A dose-response analysis of the reproductive effects of a single gestational dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin in male Long Evans Hooded rat offspring.

@article{Gray1997ADA,
  title={A dose-response analysis of the reproductive effects of a single gestational dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin in male Long Evans Hooded rat offspring.},
  author={Leon Earl Gray and Joseph S. Ostby and William R. Kelce},
  journal={Toxicology and applied pharmacology},
  year={1997},
  volume={146 1},
  pages={
          11-20
        }
}
Male rats exposed in utero to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) display reduced fertility as a consequence of the direct action of TCDD on the epididymides, as well as delayed puberty and altered reproductive organ weights. The current study provides dose-response data for the reproductive effects of TCDD, administered during pregnancy, with an emphasis on the effects of TCDD on testicular, epididymal, and ejaculated sperm numbers. Long Evans Hooded rats were dosed by gavage with 0, 0… 
Maternal exposure to a low dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) suppressed the development of reproductive organs of male rats: dose-dependent increase of mRNA levels of 5alpha-reductase type 2 in contrast to decrease of androgen receptor in the pubertal ventral prostate.
TLDR
It is highly suggested that the decrease in the size of the ventral prostate by maternal TCDD exposure might be due to decreased responsiveness of the prostate to androgen due to an insufficient expression level of androgen receptor during puberty.
Reproductive toxicity and tissue concentrations of low doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin in male offspring rats exposed throughout pregnancy and lactation.
TLDR
The effects of low doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the reproductive system of male offspring rats were examined and the male rats of the TCDD groups showed an increased number of abnormal sperm when investigated at adulthood.
Perinatal exposure of female rats to 2,3,7,8-tetrachlorodibenzo-p-dioxin induces central precocious puberty in the offspring.
TLDR
It is indicated that perinatal exposure to a low dose of TCDD induces precocious puberty, including early maturation of the hypothalamic-pituitary axis, the gonads and genitals, in female Long-Evans hooded rats.
Developmental stage-specific effects of perinatal 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure on reproductive organs of male rat offspring.
TLDR
The results suggest the presence of a critical window during development with regard to impairments of male reproductive organs by in utero and lactational exposure to a low dose of TCDD.
Interpretation of studies on the developmental reproductive toxicology of 2,3,7,8-tetrachlorodibenzo-p-dioxin in male offspring.
  • D. Bell, S. Clode, S. White
  • Medicine
    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • 2010
In utero exposure to low doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin alters reproductive development of female Long Evans hooded rat offspring.
TLDR
Administration of TCDD at dosage levels of 0.2, 0.8, and 1.0 microg/kg produces morphological reproductive alterations in female rat offspring as a consequence of in utero exposure, and these effects did not appear to result from abnormal ovarian function during prepubertal development.
The effects of maternal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin on testicular steroidogenesis in infantile male rats.
TLDR
Findings in in utero TCDD-exposed foetal testis indicating that maternal TCDd exposure does not negatively influence the developmental testosterone production of foetals type Leydig cells in rats are confirmed.
Maternal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin and the body burden in offspring of long-evans rats
TLDR
Reduced prostate weight is a sensitive and commonly observed endpoint so that the body burdens of dams and fetuses at the LOAEL of this endpoint could be served as the basis for establishing TDI for dioxins.
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TLDR
It is concluded that the route and timing of TCDD exposure during fetal and neonatal development of the rat determine the profile of male reproductive effects observed and that all effects in the present study, with the notable exception of feminized sexual behavior, can be caused by low level exposure to T CDD via the IU route alone.
Effects of in utero and lactational 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure on responsiveness of the male rat reproductive system to testosterone stimulation in adulthood.
TLDR
In utero and lactational TCDD exposure inhibits imprinting of ventral prostate weight and protein but does not result in a universal inhibition of imprinting, which provides a model to study the mechanism by which exposure to T CDD during fetal and early postnatal development modulates hormone-mediated responses in adulthood.
In utero 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) alters reproductive morphology and function in female rat offspring.
TLDR
In the LE rat, vaginal and behavioral estrous cyclicity, estrous cycle-mediated running wheel activity, and female sexual behaviors at proestrus were not affected by gestational GD 15 TCDD treatment, but untreated stud males had difficulty attaining intromission and took longer to ejaculate.
In utero and lactational exposure of the male Holtzman rat to 2,3,7,8-tetrachlorodibenzo-p-dioxin: decreased epididymal and ejaculated sperm numbers without alterations in sperm transit rate.
TLDR
The decreases in sperm number in the distal excurrent duct system were greater than the decrease in DSP, consistent with the hypothesis that TCDD exposure causes an effect other than decreased DSP that reduced epididymal and ejaculated sperm numbers.
Exposure to TCDD during development permanently alters reproductive function in male Long Evans rats and hamsters: reduced ejaculated and epididymal sperm numbers and sex accessory gland weights in offspring with normal androgenic status.
TLDR
Since T and AR levels appeared normal in the sex accessory glands and the epididymis following perinatal TCDD exposure, the alterations in these tissues are not likely to have resulted from an alteration of the androgenic status of the male offspring.
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