in pituitary LH or Testicular testosterone content could be detected. As a functional test of androgen dependence, hpg mice were treated for 70 days with estradiol plus Casodex (bicalutamide), an androgen receptor antagonist. Casodex treatment markedly attenuated both the estradiol-induced increase in Testicular weight and the proliferation of the seminiferous epithelium, as revealed by morphometric analysis. However, it did not affect the estradiol-induced increase in pituitary FSH content, nor did it affect estradiol-induced increases in the weight of the seminal vesicles and epididymides. We conclude that increased FSH production is not sufficient to explain the increase in Testicular Development induced by estradiol in hpg mice; there is a requirement for functional androgen receptors for induction of Testicular growth.
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manipulations of glutamatergic n methyl d aspartate receptor neurotransmission alter the rate of photoperiodically regulated sexual maturation in the male siberian hamster
Biology of Reproduction, 1998Co-Authors: Francis J P Ebling, Anna S CroninAbstract:: This study investigated whether central glutamatergic pathways are involved in sexual maturation in the Siberian hamster, a species in which puberty is regulated by photoperiod. The aim of the initial experiments was to determine whether exogenous activation of N-methyl-D-aspartate (NMDA) receptor-mediated glutamatergic pathways could induce premature Testicular Development in photoinhibited hamsters. Male hamsters raised in an inhibitory short-day photoperiod (8L:16D) received systemic injections of the glutamate agonist NMDA. Twice-daily treatment with 20 or 40 mg/kg BW caused significant increases in Testicular weight within 4 wk, but this was not accompanied by a significant increase in circulating testosterone. Subsequent experiments revealed that the degree of Testicular Development induced by NMDA was comparable to that induced by daily treatment with GnRH (1 microg). This study demonstrates the potential for increased glutamatergic activity to induce Testicular Development. The aim of the second series of experiments was to determine whether blockade of endogenous NMDA receptor-mediated glutamatergic pathways could prevent Testicular Development in photostimulated hamsters. Males were transferred from short (SD) to long days (LD; 16L:8D) at 80-100 days of age to induce rapid Testicular growth and were concurrently treated with MK801, a noncompetitive NMDA receptor antagonist (2 mg/kg BW per day), or CGP40116, a competitive NMDA receptor antagonist (5 or 10 mg/kg BW per day) for 4 wk. LD photoperiod caused a rapid increase in Testicular weight in vehicle-treated hamsters within 4 wk. Both antagonists significantly reduced the LD-stimulated Testicular growth. MK801 treatment induced a degree of sedation and a loss of body weight, suggesting that the reduced Testicular Development in this group may have been secondary to decreased growth rates; but no behavioral changes or loss of body weight was observed in the hamsters treated with CGP40116. These observations in a photoperiodic species provide support for the hypothesis that activation of NMDA receptor-mediated glutamatergic pathways contributes to sexual maturation.
