The expression of several reproductive hormone receptors can be modified by perfluorooctane sulfonate (PFOS) in adult male rats

López-Doval, S.; Salgado, Renato M.; Lafuente, A.

doi:10.1016/j.chemosphere.2016.04.081

Cited by 28 publications

(11 citation statements)

References 67 publications

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“…Since these three signals (noradrenaline, serotonin, nitric oxide) stimulate GnRH neurons and have a role in modulating GnRH release, the modulation of these signals by PFOS exposure suggests that adult exposure to these compounds may contribute to HPG axis dysregulation and infertility. In a final study from the same lab, PFOS exposure (1.0, 3.0, and 6.0 mg/kg/day for 28 days, oral gavage) in adult male rats did not modify pituitary GnRH receptor gene expression but suppressed receptor protein expression at all doses (López-Doval et al 2016). Thus, high doses of PFOS administered to adults disrupt the expression of hypothalamic neuropeptide expression, neurotransmitter release, and pituitary gonadotropin production.…”

Section: Adult Exposuresmentioning

confidence: 89%

REPRODUCTIVE TOXICOLOGY: Impact of endocrine disruptors on neurons expressing GnRH or kisspeptin and pituitary gonadotropins

Roepke

Sadlier

2021

Reproduction

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Reproduction is a complex process that is controlled centrally via a network of hypothalamic neurons to modulate the pulsatile release of gonadotropin-releasing hormone (GnRH) and subsequently pituitary gonadotropins. The gonadotropins, luteinizing hormone and follicle stimulating hormone, drive gametogenesis and hormone production from the gonads. The hypothalamic-pituitary exchange is controlled by gonadal steroids through negative and positive feedback mechanisms via steroid receptors. Due to the expression of these receptors, GnRH neurons, the hypothalamic neurons that control them, and pituitary gonadotropes are sensitive to exogenous compounds that interact with steroid and nuclear receptors or alter hormone production and metabolism. The compounds, called endocrine disrupting compounds (EDCs), are ubiquitous and persistent in human environments and could bioaccumulate in the body. EDCs include plasticizers (like bisphenol A), dioxin, polychlorinated biphenyls (PCBs), organochlorine pesticides, flame retardants, and perfluorinated akyl substances (PFAS). Numerous studies have reported that perinatal, juvenile, or adult exposure to these EDCs, primarily in rats, disrupt the hypothalamic control of pituitary gonadotropin production leading to disruption of gonadal steroid production and estrous cyclicity. The purpose of this review is to evaluate these studies primarily focusing on GnRH and kisspeptin neurons and anterior pituitary gonadotropins and to discuss the need for deeper investigations into the hypothalamic-pituitary-gonadal axis.

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Section: Adult Exposuresmentioning

confidence: 89%

REPRODUCTIVE TOXICOLOGY: Impact of endocrine disruptors on neurons expressing GnRH or kisspeptin and pituitary gonadotropins

Roepke

Sadlier

2021

Reproduction

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“…Deregulation of the hypothalamic-pituitary-testis (HPT) axis was also reported in male rats treated with PFOS in the long term, leading to altered GnRH, LH, FSH expression and testosterone secretion that was paralleled by histological alterations at the level of testis, hypothalamus and the pituitary gland (117). These observations were substantiated and further extended by a subsequent study from the same group, indicating that the effects of PFOS were even broader and also affected the expression and content of the respective receptors, GnRH-R, LH-R, FSH-R, in some cases producing opposite effects at the transcriptional and protein level within a specific gland (118). Similarly, transactivation and steroidogenesis assays conducted on H295R cells showed that PFOS and PFOA could impair testosterone synthesis by altering the expression of steroidogenic genes and exerting both proestrogenic and anti-estrogenic activities (119).…”

Section: Part Iii: Effects Of Pfas Exposure On the Human Endocrine Systems Pfas Effects On Human Reproductive Function And Fertilitymentioning

confidence: 59%

Endocrine disruption by PFAS: A major concern associated with legacy and replacement substances

Panieri¹,

Buha-Đorđević²,

Saso³

2021

Arhiv za farmaciju

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Perand poly-fluorinated alkyl substances (PFAS) have been used for decades in a great variety of processes and products by virtue of their exceptional properties, versatility and chemical stability. Nevertheless, it is increasingly recognized that these substances can represent a serious hazard to human health and living organisms due to their persistence, long-range transport potential and tendency to accumulate in biota. For this reason, some efforts have been made across the EU to identify alternative molecules, with a shorter carbon chain and theoretically safer profile, that might replace the previous generation of legacy PFAS. Unfortunately, this strategy has not been entirely successful and serious concerns are still posed by PFAS in different human populations. Among others, an emerging aspect is represented by the adverse effects that both legacy and alternative PFAS can exert on the human endocrine system, with respect to vulnerable target subpopulations. In this review we will briefly summarize PFAS properties, uses and environmental fate, focusing on their effects on human reproductive capacity and fertility, body weight control and obesity as well as thyroid function.

