Effects of co-administered melatonin, fructose and bisphenol A (BPA) on rat epididymis and sperm characteristics

Akarca-Dizakar, SO; Erdoğan, Deniz; Peker, Tuncay; Akçay, Neslihan Çoşkun; Türkoğlu, İsmail; Eşmekaya, Meriç Arda; Ömeroğlu, Suna

doi:10.1080/10520295.2019.1627418

Cited by 18 publications

(30 citation statements)

References 47 publications

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“…Altered expression of tight junctional proteins, occluding and ZO-1 has been reported in mice exposed to PCB (Cai, Wang, Huang, Chen, & Zuo, 2013). Similar effects have been documented in rodents exposed to BPA along with significant damage to epididymal tissue and abnormalities in the sperm head and tail (Akarca-Dizakar et al, 2019).…”

Section: Impac T Of Environmental Contaminants On Epididymal Fun C supporting

confidence: 64%

“…Several animal studies have been conducted to examine the deleterious effects of various environmental toxicants on male fertility and decipher their possible mechanism(s) of action (Akarca-Dizakar et al, 2019;Albert, Nardelli, Lalancette, Hales, & Robaire, 2018;Aydin & Erkan, 2017;Campos et al, 2019;Kim, Cheon, Choi, & Lee, 2019;Kolatorova et al, 2018). The focus of this review is to shed light on the impact of environmental contaminants on male reproduction and the underlying mechanism of action based on the recent scientific data available.…”

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confidence: 99%

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Environmental contaminants and male infertility: Effects and mechanisms

et al. 2020

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The global incidence of infertility has risen to 15% in contrast to 7%-8% in the early 1960s (Mascarenhas, Flaxman, Boerma, Vanderpoel, & Stevens, 2012). Over the past several decades, a significant deterioration in male reproductive health has been reported in association with increased industrialisation, which has contributed to a massive release of synthetic pollutants into the environment (Rim, 2017; Skakkebaek et al., 2016). The concerns over declining male reproductive health were elicited by one of the landmark publications by Carlsen et al., which revealed a worldwide reduction in the average sperm count to half between 1940 and 1990 (Carlsen, Giwercman, Keiding, & Skakkebaek, 1992). These findings prompted several scientists, mainly Swan et al. to re-evaluate the trend in semen quality over time in different regions throughout the world and eventually confirmed a significant decrease in sperm concentration in western countries (Swan, Elkin, & Fenster, 1997). Incidentally, a parallel increase in the occurrence of testicular cancer and congenital abnormalities (cryptorchidism and hypospadias) were reported in several countries (Ferguson & Agoulnik, 2013; Hutson, 2000). These observations prompted researchers to explore the potential role of common environmental factors in causing a decline in male reproductive health. In 1993, it was hypothesised that the growing incidence of male reproductive anomalies could be due to exposure to chemicals possessing oestrogenic property (Sharpe & Skakkebaek, 1993).

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Section: Impac T Of Environmental Contaminants On Epididymal Fun C supporting

confidence: 64%

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confidence: 99%

Environmental contaminants and male infertility: Effects and mechanisms

et al. 2020

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“…BPA disrupts spermatogenesis by inhibiting androgen production and reducing Sertoli cell number and function [30,[81][82][83][84]. Furthermore, BPA exposure decreased the seminiferous tubule diameters and increased tubule atrophy and damage [26,27,[85][86][87], induced germinal cell debris and congestion [27,86,88], as well as induced the reduction and/or degeneration of spermatocytes [25,27,32,89,90] and other spermatogenic cells [22,26,30,86,87,89,90]. A recent study in mice showed that chronic exposure to BPA impairs the proliferation of spermatogonia and spermatocytes, resulting in poor sperm quality, especially reduced sperm counts and motility [91].…”

Section: Bpa-induced Alterations In Testicular Structure Function Amentioning

confidence: 99%

“…Several studies investigated the role of melatonin in ameliorating BPA-induced testicular toxicity [21,25,26,85]. Anjum et al showed that the oral administration of melatonin in mice exposed to BPA reduced testicular mitochondrial LPO; restored the activity of mitochondrial enzymes (SDH, MDH, IDH, MAO, and NDH); and improved the mitochondrial antioxidants GPx, SOD, and GR [21].…”

Section: Refermentioning

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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“…Akarca-Dizakar et al [130] showed that melatonin treatment improves sperm motility and quality in BPA-exposed rats. They also showed a positive effect of melatonin on the adrenal and prostate function in male rats administered BPA for 2 weeks [131].…”

Section: Melatoninmentioning

confidence: 99%

Role of Antioxidants in Alleviating Bisphenol A Toxicity

2020

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Bisphenol A (BPA) is an oestrogenic endocrine disruptor widely used in the production of certain plastics, e.g., polycarbonate, hard and clear plastics, and epoxy resins that act as protective coating for food and beverage cans. Human exposure to this chemical is thought to be ubiquitous. BPA alters endocrine function, thereby causing many diseases in human and animals. In the last few decades, studies exploring the mechanism of BPA activity revealed a direct link between BPA-induced oxidative stress and disease pathogenesis. Antioxidants, reducing agents that prevent cellular oxidation reactions, can protect BPA toxicity. Although the important role of antioxidants in minimizing BPA stress has been demonstrated in many studies, a clear consensus on the associated mechanisms is needed, as well as the directives on their efficacy and safety. Herein, considering the distinct biochemical properties of BPA and antioxidants, we provide a framework for understanding how antioxidants alleviate BPA-associated stress. We summarize the current knowledge on the biological function of enzymatic and non-enzymatic antioxidants, and discuss their practical potential as BPA-detoxifying agents.

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Effects of co-administered melatonin, fructose and bisphenol A (BPA) on rat epididymis and sperm characteristics

Cited by 18 publications

References 47 publications

Environmental contaminants and male infertility: Effects and mechanisms

Environmental contaminants and male infertility: Effects and mechanisms

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

Role of Antioxidants in Alleviating Bisphenol A Toxicity

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