Delayed onset of puberty in male offspring from bisphenol A-treated dams is followed by the modulation of gene expression in the hypothalamic–pituitary–testis axis in adulthood

Oliveira, Isabela Medeiros de; Romano, Renata Marino; Campos, Patricia de; Cavallin, Mônica Degraf; Oliveira, Cláudio Alvarenga de; Romano, Marco Aurélio

doi:10.1071/rd17107

Cited by 19 publications

(8 citation statements)

References 56 publications

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“…Other rodent studies suggest that BPA exposure can affect T production with one report suggesting developmental exposure to BPA increases this hormone [84], whereas other studies suggest this chemical decreases T production [85; 86; 87; 88; 89]. Similar to the BPA-analogue studies reported above, BPA can also affect sperm production and quality and increase sperm DNA damage in rodent models [90; 91; 92; 93; 94].…”

Section: Neuroendocrine Disruption Due To Exposure Of Rodent Models Tmentioning

confidence: 72%

Neuroendocrine disruption in animal models due to exposure to bisphenol A analogues

Rosenfeld

2017

Frontiers in Neuroendocrinology

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Animal and human studies provide evidence that exposure to the endocrine disrupting chemical (EDC), bisphenol A (BPA), can lead to neurobehavioral disorders. Consequently, there is an impetus to identify safer alternatives to BPA. Three bisphenol compounds proposed as potential safer alternatives to BPA are bisphenol S (BPS), bisphenol F (BPF), and bisphenol AF (BPAF). However, it is not clear whether these other compounds are safer in terms of inducing less endocrine disrupting effects in animals and humans who are now increasingly coming into contact with these BPA-substitutes. In the past few years, several animal studies have shown exposure to these other bisphenols induce similar neurobehavioral disruption as BPA. We will explore in this review article the current studies suggesting these other bisphenols result in neuroendocrine disruptions that may be estrogen receptor-dependent. Current work may aide in designing future studies to test further whether these BPA-substitutes can act as neuroendocrine disruptors.

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Section: Neuroendocrine Disruption Due To Exposure Of Rodent Models Tmentioning

confidence: 72%

Neuroendocrine disruption in animal models due to exposure to bisphenol A analogues

Rosenfeld

2017

Frontiers in Neuroendocrinology

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“…The activity of HPG axis in male rat offspring is affected by low BPA dose exposure from gestational day 18 to 5PND and causes delayed onset of puberty [162]. The expression rates of hypothalamic GnRH and esr2, pituitary FSH β subunit and AR, testicular FSH receptor and inhibin β subunit are increased in the adult exposed to low BPA doses (0.5 mg/kg), whereas serum T and LH levels are affected at higher doses (5 mg/kg) [162].…”

Section: Fig (3) the Targets Of Bpa Along The Hpg Axis And The Possible Interplay With Metabolic And Environmental Factors (A Higher Resomentioning

confidence: 99%

Neuro-toxic and Reproductive Effects of BPA

et al. 2019

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Background: Bisphenol A (BPA) is one of the highest volume chemicals produced worldwide. It has recognized activity as an endocrine-disrupting chemical and has suspected roles as a neurological and reproductive toxicant. It interferes in steroid signaling, induces oxidative stress, and affects gene expression epigenetically. Gestational, perinatal and neonatal exposures to BPA affect developmental processes, including brain development and gametogenesis, with consequences on brain functions, behavior, and fertility. Methods: This review critically analyzes recent findings on the neuro-toxic and reproductive effects of BPA (and its analogues), with focus on neuronal differentiation, synaptic plasticity, glia and microglia activity, cognitive functions, and the central and local control of reproduction. Results: BPA has potential human health hazard associated with gestational, peri- and neonatal exposure. Beginning with BPA’s disposition, this review summarizes recent findings on the neurotoxicity of BPA and its analogues, on neuronal differentiation, synaptic plasticity, neuroinflammation, neuro-degeneration, and impairment of cognitive abilities. Furthermore, it reports the recent findings on the activity of BPA along the HPG axis, effects on the hypothalamic Gonadotropin Releasing Hormone (GnRH), and the associated effects on reproduction in both sexes and successful pregnancy. Conclusion: BPA and its analogues impair neuronal activity, HPG axis function, reproduction, and fertility. Contrasting results have emerged in animal models and human. Thus, further studies are needed to better define their safety levels. This review offers new insights on these issues with the aim to find the “fil rouge”, if any, that characterize BPA’s mechanism of action with outcomes on neuronal function and reproduction.

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“…Endocrine disrupting chemicals (EDCs) might impact the production of various steroid and peptide hormones. For example, the classic EDC, BPA, can alter production of estrogen, testosterone, glucocorticoids, insulin, and likely other hormones (Akingbemi et al, 2004 ; Nakamura et al, 2010 ; Poimenova et al, 2010 ; Peretz et al, 2011 ; D'Cruz et al, 2012 ; Nanjappa et al, 2012 ; Castro et al, 2013 ; Garcia-Arevalo et al, 2016 ; Oliveira et al, 2017 ; Weldingh et al, 2017 ). Such EDC-induced endocrinopathies might be another mechanism by which host changes can influence the gut microbiota.…”

Section: Introductionmentioning

confidence: 99%

Gut Dysbiosis in Animals Due to Environmental Chemical Exposures

Rosenfeld

2017

Front. Cell. Infect. Microbiol.

181

104

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The gut microbiome consists of over 103–104 microorganism inhabitants that together possess 150 times more genes that the human genome and thus should be considered an “organ” in of itself. Such communities of bacteria are in dynamic flux and susceptible to changes in host environment and body condition. In turn, gut microbiome disturbances can affect health status of the host. Gut dysbiosis might result in obesity, diabetes, gastrointestinal, immunological, and neurobehavioral disorders. Such host diseases can originate due to shifts in microbiota favoring more pathogenic species that produce various virulence factors, such as lipopolysaccharide. Bacterial virulence factors and metabolites may be transmitted to distal target sites, including the brain. Other potential mechanisms by which gut dysbiosis can affect the host include bacterial-produced metabolites, production of hormones and factors that mimic those produced by the host, and epimutations. All animals, including humans, are exposed daily to various environmental chemicals that can influence the gut microbiome. Exposure to such chemicals might lead to downstream systemic effects that occur secondary to gut microbiome disturbances. Increasing reports have shown that environmental chemical exposures can target both host and the resident gut microbiome. In this review, we will first consider the current knowledge of how endocrine disrupting chemicals (EDCs), heavy metals, air pollution, and nanoparticles can influence the gut microbiome. The second part of the review will consider how potential environmental chemical-induced gut microbiome changes might subsequently induce pathophysiological responses in the host, although definitive evidence for such effects is still lacking. By understanding how these chemicals result in gut dysbiosis, it may open up new remediation strategies in animals, including humans, exposed to such chemicals.

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Delayed onset of puberty in male offspring from bisphenol A-treated dams is followed by the modulation of gene expression in the hypothalamic–pituitary–testis axis in adulthood

Cited by 19 publications

References 56 publications

Neuroendocrine disruption in animal models due to exposure to bisphenol A analogues

Neuroendocrine disruption in animal models due to exposure to bisphenol A analogues

Neuro-toxic and Reproductive Effects of BPA

Gut Dysbiosis in Animals Due to Environmental Chemical Exposures

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