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“…In contrast, Alam et al revealed that low doses of PFOS (0.015 mg/kg/d) can promote the synthetic secretion of testosterone 54 . Another study reported that PFOS did not affect the secretion of testosterone but can affect the bioavailability of testosterone, resulting in male reproductive system damage 55 . In addition, evidence highlighted a positive correlation between hypovitaminosis D and low testosterone, while 1α,25(OH) 2 D 3 supplementation increased testosterone biosynthesis 42,56–58 .…”

Section: Discussionmentioning

confidence: 96%

1α,25‐dihydroxyvitamin D₃ supplementation alleviates perfluorooctanesulfonate acid‐induced reproductive injury in male mice: Modulation of Nrf2 mediated oxidative stress response

Liang

et al. 2022

Environmental Toxicology

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Perfluorooctanesulfonate acid (PFOS) is a typical persistent organic pollutant that widely exists in the environment. To clarify the toxic effects and mechanisms of PFOS and to find effective intervention strategies have been attracted global attention. Here, we investigated the effects of PFOS on the male reproductive system and explored the potential protective role of 1α,25-dihydroxyvitamin D 3 (1α,25(OH) 2 D 3 ).Our results showed that 1α,25(OH) 2 D 3 intervention significantly improved PFOSinduced sperm quality decline and testicular damage. Moreover, 1α,25(OH) 2 D 3 aggrandized the total antioxidant capacity. Furthermore, after PFOS exposure, the transcription factor nuclear factor erythroid-related factor 2 (Nrf2) was adaptively increased together with its target genes, such as HO-1, NQO1, and SOD2. Meanwhile, 1α,25(OH) 2 D 3 ameliorated PFOS-induced augment of Nrf2 and target genes.These findings indicated that 1α,25(OH) 2 D 3 might attenuate PFOS-induced reproductive injury in male mice via Nrf2-mediated oxidative stress. K E Y W O R D S 1α,25(OH) 2 D 3 , Nrf2, oxidative stress, perfluorooctanesulfonate acid, reproductive toxicity 1 | INTRODUCTION Perfluorooctanesulfonic acid (PFOS) is a representative synthetic organo-fluorine compound, which has been widely used as a stain repellent and anti-stick material due to its excellent hydrophobic and lipophobic properties. 1 However, PFOS is difficult to degrade and widely exists in water, dust, soil, and other environmental media. 2,3 Noteworthy, PFOS generates a bioaccumulation effect. Drinking water, contaminated food consumption, product usage, and occupational exposure are the main approaches to PFOS exposure. PFOS has been extensively detected in human blood, umbilical cord blood, breast milk, and other samples worldwide. 4 Therefore, PFOS exposure has become a global environmental problem, and it is of great importance to clarify the toxic effects and mechanisms of PFOS and to find effective intervention strategies.In human body, PFOS combines with proteins, such as liver fatty acid transporters in the liver and albumin in the plasma. Liver is the primary target of PFOS, which can cause typical hepatic toxicity by disrupting glucose and lipid metabolism. [5][6][7][8] Recent studies have discovered that PFOS can also induce immune toxicity, 9 cardiotoxicity, 10 and neurotoxicity. 11 Furthermore, PFOS has significant reproductive

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The expression of several reproductive hormone receptors can be modified by perfluorooctane sulfonate (PFOS) in adult male rats

Cited by 28 publications

References 67 publications

REPRODUCTIVE TOXICOLOGY: Impact of endocrine disruptors on neurons expressing GnRH or kisspeptin and pituitary gonadotropins

REPRODUCTIVE TOXICOLOGY: Impact of endocrine disruptors on neurons expressing GnRH or kisspeptin and pituitary gonadotropins

Endocrine disruption by PFAS: A major concern associated with legacy and replacement substances

1α,25‐dihydroxyvitamin D₃ supplementation alleviates perfluorooctanesulfonate acid‐induced reproductive injury in male mice: Modulation of Nrf2 mediated oxidative stress response

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The expression of several reproductive hormone receptors can be modified by perfluorooctane sulfonate (PFOS) in adult male rats

Cited by 28 publications

References 67 publications

REPRODUCTIVE TOXICOLOGY: Impact of endocrine disruptors on neurons expressing GnRH or kisspeptin and pituitary gonadotropins

REPRODUCTIVE TOXICOLOGY: Impact of endocrine disruptors on neurons expressing GnRH or kisspeptin and pituitary gonadotropins

Endocrine disruption by PFAS: A major concern associated with legacy and replacement substances

1α,25‐dihydroxyvitamin D3 supplementation alleviates perfluorooctanesulfonate acid‐induced reproductive injury in male mice: Modulation of Nrf2 mediated oxidative stress response

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1α,25‐dihydroxyvitamin D₃ supplementation alleviates perfluorooctanesulfonate acid‐induced reproductive injury in male mice: Modulation of Nrf2 mediated oxidative stress response