In utero exposure to diisononyl phthalate caused testicular dysgenesis of rat fetal testis

Li, Linxi; Bu, Tiao; Su, Huina; Chen, Zhichuan; Liang, Yuyuan; Zhang, Gaolong; Zhu, Danyan; Shan, Yuanyuan; Xu, Ren-ai; Hu, Yuanyuan; Li, Junwei; Hu, Guoxin; Lian, Qingquan; Ge, Ren‐Shan

doi:10.1016/j.toxlet.2014.11.024

Cited by 68 publications

(54 citation statements)

References 37 publications

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“…Some endocrine disruptors, such as anti-androgenic phthalates (Mahood et al, 2005; Li et al, 2014, 2016) and estrogen-like insecticide methoxychlor metabolites (Liu et al, 2016), can significantly increase the incidence of MNGs after in utero exposure. However, ATR did not have such effects (Supplementary Figure S1), suggesting that ATR has a different reproductive toxicity mechanism from the phthalates and methoxychlor.…”

Section: Discussionmentioning

confidence: 99%

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In utero Exposure to Atrazine Disrupts Rat Fetal Testis Development

Fang

Dong

et al. 2018

Front. Pharmacol.

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Atrazine (ATR) is a commonly used agricultural herbicide and a potential endocrine disruptor that may cause testicular dysgenesis. The objective of the present study was to investigate the effects of atrazine on fetal testis development after in utero exposure. Female Sprague-Dawley rats were gavaged daily with vehicle (corn oil, control) or atrazine (25, 50, and 100 mg/kg body weight/day) from gestational day 12 to 21. Atrazine dose-dependently decreased serum testosterone levels of male pups, with a significant difference from the control recorded at a dose of 100 mg/kg. In addition, atrazine significantly increased fetal Leydig cell aggregation at a dose of 100 mg/kg. Atrazine increased fetal Leydig cell number but not Sertoli cell number. However, atrazine down-regulated Scarb1 and Cyp17a1 in the fetal Leydig cell per se and Hsd17b3 and Dhh in the Sertoli cell per se. These results demonstrated that in utero exposure to atrazine disrupted rat fetal testis development.

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Section: Discussionmentioning

confidence: 99%

“…Some endocrine disruptors induce the increased incidence of multinucleated gonocytes (MNGs) in the fetal testis during the gestational exposure (Borch et al, 2006; Li et al, 2014). Bouin’s solution fixed testes were arranged in a tissue-array in one paraffin block.…”

Section: Methodsmentioning

confidence: 99%

In utero Exposure to Atrazine Disrupts Rat Fetal Testis Development

Fang

Dong

et al. 2018

Front. Pharmacol.

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“…The potentially reprotoxic effects of DiNP are similar to those of DEHP, but at higher doses: the highest NOAEL is 15 mg/kg/day for DiNP as against 5 for DEHP [2]. In rodents, prenatal exposure to DiNP was associated with anti-androgenic effects such as impairment of germinal and Leydig cells, a decrease in testicular production of testosterone, testicular atrophy, reduced anogenital distance and reduced sperm motility [18, 51–54]. DiNP is the only plasticizer whose effects on humans have been studied.…”

Section: Discussionmentioning

confidence: 99%

Exposure of hospitalised pregnant women to plasticizers contained in medical devices

