This study was conducted to evaluate the potential reproductive toxicity of epichlorohydrin in a one-generation reproduction toxicity study. The test chemical was administered daily by gavage at 0, 3.3, 10, and 30 mg/kg/day. Males were dosed for 10 weeks prior to mating and during mating. Females we...
This study was conducted to evaluate the potential reproductive toxicity of epichlorohydrin in a one-generation reproduction toxicity study. The test chemical was administered daily by gavage at 0, 3.3, 10, and 30 mg/kg/day. Males were dosed for 10 weeks prior to mating and during mating. Females were dosed from 2 weeks before mating to day 21 of lactation. At 30 mg/kg, an increase in the incidence of clinical signs; gross findings in epididymidis and kidney; and the weights of heart, liver and epididymidis a decrease in the male fertility; and an increased incidence of histopathological changes of the testis, epididymidis and kidney were observed. At 10 mg/kg, decreased male fertility and increased kidney weight and incidence of histopathological changes of the epididymidis were found. No treatment-related effects were observed at 3.3 mg/kg. Under these experimental conditions, the no-observed-adverse-effect level of epichlorohydrin was 3.3 mg/kg/day for parent animals and their offspring.This study was designed to investigate the potential effects of epichlorohydrin (ECH) on rat spermatogenesis. Oxidative stress was also assessed in epididymal tissue to determine a possible mechanism for the reproductive dysfunction. Male rats aged 6 weeks were administered ECH daily by gavage at 0, 3.3, 10, and 30 mg/kg/day for 10 weeks and sacrificed 24h after the last administration of ECH. Spermatotoxicity was assessed through reproductive organ weights, sperm analysis, histopathology, and oxidative stress in the epididymis. At 30 mg/kg, there was an increase in the incidence of clinical signs, gross pathology findings in the epididymidis, and sperm abnormalities and a decrease in the testicular spermatid counts, epididymal sperm counts, and sperm motility. Increases in the incidence of histopathological changes of the epididymidis were also observed. In addition, an increased malondialdehyde (MDA) concentration and decreased glutathione (GSH), catalase, superoxide dismutase (SOD), and glutathione-S-transferase (GST) were observed in the epididymal tissues. At 10 mg/kg, an increased MDA concentration and decreased GSH, catalase, SOD, and GST were observed in the epididymal tissues. Epididymal GSH content also decreased at 3.3 mg/kg/day. However, no treatment-related effects on body weight and reproductive organ weight were found at any dose tested. The results show that repeated oral administration of ECH to male rats at ≥ 10 mg/kg/day elicits spermatotoxicity and oxidative damage in the epididymis, and that the adverse effects of ECH on male reproductive function may be due to the induction of oxidative stress in the epididymis.
This study was conducted to evaluate the potential reproductive toxicity of epichlorohydrin in a one-generation reproduction toxicity study. The test chemical was administered daily by gavage at 0, 3.3, 10, and 30 mg/kg/day. Males were dosed for 10 weeks prior to mating and during mating. Females were dosed from 2 weeks before mating to day 21 of lactation. At 30 mg/kg, an increase in the incidence of clinical signs; gross findings in epididymidis and kidney; and the weights of heart, liver and epididymidis a decrease in the male fertility; and an increased incidence of histopathological changes of the testis, epididymidis and kidney were observed. At 10 mg/kg, decreased male fertility and increased kidney weight and incidence of histopathological changes of the epididymidis were found. No treatment-related effects were observed at 3.3 mg/kg. Under these experimental conditions, the no-observed-adverse-effect level of epichlorohydrin was 3.3 mg/kg/day for parent animals and their offspring.This study was designed to investigate the potential effects of epichlorohydrin (ECH) on rat spermatogenesis. Oxidative stress was also assessed in epididymal tissue to determine a possible mechanism for the reproductive dysfunction. Male rats aged 6 weeks were administered ECH daily by gavage at 0, 3.3, 10, and 30 mg/kg/day for 10 weeks and sacrificed 24h after the last administration of ECH. Spermatotoxicity was assessed through reproductive organ weights, sperm analysis, histopathology, and oxidative stress in the epididymis. At 30 mg/kg, there was an increase in the incidence of clinical signs, gross pathology findings in the epididymidis, and sperm abnormalities and a decrease in the testicular spermatid counts, epididymal sperm counts, and sperm motility. Increases in the incidence of histopathological changes of the epididymidis were also observed. In addition, an increased malondialdehyde (MDA) concentration and decreased glutathione (GSH), catalase, superoxide dismutase (SOD), and glutathione-S-transferase (GST) were observed in the epididymal tissues. At 10 mg/kg, an increased MDA concentration and decreased GSH, catalase, SOD, and GST were observed in the epididymal tissues. Epididymal GSH content also decreased at 3.3 mg/kg/day. However, no treatment-related effects on body weight and reproductive organ weight were found at any dose tested. The results show that repeated oral administration of ECH to male rats at ≥ 10 mg/kg/day elicits spermatotoxicity and oxidative damage in the epididymis, and that the adverse effects of ECH on male reproductive function may be due to the induction of oxidative stress in the epididymis.
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#Epichlorohydrin Repoductive Toxicity Toxic Mechanism Oxidative Stress Rats
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