Exposure of Neonatal Female Rats to p-tert-Octylphenol Disrupts Afternoon Surges of Luteinizing Hormone, Follicle-Stimulating Hormone and Prolactin Secretion, and Interferes with Sexual Receptive Behavior in Adulthood1

@inproceedings{Herath2001ExposureON,
  title={Exposure of Neonatal Female Rats to p-tert-Octylphenol Disrupts Afternoon Surges of Luteinizing Hormone, Follicle-Stimulating Hormone and Prolactin Secretion, and Interferes with Sexual Receptive Behavior in Adulthood1},
  author={C. Herath and G. Watanabe and S. Katsuda and M. Yoshida and A. Suzuki and K. Taya},
  booktitle={Biology of reproduction},
  year={2001}
}
Abstract The present study investigated the effects of exposure of neonatal female rats to p-tert-octylphenol (OP) on estrogen-induced afternoon surges of LH, FSH, and prolactin (PRL) secretion, and on sexual behavior in adulthood. After birth, one group of female Wistar rat pups received s.c. injections of OP (100 mg/kg body weight [BW]; OP group) dissolved in DMSO, while the control group received DMSO only (DMSO group). In order to make a qualitative comparison, a third group was injected… Expand
Effect of maternal exposure to octylphenol (4-tert-octylphenol) on the growth of the adrenal gland in male albino rats
TLDR
There is increased in the average body weight and percentage of gain in body weight of male rats from mothers of small treatment and the control group for 12 weeks of age and histological results showed that the adrenal gland in the group which was given high dose of octylphenol show that Severe histological changes in the cortex. Expand
Neonatally administered tert-octylphenol affects onset of puberty and reproductive development in female rats
TLDR
Exposure to OP during the critical period of sexual brain differentiation affects the onset of puberty and reproductive development, and data suggest that exposure to OP after the early postnatal period is hazardous to the developing reproductive system and neuroendocrine brain. Expand
Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression.
TLDR
The results indicate that the effect of OP on the infantile ovary is reversible, while more permanent effects in the hypothalamus and pituitary are involved in the reduction of circulating FSH levels and premature vaginal opening. Expand
Exposure of neonatal female rats to bisphenol A disrupts hypothalamic LHRH pre-mRNA processing and estrogen receptor alpha expression in nuclei controlling estrous cyclicity.
TLDR
It is shown that BPA permanently disrupts hypothalamic LHRH pre-mRNA processing and steroid receptors expression in nuclei that control estrous cyclicity in adult rats. Expand
Adverse effects of environmental toxicants, octylphenol and bisphenol A, on male reproductive functions in pubertal rats
TLDR
It is demonstrated that OP and BPA can reduce sperm counts resulting from lowered plasma testosterone in male rats just after puberty, raising the possibility of a link between these chemicals and prostate diseases because IGF-I has been implicated in the pathogenesis of human prostate cancers. Expand
Neonatal exposure to bisphenol A alters estrogen-dependent mechanisms governing sexual behavior in the adult female rat.
TLDR
The results show that BPA permanently alters the hypothalamic estrogen-dependent mechanisms that govern sexual behavior in the adult female rat. Expand
In utero and lactational exposure to TCDD; steroidogenic outcomes differ in male and female rat pups.
TLDR
It is concluded that developing testis and male gonadotropin secretion are resistant to TCDD-induced toxicity, and reduced estradiol, ovarian P450arom expression and enzyme activity levels, and elevated FSH levels may have a role in the development of ovarian dysfunction reported in T CDD-exposed females. Expand
Neonatal exposure to 17α-ethynyl estradiol (EE) disrupts follicle development and reproductive hormone profiles in female rats.
TLDR
It is suggested that neonatal exposure to EE disrupted the system regulating the interactions between the reproductive hormones and follicle development in pre-pubertal rats, which may result in reproduction dysfunction in adulthood. Expand
In vitro effects of diethylstilbestrol, genistein, 4-tert-butylphenol, and 4-tert-octylphenol on steroidogenic activity of isolated immature rat ovarian follicles.
TLDR
The results indicate that isolated ovarian follicles representing intact morphological and functional units offer a sensitive model system for elucidating the female-specific reproductive effects of environmental chemicals. Expand
Effects of 4-tert-octylphenol, 4-tert-butylphenol, and diethylstilbestrol on prenatal testosterone surge in the rat.
TLDR
The present in vivo and in vitro analyses confirm different effects of alkylphenols and DES on fetal rat steroidogenesis and tissue structure. Expand
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TLDR
The results demonstrate that chronic administration of OP to adult male rats can adversely affect the secretion of reproductive hormones and strongly suggest that OP exerts these effects by acting like an estrogen. Expand
Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats.
TLDR
It is suggested that neonatal exposure to a high dose of OP alters developmental hormonal secretion presumably due to a hypothalamo-pituitary-ovarian disorder, with accelerated vaginal opening, subsequent persistent estrus, and uterine endometrial hyperplasia. Expand
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TLDR
Evidence is provided that OP acts like estrogen in vivo in both neonatal and adult female rats to exert effects that block reproductive cyclicity and ovulation. Expand
Chronic administration of 4-tert-octylphenol to adult male rats causes shrinkage of the testes and male accessory sex organs, disrupts spermatogenesis, and increases the incidence of sperm deformities.
TLDR
The results clearly demonstrate that OP can severely reduce the size and/or function of all of the male gametogenic and accessory reproductive organs studied and suggests that OP may exert its action in an estrogenic-like manner. Expand
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TLDR
Exposure of male rats to two estrogenic, environmental chemicals during gestation or during the first 21 days of postnatal life, affected testicular size or spermatogenesis in adulthood, and none of the treatments had any adverse effect on testicular morphology or on the cross-sectional area of the lumen or seminiferous epithelium. Expand
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TLDR
The results indicate that the lack of spontaneous ovulation in androgenized rats may be due to the absence of positive feedback to ovarian steroids, and Constant light-exposed ovex rats do not respond to the positive feedback action of estrogen and show a different response to P than ovex normal rats. Expand
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TLDR
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Central Administration of Antiserum to Vasoactive Intestinal Peptide Delays and Reduces Luteinizing Hormone and Prolactin Surges in Ovariectomized, Estrogen-Treated Rats
TLDR
The results suggest that hypothalamic VIP is an important regulator of both the timing and the magnitude of the EB-induced LH and PRL surge in the OVX rat, and suggest that its role may be stimulatory in this respect. Expand
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TLDR
The concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in serum following progesterone injection into spayed, estrogen-treated rats were measured by radioimmunoassay androgen priming is essential since no effect of progester one was observed in spayed treated animals. Expand
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