et al. 2017

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BackgroundMedical devices (MDs) in polyvinyl chloride (PVC) are not a well-known source of exposure to plasticizers, in particular during pregnancy. Because of its toxicity, the di-(2-ethylhexyl) phthalate (DEHP) has been replaced by other plasticizers such as di (isononyl)-cyclohexane-1,2-dicarboxilic acid (DINCH), tri-octyltrimellitate (TOTM) and di-(isononyl) phthalate (DiNP). Our study aimed to quantify the plasticizers (DEHP and alternative plasticizers) contained in PVC medical devices used for hospitalised pregnant women and to describe which these MDs had been used (type, number, duration of exposure).MethodsThe plasticizers contained in the MDs used for daily care in the Obstetrics Department of a French University Hospital were extracted from PVC (after contact with a chloroform solution), identified and quantified by gas-chromatography-mass-spectrometry analysis. A total of 168 pregnant women hospitalised in the Obstetrics Department with at least one catheter were included in the observational study. The median number of MDs containing plasticizers used and the daily duration of exposure to the MDs were compared in three groups of pregnant women: “Pathology group” (women hospitalised for an obstetric disorder who did not give birth during this hospitalisation; n = 52), “Pathology and delivery group” (hospitalised for an obstetric disorder and who gave birth during this stay; n = 23) and “Delivery group” (admitted for planned or spontaneous delivery without obstetric disorder; n = 93).ResultsDiNP, TOTM and DINCH were the predominant plasticizers contained in the MDs at an amount of 29 to 36 g per 100 g of PVC. Women in the “Pathology group” (preterm labour or other pathology) were exposed to a median number of two MDs containing TOTM and one MD containing DiNP, fewer than those in the “Pathology and delivery group” (p < 0.05). Women in the “Pathology group” had a median exposure of 3.4 h/day to MDs containing DiNP and 8.2 h/day to MDs containing TOTM, longer than those in the “Delivery group” (p < 0.01).ConclusionsOur study shows that the medical management of pregnant women in a hospital setting entails exposure to MDs containing alternative plasticizers (DiNP, TOTM and DINCH).Electronic supplementary materialThe online version of this article (doi:10.1186/s12905-017-0398-7) contains supplementary material, which is available to authorized users.

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“…Subsequently, Pathirana et al (2011) showed that in vitro exposure to monobutyl phthalate (MBP) and DHEP inhibited hCG-induced testosterone secretion as well as INSL3 secretion from interstitial cell cultures of dog testes [42]. Furthermore, male fetal rat exposure to diisononyl phthalate (DiNP) and dicyclohexyl phthalate (DCHP) appeared to cause inhibition of gene expression and reduced protein levels of INSL3 and 3β-hydroxysteroid dehydrogenase [43], and exposure to relatively high levels of DCHP reduced the expression levels of key steroidogenesis genes [44].…”

Section: Pre-natal Exposure: Can Testicular Function Already Be Comprmentioning

confidence: 99%

Mechanisms of Testicular Disruption from Exposure to Bisphenol A and Phtalates

Pallotti

Pelloni

Gianfrilli

et al. 2020

JCM

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Great attention has been paid in recent years to the harmful effects of various chemicals that interfere with our natural hormone balance, collectively known as endocrine-disrupting chemicals (EDCs) or endocrine disruptors. The effects on the reproductive system of bisphenol A (BPA) and phthalates have received particular attention: while they have a short half-life, they are so widespread that human exposure can be considered as continuous. Evidence is often limited to the animal model, disregarding the likelihood of human exposure to a mixture of contaminants. Data from animal models show that maternal exposure probably has harmful effects on the male fetus, with an increased risk of urogenital developmental abnormalities. After birth, exposure is associated with changes in the hypothalamic-pituitary-testicular axis, hindering the development and function of the male genital pathways through the mediation of inflammatory mechanisms and oxidative stress. The epidemiological and clinical evidence, while generally confirming the association between reproductive abnormalities and some phthalate esters and BPA, is more contradictory, with wildly different findings. The aim of this review is therefore to provide an update of the potential mechanisms of the damage caused by BPA and phthalates to reproductive function and a review of the clinical evidence currently available in the literature.

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In utero exposure to diisononyl phthalate caused testicular dysgenesis of rat fetal testis

Cited by 68 publications

References 37 publications

In utero Exposure to Atrazine Disrupts Rat Fetal Testis Development

In utero Exposure to Atrazine Disrupts Rat Fetal Testis Development

Exposure of hospitalised pregnant women to plasticizers contained in medical devices

Mechanisms of Testicular Disruption from Exposure to Bisphenol A and Phtalates

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