Disposition of [14C]nonoxynol-9 after intravenous or vaginal administration to female Sprague-Dawley rats

Walter, Brian A.; Agha, Bushra J.; Digenis, George A.

doi:10.1016/0041-008x(88)90085-3

Cited by 24 publications

(10 citation statements)

References 5 publications

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“…There is also evidence that nonoxynol-9 can be metabolized to nonylphenol, which after glucuronidation was excreted through urine and bile (60). Intravaginal administration of nonoxynol-9 in rats caused damage to the vaginal epithelium and acute inflammation in the vagina, cervix, and uterus (61).…”

Section: Industrial Chemicals and Environmental Poliutantsmentioning

confidence: 99%

Male Reproductive Health and Environmental Xenoestrogens

Toppari¹,

Larsen²,

Christiansen³

et al. 1996

Environmental Health Perspectives

361

340

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Male reproductive health has deteriorated in many countries during the last few decades. In the 1990s, declining semen quality has been reported from Belgium, Denmark, France, and Great Britain. The incidence of testicular cancer has increased during the same time. Incidences of hypospadias and cryptorchidism also appear to be increasing. Similar reproductive problems occur in many wildlife species. There are marked geographic differences in the prevalence of male reproductive disorders. While the reasons for these differences are currently unknown, both clinical and laboratory research suggest that the adverse changes may be inter-related and have a common origin in fetal life or childhood. Exposure of the male fetus to supranormal levels of estrogens, such as diethlylstilbestrol, can result in the above-mentioned reproductive defects. The growing number of reports demonstrating that common environmental contaminants and natural factors possess estrogenic activity presents the working hypothesis that the adverse trends in male reproductive health may be, at least in part, associated with exposure to estrogenic or other hormonally active (e.g., antiandrogenic) environmental chemicals during fetal and childhood development. An extensive research program is needed to understand the extent of the problem, its underlying etiology, and the development of a strategy for prevention and intervention. Environ Health Perspect 104(Suppl 4): 741-803 (1996)

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Section: Industrial Chemicals and Environmental Poliutantsmentioning

confidence: 99%

Male Reproductive Health and Environmental Xenoestrogens

Toppari¹,

Larsen²,

Christiansen³

et al. 1996

Environmental Health Perspectives

361

340

View full text Add to dashboard Cite

show abstract

“…Hence, it is highly possible that many oestrogenic chemicals remain unidentified. Li and Hansen (1997); Mendola et al (1997); Kester et al (2000); Birkett (2003) Dioxins 6.15-7.28 Altered serum testosterone levels and decline in sperm concentrations Sharpe and Skakkebaek (1993); Egeland et al (1994); Carlsen et al (1992); Auger et al (1995); Menchini-Fabris et al (1996); Toppari et al (1996); Swan et al (2000) PAHs E6.0 Preterm birth and intrauterine growth restriction Perera et al (2002); Birkett (2003) Phthalates 1.46-13.1 Reduced anogenital distance, nipple and areola retention, cleft phallus, hypospadias, cryptorchidism, reduction in fetal testosterone levels, abnormally located Leydig cells, abnormal seminiferous cord formation Harris et al (1997); Mylchreest et al (1998Mylchreest et al ( , 1999; Gray et al (1999); Parks et al (2000); McIntyre et al (2001); Fisher et al (2003) BPA 3.4 Decrease in the quantity and quality of sperm production, decreased fertility in males, hypospadias, cryptorchidism, endometrial hyperplasia, recurrent miscarriages, polycystic ovarian syndrome Carlsen et al (1992); Giwercman et al (1993); Chitra et al (2003); Muñoz de Toro et al 2005Pesticides 0.2-7.0 Decrease in the quantity of sperm production, miscarriage, genital deformities, hypospadias Singer (1949); Toppari et al (1996); Walter et al (1988); Finizio et al (1997); Baskin et al (2001) Sharara et al (1998); Schuurs (1999); Gardella and Hill (2000); Yoshida (2002) In general, EDCs modulate the hormonal function in the body and, i...…”

Section: Oestrogenic Propertiesmentioning

confidence: 99%

Negative impact of endocrine-disrupting compounds on human reproductive health

Balabanič

Rupnik

Klemenčić

2011

Reprod. Fertil. Dev.

