Desfechos reprodutivos intergeracionais da exposição oral de ratas Wistar ao dimetanossulfonato de etano durante a prenhez e lactação
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Data
2021-05-31
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Universidade Estadual Paulista (Unesp)
Resumo
Hormônios esteroides são fundamentais para a diferenciação sexual, instalação da puberdade e manutenção da fertilidade em animais adultos. Em machos, a esteroidogênese se inicia no período fetal e auxilia no processo de masculinização. Em fêmeas, a esteroidogênese tem início apenas no período pós-natal. Um dos principais hormônios esteroides responsáveis por estes processos é a testosterona, produzida pelas células de Leydig em machos e pelas células da teca em fêmeas. Compostos que comprometem a concentração plasmática de testosterona têm influência direta sobre a fertilidade. O dimetanossulfonato de etano (EDS) é um agente citotóxico para as células de Leydig, causando sua destruição nos 3 dias subsequentes à administração de uma dose única de 75mg/kg de peso corpóreo via injeção intraperitoneal em ratos, com consequente queda da produção de testosterona. Neste trabalho, foram investigados os efeitos da exposição oral materna ao EDS durante a gestação e lactação de ratas Wistar, do dia gestacional (DG) 12 ao 21º dia pós-natal (DPN), sobre as matrizes (F0) e sobre o desenvolvimento e os parâmetros reprodutivos das proles F1 (masculina e feminina) e F2 (masculina). A geração F1 foi avaliada quanto a parâmetros de desenvolvimento físico, sensorial e sexual. Houve atraso na abertura de olhos de fêmeas F1 do grupo EDS. Tanto F0 quanto F1 do grupo EDS apresentaram ingestão de ração e peso corpóreo reduzidos em relação ao controle. Na prole masculina observou-se redução da distância anogenital, peso de testículo e epidídimo, produção espermática diária e redução na inseminação de fêmeas receptivas. Os machos foram acasalados com fêmeas sem tratamento e deram origem à F2. A F2 apresentou redução do peso absoluto do testículo apenas no DPN 21. Na prole feminina da F1, observou-se atraso na instalação da puberdade, redução do peso do útero (DPN 90) e diminuição da contribuição do endométrio para a altura total do epitélio uterino. Essas fêmeas foram acasaladas com machos sem tratamento e eutanasiadas no DG 20 para avaliação de parâmetros de fertilidade. Foi observada a redução do número de corpos lúteos e implantações e aumento no número de reabsorções. Em suma, o tratamento ocasionou redução de peso corpóreo e ingestão alimentar total em F0 e F1, redução do peso de órgãos do sistema genital na F1 masculina (testículo e epidídimo) e feminina (útero) e de parâmetros de fertilidade, bem como redução do peso testicular no início do desenvolvimento da F2. Conclui-se que a combinação das alterações intergeracionais causadas pela ingestão de EDS adicionado ao alimento sólido nas condições acima referidas, leva à redução da fertilidade em ratos, e apresenta um método novo e promissor para o controle populacional de animais sinantrópicos.
Steroid hormones are essential for sexual differentiation, puberty onset and maintenance of fertility in adult animals. In males, steroidogenesis begins in the fetal period and contributes to the masculinization process. In females, steroidogenesis starts only in the postnatal period. One of the main steroid hormones responsible for these processes is testosterone, produced by Leydig cells in males and by theca cells in females. Compounds that compromise testosterone plasmatic levels have a direct influence on fertility. Ethane dimethanesulfonate (EDS) is a cytotoxic agent for Leydig cells, causing its destruction in the 3 days following the administration of a single dose of 75mg / kg body weight via intraperitoneal injection in rats, with a consequent drop in testosterone production. In the present study we investigated the effects of maternal exposure to EDS during pregnancy and lactation of Wistar rats, from gestational day (GD) 12 to postnatal day (PND) 21, on the dams (F0) and on the development and reproductive parameters of the F1 and F2 offspring. F1 was evaluated for parameters of physical, sensorial, and sexual development. Eye opening was delayed on F1 females from EDS group. Both F0 and F1 of the EDS-treated group had reduced food intake and body weight compared to the control group. In the male offspring, there was a reduction in anogenital distance, testis and epididymis weight, daily sperm production and insemination rate. Males were mated with untreated females to obtain the second generation (F2). F2 had reduced absolute testis weight only on PND 21. In F1 female offspring, there was a delay in the onset of puberty, a reduction of the weight of the uterus (PND 90) and of the contribution of the endometrium to the total uterine epithelium height. These females were mated with untreated males and euthanized on GD 20 to assess fertility parameters. To summarize, the treatment caused a reduction in body weight and total food intake in F0 and F1, a reduction in the weight of organs of the genital system in male (testis and epididymis) and female (uterus) F1 and in fertility parameters, as well as reduced testicular weight at the beginning of F2 development. It was observed a reduction in the number of corpora lutea and implantation sites and an increase in the number of resorbed fetuses. We conclude that the combination of intergenerational alterations caused by EDS added to the solid food intake, in the specified conditions, leads to reduced fertility in rats, and presents a new and promising method for populational control of synanthropic animals.
Steroid hormones are essential for sexual differentiation, puberty onset and maintenance of fertility in adult animals. In males, steroidogenesis begins in the fetal period and contributes to the masculinization process. In females, steroidogenesis starts only in the postnatal period. One of the main steroid hormones responsible for these processes is testosterone, produced by Leydig cells in males and by theca cells in females. Compounds that compromise testosterone plasmatic levels have a direct influence on fertility. Ethane dimethanesulfonate (EDS) is a cytotoxic agent for Leydig cells, causing its destruction in the 3 days following the administration of a single dose of 75mg / kg body weight via intraperitoneal injection in rats, with a consequent drop in testosterone production. In the present study we investigated the effects of maternal exposure to EDS during pregnancy and lactation of Wistar rats, from gestational day (GD) 12 to postnatal day (PND) 21, on the dams (F0) and on the development and reproductive parameters of the F1 and F2 offspring. F1 was evaluated for parameters of physical, sensorial, and sexual development. Eye opening was delayed on F1 females from EDS group. Both F0 and F1 of the EDS-treated group had reduced food intake and body weight compared to the control group. In the male offspring, there was a reduction in anogenital distance, testis and epididymis weight, daily sperm production and insemination rate. Males were mated with untreated females to obtain the second generation (F2). F2 had reduced absolute testis weight only on PND 21. In F1 female offspring, there was a delay in the onset of puberty, a reduction of the weight of the uterus (PND 90) and of the contribution of the endometrium to the total uterine epithelium height. These females were mated with untreated males and euthanized on GD 20 to assess fertility parameters. To summarize, the treatment caused a reduction in body weight and total food intake in F0 and F1, a reduction in the weight of organs of the genital system in male (testis and epididymis) and female (uterus) F1 and in fertility parameters, as well as reduced testicular weight at the beginning of F2 development. It was observed a reduction in the number of corpora lutea and implantation sites and an increase in the number of resorbed fetuses. We conclude that the combination of intergenerational alterations caused by EDS added to the solid food intake, in the specified conditions, leads to reduced fertility in rats, and presents a new and promising method for populational control of synanthropic animals.
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Palavras-chave
Animais sinantrópicos, Controle populacional, Dimetanossulfonato de etano, Fertilidade, Rato