Endocrine‐disrupting chemicals and male reproductive health

Sharma, Aditi; Mollier, Josephine; Brocklesby, Richard W. K.; Caves, Charlotte; Jayasena, Channa N.; Minhas, Suks

doi:10.1002/rmb2.12326

Cited by 97 publications

(47 citation statements)

References 84 publications

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“…EDCs affect the reproductive system and the cellular processes in both sexes, leading to congenital abnormalities and infertility [ 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 ]. Mechanisms through which EDCs exert their pathophysiological effects have not yet been fully elucidated in human studies [ 19 ]. Despite a growing literature on couple exposure to non-persistent EDCs and fecundability, evidence for associations between biologically measured exposures and time to pregnancy is limited with equivocal results that do not preclude action, given the documented endocrine disrupting effects on other reproductive outcomes/fetal development [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

Endocrine Disruptors Acting on Estrogen and Androgen Pathways Cause Reproductive Disorders through Multiple Mechanisms: A Review

Amir

Shah

Mamoulakis

et al. 2021

IJERPH

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Increasing contamination of the environment by toxic compounds such as endocrine disrupting chemicals (EDCs) is one of the major causes of reproductive defects in both sexes. Estrogen/androgen pathways are of utmost importance in gonadal development, determination of secondary sex characteristics and gametogenesis. Most of the EDCs mediate their action through respective receptors and/or downstream signaling. The purpose of this review is to highlight the mechanism by which EDCs can trigger antagonistic or agonistic response, acting through estrogen/androgen receptors causing reproductive defects that lead to infertility. In vitro, in vivo and in silico studies focusing on the impact of EDCs on estrogen/androgen pathways and related proteins published in the last decade were considered for the review. PUBMED and PUBCHEM were used for literature search. EDCs can bind to estrogen receptors (ERα and ERβ) and androgen receptors or activate alternative receptors such as G protein-coupled receptors (GPCR), GPR30, estrogen-related receptor (ERRγ) to activate estrogen signaling via downstream kinases. Bisphenol A, dichlorodiphenyltrichloroethane, dichlorodiphenyldichloroethylene, polychlorinated biphenyls and phthalates are major toxicants that interfere with the normal estrogen/androgen pathways leading to infertility in both sexes through many ways, including DNA damage in spermatozoids, altered methylation pattern, histone modifications and miRNA expression.

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Section: Introductionmentioning

confidence: 99%

Endocrine Disruptors Acting on Estrogen and Androgen Pathways Cause Reproductive Disorders through Multiple Mechanisms: A Review

Amir

Shah

Mamoulakis

et al. 2021

IJERPH

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“…Early-life exposures have also been associated with developmental abnormalities and may increase the risk of several diseases later-in-life [ 4 ]. In adulthood, increasing incidences of several human reproductive disorders, such as testicular cancers and reduced sperm counts, may be partially attributed to an increased exposure to environmental EDCs that have estrogenic activity [ 7 , 8 , 9 , 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

Fighting Bisphenol A-Induced Male Infertility: The Power of Antioxidants

et al. 2021

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Bisphenol A (BPA), a well-known endocrine disruptor present in epoxy resins and polycarbonate plastics, negatively disturbs the male reproductive system affecting male fertility. In vivo studies showed that BPA exposure has deleterious effects on spermatogenesis by disturbing the hypothalamic–pituitary–gonadal axis and inducing oxidative stress in testis. This compound seems to disrupt hormone signalling even at low concentrations, modifying the levels of inhibin B, oestradiol, and testosterone. The adverse effects on seminal parameters are mainly supported by studies based on urinary BPA concentration, showing a negative association between BPA levels and sperm concentration, motility, and sperm DNA damage. Recent studies explored potential approaches to treat or prevent BPA-induced testicular toxicity and male infertility. Since the effect of BPA on testicular cells and spermatozoa is associated with an increased production of reactive oxygen species, most of the pharmacological approaches are based on the use of natural or synthetic antioxidants. In this review, we briefly describe the effects of BPA on male reproductive health and discuss the use of antioxidants to prevent or revert the BPA-induced toxicity and infertility in men.

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“…In this paper, we evaluated whether the use of D-Asp may have a protective role in preventing the testicular injury produced by the exposure to EDS, a toxicant that selectively destroys LC. Indeed, it must be considered that recently, some pollutants, such as cadmium [ 41 , 42 , 43 ] and BPA [ 44 , 45 , 46 ] may act as endocrine disrupters and/or toxicants that specifically affect gametogenesis leading to the production of low-quality gametes and, consequently, giving rise to a low rate of reproduction [ 47 , 48 ]. Firstly, to evaluate the effectiveness of the treatments, we measured the serum T levels.…”

Section: Resultsmentioning

confidence: 99%

Preliminary Investigation on the Ameliorative Role Exerted by D-Aspartic Acid in Counteracting Ethane Dimethane Sulfonate (EDS) Toxicity in the Rat Testis

Venditti

Romano

Aniello

et al. 2021

Animals

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Herein is reported the first evidence of the protective role of D-aspartic acid (D-Asp) in preventing the toxic effect exerted by the alkylating agent ethane dimethane sulfonate (EDS) in the rat testis. We confirmed that EDS treatment specifically destroyed Leydig cells (LC), resulting in the drastic decrease of the serum testosterone level and producing morphological changes in the germinal tubules, i.e., altered organization of the epithelium, loss of cell contacts and the consequent presence of empty spaces between them, and a reduce number of spermatozoa. Moreover, an increase of TUNEL-positive germ cells, other than alteration in the protein level and localization of two LC “markers”, StAR and PREP, were observed. Interestingly, results obtained from rats pre-treated with D-Asp for 15 days before EDS-injection showed that all the considered parameters were quite normal. To explore the probable mechanism(s) involved in the protection exerted by D-Asp, we considered the increased oxidative stress induced by EDS and the D-Asp antioxidant effects. Thiobarbiturc acid-reactive species (TBARS) levels increased following EDS-injection, while no change was observed in the D-Asp + EDS treated rats. Our results showed that D-Asp may be used as a strategy to mitigate the toxic effects exerted by environmental pollutants, as endocrine disrupters, in order to preserve the reproductive function.

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Endocrine‐disrupting chemicals and male reproductive health

Cited by 97 publications

References 84 publications

Endocrine Disruptors Acting on Estrogen and Androgen Pathways Cause Reproductive Disorders through Multiple Mechanisms: A Review

Endocrine Disruptors Acting on Estrogen and Androgen Pathways Cause Reproductive Disorders through Multiple Mechanisms: A Review

Fighting Bisphenol A-Induced Male Infertility: The Power of Antioxidants

Preliminary Investigation on the Ameliorative Role Exerted by D-Aspartic Acid in Counteracting Ethane Dimethane Sulfonate (EDS) Toxicity in the Rat Testis

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