185

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There is increasing concern about chemical pollutants that are able to mimic hormones, the so-called endocrine-disrupting compounds (EDCs), because of their structural similarity to endogenous hormones, their ability to interact with hormone transport proteins or because of their potential to disrupt hormone metabolic pathways. Thus, the effects of endogenous hormones can be mimicked or, in some cases, completely blocked. A substantial number of environmental pollutants, such as polychlorinated biphenyls, dioxins, polycyclic aromatic hydrocarbons, phthalates, bisphenol A, pesticides, alkylphenols and heavy metals (arsenic, cadmium, lead, mercury), have been shown to disrupt endocrine function. These compounds can cause reproductive problems by decreasing sperm count and quality, increasing the number of testicular germ cells and causing male breast cancer, cryptorchidism, hypospadias, miscarriages, endometriosis, impaired fertility, irregularities of the menstrual cycle, and infertility. Although EDCs may be released into the environment in different ways, the main sources is industrial waste water. The present paper critically reviews the current knowledge of the impact of EDCs on reproductive disorders in humans.

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“…Systemic biotransformation of absorbed NPEs in rats is extensive ( Walter et al, 1988 ). Based on metabolism of similar non-ionic surfactants, biotransformation consists of alkyl group oxidation, removal of ethylene oxide units, and oxidation of the terminal ethoxy group, followed by conjugation of the resulting metabolites (Gardner et al, 1980;French et al, 1993) .…”

Section: Introductionmentioning

confidence: 99%

Comparative in vitro percutaneous absorption of nonylphenol and nonylphenol ethoxylates (NPE-4 and NPE-9) through human, porcine and rat skin

Monteiro‐Riviere

Miller²,

Simon³

et al. 2000

Toxicol Ind Health

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The purpose of this study was to assess the percutaneous absorption of nonylphenol (NP) and the nonylphenol ethoxylates, NPE-4 and NPE-9, in human, porcine and rat skin. In vitro studies with the NPEs were conducted for 8 h in flowthrough diffusion cells using topical solutions of 0.1, 1.0 and 10% in PEG-400 or 1% in water (NPE-9 only). NP absorption was assessed as a 1% solution in PEG-400. All compounds were 14C ring-labeled and radioactivity in perfusate was monitored over time. Skin deposition was measured at the termination of the experiment. Absorption into perfusate and total penetration (compound absorbed plus compound sequestered in skin) were calculated. Absorption of NPE-4, NPE-9 and NP was similar across all species at less than 1% of the applied dose over 8 h. Penetration was generally below 5% of applied dose, the majority located in the stratum corneum. In all species and for both NPEs, the fraction of dose absorbed was highest for the lowest applied dose. Absorptions expressed as actual mass absorbed over 8 h were similar (approximately 0.3 microg/cm2) across all concentrations. Penetration, but not absorption, was greater from a water vehicle compared to a PEG-400 vehicle, particularly in rat skin. These studies suggest that NP, NPE-4 and NPE-9 were minimally absorbed across skin from all three species. Fractional absorption was concentration-dependent, making the actual absorbed flux constant across all doses.

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Disposition of [14C]nonoxynol-9 after intravenous or vaginal administration to female Sprague-Dawley rats

Cited by 24 publications

References 5 publications

Male Reproductive Health and Environmental Xenoestrogens

Male Reproductive Health and Environmental Xenoestrogens

Negative impact of endocrine-disrupting compounds on human reproductive health

Comparative in vitro percutaneous absorption of nonylphenol and nonylphenol ethoxylates (NPE-4 and NPE-9) through human, porcine and rat skin

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