II. The effect of p-nonylphenol on the fertility potential of male rats after gestational, lactational and direct exposure

Jager, Christiaan De; Bornman, M. S.; Oosthuizen, J. M. C.

doi:10.1046/j.1439-0272.1999.00246.x

Cited by 63 publications

(37 citation statements)

References 21 publications

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“…De Jager et al demonstrated that the weights of the testis and epididymis were negatively affected by NP in proportion to dose [16]. Furthermore, Hossaini et al showed a dosedependent reduction in the weight of the right epididymis of male pups when dams were administered NP on days 11 to 18 of gestation at Different superscripts denote significant differences (P<0.05).…”

Section: Discussionmentioning

confidence: 99%

“…A reduction in the weight of the epididymis in rats implies a decrease in epididymal sperm density [16,20,21]. Han et al have shown that control animals have a compact and regular arrangement of cells in the seminiferous tubules, whereas animals exposed to NP display an irregular and disordered arrangement with the shedding of cellular material from the seminiferous epithelium [21].…”

Section: Discussionmentioning

confidence: 99%

“…Neonatal exposure to NP (8 mg/kg/day) through daily intraperitoneal injections had an effect on the weight of the reproductive organs and delayed the descent of the testes [15]. In a study of the fertility of male rats after gestation and early postnatal life, NP (100 mg/kg, 250 mg/kg, 400 mg/kg) was found to effect both the testis and epididymis [16,17]. However, Odum and Ashby did not find any effect of NP (8 mg/kg/day) on the male reproductive tract [18].…”

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confidence: 99%

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Effect of Gestational Exposure to Nonylphenol on the Development and Fertility of Mouse Offspring

Kimura

Suzuki

et al. 2006

Journal of Reproduction and Development

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Abstract. Nonylphenol (NP), a kind of environmental chemical, is thought to imitate endogenous hormones, inhibit the actions of hormones, and induce reproductive abnormalities. A number of experimental animals, usually rats, have been used to evaluate the potential reproductive toxicity of NP. However, the findings of previous studies were contradictory in some cases. Therefore, we used ICR mice as a biomodel for in utero study of NP. After mating, 8-to 12-week-old females were assigned to four groups (n=8) for subcutaneous injections from day 5 to 20 of gestation. Group I animals received corn oil alone as a control, while the mice of groups II, III and IV received NP at concentrations of 1/1000, 1/100 and 1/10 of the LD50, respectively. A dose-dependent decrease was observed in terminal body weights of males of the F1 generation; however, a very small negative effect was only found in the females of the NP1/10 group. No significant effect was found on the liver weights of both sexes. The weights of the testis and epididymis were slightly decreased in the NP1/ 10 group. The NP1/100 treatment increased ovary weight considerably. The uterus weight tended to be increased in the NP treatment groups; however, there were large variations. The gestational exposure of the groups had no significant effect on the rate of pregnancy (94.4-100%) and the number of fetuses per litter (13.6-14.3 males, 12.3-13.7 females) compared with the control group. However, the overall mortality of fetuses/embryos was increased considerably in the NP1/100 (male: 13.9%) and NP1/10 (female: 9.8%) groups. These results suggest that exposure to NP in utero possibly affects the body weight and some reproductive organ weights, but does not influence the potential fertility of the F1 generation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Effect of Gestational Exposure to Nonylphenol on the Development and Fertility of Mouse Offspring

Kimura

Suzuki

et al. 2006

Journal of Reproduction and Development

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“…In addition, disruption of vimentin fi laments by MEHP promotes germ cell detachment due to Sertoli cells shrinking. NP administration to pregnant rats during gestation, lactancy and 10 weeks after weaning (corresponding to a complete lifespan exposed to NP) have been shown to decrease epithelial thickness, probably due to Sertoli cells shrinking and an increase in germ cell apoptosis (de Jager et al, 1999;McClusky et al, 2007). ).…”

Section: Eds Affect Spermatogenesis and Induce Germ Cell Apoptosis Inmentioning

confidence: 99%

Contribution of environmental pollutants to male infertily: A working model of germ cell apoptosis induced by plasticizers

Lagos-Cabré¹,

Moreno

2012

Biol. Res.

