Possible effects of melatonin against rat uterus exposure to bisphenol A during neonatal period

Dernek, Damla; Ömeroğlu, Suna; Akçay, Neslihan Çoşkun; Kartal, Bahar; Dizakar, Saadet Özen Akarca; Türkoğlu, İsmail; Aydin, Vildan

doi:10.1007/s11356-017-0187-8

Cited by 8 publications

(4 citation statements)

References 31 publications

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“…Moreover, melatonin protects the uterus degeneration induced by BPA exposure during the neonatal period, as histologically and morphometrically evidenced [176].…”

Section: Melatoninmentioning

confidence: 87%

Oxidative Stress and BPA Toxicity: An Antioxidant Approach for Male and Female Reproductive Dysfunction

et al. 2020

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Bisphenol A (BPA) is a non-persistent anthropic and environmentally ubiquitous compound widely employed and detected in many consumer products and food items; thus, human exposure is prolonged. Over the last ten years, many studies have examined the underlying molecular mechanisms of BPA toxicity and revealed links among BPA-induced oxidative stress, male and female reproductive defects, and human disease. Because of its hormone-like feature, BPA shows tissue effects on specific hormone receptors in target cells, triggering noxious cellular responses associated with oxidative stress and inflammation. As a metabolic and endocrine disruptor, BPA impairs redox homeostasis via the increase of oxidative mediators and the reduction of antioxidant enzymes, causing mitochondrial dysfunction, alteration in cell signaling pathways, and induction of apoptosis. This review aims to examine the scenery of the current BPA literature on understanding how the induction of oxidative stress can be considered the “fil rouge” of BPA’s toxic mechanisms of action with pleiotropic outcomes on reproduction. Here, we focus on the protective effects of five classes of antioxidants—vitamins and co-factors, natural products (herbals and phytochemicals), melatonin, selenium, and methyl donors (used alone or in combination)—that have been found useful to counteract BPA toxicity in male and female reproductive functions.

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“…Moreover, melatonin protects the uterus degeneration induced by BPA exposure during the neonatal period, as histologically and morphometrically evidenced [176].…”

Section: Melatoninmentioning

confidence: 87%

Oxidative Stress and BPA Toxicity: An Antioxidant Approach for Male and Female Reproductive Dysfunction

et al. 2020

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“…Based on these findings, it is suggested that melatonin plays a role in protecting the ovary from toxicity caused by DEHP. 55 This antioxidative compound may also alleviate possible similar effects of other endocrinedisrupting compounds on the human ovary.…”

mentioning

confidence: 99%

Identification of oxidative stress–related Xdh gene as a di(2‐ethylhexyl)phthalate (DEHP) target and the use of melatonin to alleviate the DEHP‐induced impairments in newborn mouse ovaries

Liu

Yan

et al. 2019

Journal of Pineal Research

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This study, using an in vitro ovary culture model, investigates the mechanisms through which di(2‐ethylhexyl)phthalate (DEHP) impairs germ cell cyst breakdown and primordial follicle assembly. The results indicate the latter effects exerted by 10 or 100 µmol/L DEHP in cultured newborn ovaries were associated with increased levels of reactive oxygen species (ROS) and apoptosis. Based on a transcriptome analysis, we found the expression of the oxidative stress–related gene Xdh (xanthine dehydrogenase) was significantly upregulated in DEHP‐cultured ovaries. Two treatments, namely Xdh RNAi or the addition of melatonin to the ovary culture, inhibited the increase in Xdh expression and ROS levels caused by DEHP and, at the same time, reduced apoptosis and the impairment of primordial follicle assembly in the treated ovaries. Together, the results identify Xdh gene as one of the major targets of DEHP in newborn ovaries and that the consequent increased level of ROS is possibly responsible for the increment of apoptosis and primordial follicle assembly impairment. At the same time, they highlight that melatonin alleviates the effects of DEHP as with other endocrine‐disrupting compounds on the ovary.

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“…Oral administration of melatonin increased the in vitro fertilization rate, alleviating the alterations in fertility related proteins, reducing ROS levels, and preventing oocyte apoptosis induced by BPA. Melatonin also protects the uterus from deterioration induced by BPA exposure during the neonatal period in rats [132]. In another study, Wu et al [62] reported that male rats treated with BPA did not change the weight of the reproductive organs.…”

Section: Melatoninmentioning

confidence: 95%

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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Possible effects of melatonin against rat uterus exposure to bisphenol A during neonatal period

Cited by 8 publications

References 31 publications

Oxidative Stress and BPA Toxicity: An Antioxidant Approach for Male and Female Reproductive Dysfunction

Oxidative Stress and BPA Toxicity: An Antioxidant Approach for Male and Female Reproductive Dysfunction

Identification of oxidative stress–related Xdh gene as a di(2‐ethylhexyl)phthalate (DEHP) target and the use of melatonin to alleviate the DEHP‐induced impairments in newborn mouse ovaries

Role of Antioxidants in Alleviating Bisphenol A Toxicity

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