Maternal exposure to environmentally relevant doses of bisphenol A causes reproductive dysfunction in F1 adult male rats: protective role of melatonin

Olukole, Samuel Gbadebo; Lanipekun, Damilare Olaniyi; Ola-Davies, Eunice Olufunke; Oke, B. O.

doi:10.1007/s11356-019-06153-3

Cited by 23 publications

(11 citation statements)

References 43 publications

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“…In rat testes and epididymal sperm, similar results were reported-the administration of melatonin with BPA [26] and BPA exposure in utero [86] decreased OS by restoring GSH, GPx, SOD, CAT, and Glutathione-S-transferase (GST) activity and MDA and H2O2 levels. This potent antioxidant also normalizes testosterone levels, improves histopathological alterations and allows the occurrence of normal spermatogenesis, leading to normal sperm count, motility, viability, and morphology [26,86]. By studying the genotoxic effects of BPA in male Sprague Dawley rats' germ cells and the potential protective action of melatonin, Wu and colleagues showed that animals exposed to 200 mg/kg BPA per day for ten days presented higher levels of thiobarbituric acid reactive substances (TBARS) and decreased activity of SOD than controls [25].…”

Section: Refersupporting

confidence: 78%

“…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]. In rat testes and epididymal sperm, similar results were reported-the administration of melatonin with BPA [26] and BPA exposure in utero [86] decreased OS by restoring GSH, GPx, SOD, CAT, and Glutathione-S-transferase (GST) activity and MDA and H2O2 levels. This potent antioxidant also normalizes testosterone levels, improves histopathological alterations and allows the occurrence of normal spermatogenesis, leading to normal sperm count, motility, viability, and morphology [26,86].…”

Section: Refermentioning

confidence: 65%

“…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 Functionmentioning

confidence: 99%

“…Additionally, results showed that BPA caused LPO [ 21 , 22 ] and decrease GSH content in mitochondria [ 21 , 131 ]. In rats, it was also found that BPA deregulate not only testosterone levels and semen quality but also induced OS in testis and epididymal sperm, by increasing the levels of MDA [ 26 , 27 , 30 , 32 , 86 , 88 ], H 2 O 2 [ 26 , 86 , 102 , 105 , 132 ], and LPO [ 105 , 132 ] and decreasing the GSH content [ 26 , 27 , 30 , 86 , 88 ] and CAT [ 26 , 88 , 105 , 132 ], SOD [ 25 , 26 , 30 , 86 , 88 , 105 , 132 ], GR [ 105 ], and GPx activity [ 26 , 30 , 86 , 88 , 105 , 132 ]. Increased MDA and decreased GSH concentrations are usually associated to higher concentrations of free oxygen radicals, inducing LPO in tissues.…”

Section: Impact Of Bpa Exposure On Oxidative Stress In Testis and mentioning

confidence: 99%

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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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Section: Refersupporting

confidence: 78%

Section: Refermentioning

confidence: 65%

Section: Bpa-induced Alterations In Testicular Structure Functionmentioning

confidence: 99%

Section: Impact Of Bpa Exposure On Oxidative Stress In Testis and mentioning

confidence: 99%

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

et al. 2021

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“…Rodent studies have shown that exposure to BPA during pregnancy and lactation increases the risk of diabetes in the next generation (Ma et al 2013 ). Moreover, maternal exposure to environmental doses of BPA was shown to induce reproductive dysfunction in offspring (Olukole et al 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Bisphenol A disturbs metabolism of primary rat adipocytes without affecting adipokine secretion

Szkudelska

Okulicz

Szkudelski

2021

Environ Sci Pollut Res

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Bisphenol A (BPA) is an ubiquitous synthetic chemical exerting numerous adverse effects. Results of rodent studies show that BPA negatively affects adipose tissue. However, the short-term influence of this compound addressing adipocyte metabolism and adipokine secretion is unknown. In the present study, isolated rat adipocytes were exposed for 2 h to 1 and 10 nM BPA. Insulin-induced glucose conversion to lipids along with glucose transport was significantly increased in the presence of BPA. However, basal glucose conversion to lipids, glucose oxidation, and formation of lipids from acetate were unchanged in adipocytes incubated with BPA. It was also shown that BPA significantly increases lipolytic response of adipocytes to epinephrine. However, lipolysis stimulated by dibutyryl-cAMP (a direct activator of protein kinase A) and the antilipolytic action of insulin were not affected by BPA. Moreover, BPA did not influence leptin and adiponectin secretion from adipocytes. Our new results show that BPA is capable of disturbing processes related to lipid accumulation in isolated rat adipocytes. This is associated with the potentiation of insulin and epinephrine action. The effects of BPA appear already after short-term exposure to low doses of this compound. However, BPA fails to change adipokine secretion.

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