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Bisphenol A [2,2-bis(4-hydroxyphenyl)propane] (BPA), 4-nonylphenol (NP) and di(2-ethylhexyl)phthalate (DEHP), and its metabolite mono-2-ethylhexyl phthalate (MEHP) are chemicals found in plastics, which act as endocrine disruptors (EDs) in animals, including human. EDs act like hormones in the endocrine system, and disrupt the physiologic function of endogenous hormones. Most people are exposed to different endocrine disruptors and concern has been raised about their true effect on reproductive organs. In the testis, they seem to preferentially attack developing testis during puberty rather than adult organs. However, the lack of information about the molecular mechanism, and the apparently controversial effect observed in different models has hampered the understanding of their effects on mammalian spermatogenesis. In this review, we critically discuss the available information regarding the effect of BPA, NP and DEHP/ MEHP upon mammalian spermatogenesis, a major target of EDs. Germ cell sloughing, disruption of the blood-testis-barrier and germ cell apoptosis are the most common effects reported in the available literature. We propose a model at the molecular level to explain the effects at the cellular level, mainly focused on germ cell apoptosis.

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“…A variety of stressors have been shown to inhibit spermatogenesis: hyperthermia (Lue et al, 1999;Rockett et al, 2001), anti-tumor drugs (Tates, 1992;Vecino et al, 2001), heavy metals (Bouissou and Fabre, 1966;Hew et al, 1993) and environmental hormones (de Jager et al, 1999;Raychoudhury et al, 1999) are involved in such stressors. Recent studies have noticed that heme oxygenase-1 (HO-1) and metallothionein-1/ 2 (MT-1/2) not only play roles as molecular markers for stress but are also biological defense proteins (Oguro and Yoshida, 1998;Bourdon and Blache, 2001;Suntres, 2002), because they are induced by various similar oxidative stimuli, including heat shock, heavy metals, endotoxin and cytokines, and function as a radical scavenger for reactive oxygen species (ROS) such as superoxide and hydroxyl radical produced by stress (Elbirt and Bonkovsky, 1999;Davis and Cousins, 2000).…”

Section: Introductionmentioning

confidence: 99%

Tissue-Dependent Induction of Heme Oxygenase-1 and Metallothionein-1/2 by Methyl Methanesulfonate

Ashino¹,

Ozawa

Numazawa³

et al. 2003

J. Toxicol. Sci.

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-Methyl methanesulfonate (MMS), a methylating agent, is known to be a genotoxicant in testis. The purpose of this study was to investigate roles of oxidative stress-responsive proteins, heme oxygenase-1 (HO-1) and metallothionein-1/2 (MT-1/2), in genotoxicity of MMS. Cadmium, a potent genotoxicity inducer, induced HO-1 and MT-1/2 in rat livers and kidneys. Then we comparatively investigated MMS-induced HO-1 and MT-1/2 in rat livers, kidneys and testes. We found that a single administration of MMS (40 mg/kg) resulted in the induction of MT-1/2 mRNA in the liver, but not HO-1 mRNA, reaching maximum level at 6 hr and returning to the control levels by 24 hr. Interestingly, MMS induced both HO-1 and MT-1/2 mRNAs in the kidney. In contrast, MMS induced HO-1 mRNA, but not MT-1/2 mRNA in the testis. Since HO-1 and MT-1/2 have been recognized to respond to various oxidative stimuli, we further examined the inducing effect of MMS on these two proteins. MMS at dosages of 20 to 40 mg/kg for 2 consecutive weeks induced HO-1 mRNA (123 to 187% of the control) and protein (274 to 404% of the control) in rat testes. However, MT-1/2 mRNA was not induced by MMS administration, although a high level of expression was observed in comparison with the liver and kidney. These findings suggest that MMS induces HO-1 and/or MT-1/2 mRNA and its protein tissue-dependently, and the heme catabolites by HO-1 in the testis may contribute in some manner to its genotoxicity.

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II. The effect of p-nonylphenol on the fertility potential of male rats after gestational, lactational and direct exposure

Cited by 63 publications

References 21 publications

Effect of Gestational Exposure to Nonylphenol on the Development and Fertility of Mouse Offspring

Effect of Gestational Exposure to Nonylphenol on the Development and Fertility of Mouse Offspring

Contribution of environmental pollutants to male infertily: A working model of germ cell apoptosis induced by plasticizers

Tissue-Dependent Induction of Heme Oxygenase-1 and Metallothionein-1/2 by Methyl Methanesulfonate

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