In utero exposure to bisphenol A disrupts fetal testis development in rats

Lv, Yao; Li, Lili; Fang, Yinghui; Chen, Panpan; Wu, Siwen; Chen, Xiuxiu; Ni, Chaobo; Zhu, Qiqi; Huang, Tongliang; Lian, Qingquan; Ge, Ren‐Shan

doi:10.1016/j.envpol.2018.12.006

Cited by 43 publications

(29 citation statements)

References 36 publications

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“…A more recent study by Lv et al (2019) further confirmed these results, finding a downregulation of the mRNA and protein levels of some steroidogenic enzymes and AMH transcribed and translated by Leydig cells and Sertoli cells, respectively. In addition to the reduced proliferation of fetal Leydig cells, the authors also hypothesized that exposure to these phenol compounds might be involved in the impaired development of the fetal testicle [52]. Key steroidogenic enzyme Cyp11a expression also seems reduced in a dose dependent way from prenatal BPA exposure [53].…”

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

confidence: 61%

“…However, the authors noted that the possibility of a different response between humans and animal models should be taken into account [51]. A more recent study by Lv et al (2019) further confirmed these results, finding a downregulation of the mRNA and protein levels of some steroidogenic enzymes and AMH transcribed and translated by Leydig cells and Sertoli cells, respectively. In addition to the reduced proliferation of fetal Leydig cells, the authors also hypothesized that exposure to these phenol compounds might be involved in the impaired development of the fetal testicle [52].…”

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

confidence: 87%

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

confidence: 61%

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

confidence: 87%

Mechanisms of Testicular Disruption from Exposure to Bisphenol A and Phtalates

Pallotti

Pelloni

Gianfrilli

et al. 2020

JCM

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“…In another study, BPA concentration in the blood was negatively correlated with INSL3 expression level (53). Several other studies have indicated that BPA and its analogs reduced both Leydig cell number and testosterone production (54)(55)(56)(57)(58)(59). Interestingly, a clinical study conducted on 160 neonate males (Control:80, hypospadias patients: 80) suffering from hypospadias had seven folds BPA concentration in their blood compared to normal newborns (60).…”

Section: The Effects Of Bisphenols On Leydig Cells and The Developmenmentioning

confidence: 98%

Bisphenols Threaten Male Reproductive Health via Testicular Cells

2020

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Male reproductive function and health are largely dependent on the testes, which are strictly regulated by their major cell components, i. e., Sertoli, Leydig, and germ cells. Sertoli cells perform a crucial phagocytic function in addition to supporting the development of germ cells. Leydig cells produce hormones essential for male reproductive function, and germ cell quality is a key parameter for male fertility assessment. However, these cells have been identified as primary targets of endocrine disruptors, including bisphenols. Bisphenols are a category of man-made organic chemicals used to manufacture plastics, epoxy resins, and personal care products such as lipsticks, face makeup, and nail lacquers. Despite long-term uncertainty regarding their safety, bisphenols are still being used worldwide, especially bisphenol A. While considerable attention has been paid to the effects of bisphenols on health, current bisphenol-related reproductive health cases indicate that greater attention should be given to these chemicals. Bisphenols, especially bisphenol A, F, and S, have been reported to elicit various effects on testicular cells, including apoptosis, DNA damage, disruption of intercommunication among cells, mitochondrial damage, disruption of tight junctions, and arrest of proliferation, which threaten male reproductive health. In addition, bisphenols are xenoestrogens, which alter organs and cells functions via agonistic or antagonistic interplay with hormone receptors. In this review, we provide in utero, in vivo, and in vitro evidence that currently available brands of bisphenols impair male reproductive health through their action on testicular cells.

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“…Oral administration of BPA from GD1 to GD22 to pregnant rats inhibited T production in neonates (129). Pregnant Sprague Dawley rats were administered 4, 40, and 400 mg/kg BW BPA via gavage daily from GD12 to 21, and BPA dose-dependently reduced serum T levels and down-regulated the expression of Insl3 and Hsd17b3 and their proteins at 40 and 400 mg/kg and that of Lhcgr, Cyp11a1, and Cyp17a1 and their proteins at 400 mg/kg (26). BPA inhibited FLC proliferation at 400 mg/kg (26).…”

Section: Effect Of In Utero Bpa Exposure On Male Reproductive Tract Dmentioning

confidence: 99%

“…There is increasing evidence that BPA is associated with the occurrence of reproductive toxicity (25,26) and other health problems such as diabetes (27), neurotoxicity (28)(29)(30), immunotoxicity (31), and cancer (32)(33)(34).…”

Section: Introductionmentioning

confidence: 99%

Bisphenols and Leydig Cell Development and Function

Zhu²,

Wang

et al. 2020

Front. Endocrinol.

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Bisphenol A (BPA) is a ubiquitous environmental pollutant, mainly from the production and use of plastics and the degradation of wastes related to industrial plastics. Evidence from laboratory animal and human studies supports the view that BPA has an endocrine disrupting effect on Leydig cell development and function. To better understand the adverse effects of BPA, we reviewed its role and mechanism by analyzing rodent data in vivo and in vitro and human epidemiological evidence. BPA has estrogen and anti-androgen effects, thereby destroying the development and function of Leydig cells and causing related reproductive diseases such as testicular dysgenesis syndrome, delayed puberty, and subfertility/infertility. Due to the limitation of BPA production, the increased use of BPA analogs has also attracted attention to these new chemicals. They may share actions and mechanisms similar to or different from BPA.

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In utero exposure to bisphenol A disrupts fetal testis development in rats

Cited by 43 publications

References 36 publications

Mechanisms of Testicular Disruption from Exposure to Bisphenol A and Phtalates

Mechanisms of Testicular Disruption from Exposure to Bisphenol A and Phtalates

Bisphenols Threaten Male Reproductive Health via Testicular Cells

Bisphenols and Leydig Cell Development and Function

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