Bisphenol A,  an endocrine-disruptor compund,  that modulates the immune response to infections

Río-Araiza, Víctor Hugo Del; Mendoza, María Luisa; Nava-Castro, Karen Elizabeth; Muñoz-Cruz, Samira; Chávez-Rueda, Karina; León, Carmen T. Gómez de; Montor, Jorge Morales

doi:10.2741/4897

Cited by 20 publications

(4 citation statements)

References 14 publications

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“…The transcription factor NF-κB, as an important immunoregulatory factor, promotes the high expression of pro-inflammatory cytokine TNF-α and interleukin family, which have a significant disruptive effect on the expression and distribution of tight junction proteins and impair the intestinal epithelial barrier function [ 49 , 50 ]. BPA has been demonstrated to modulate the function of the immune system and increases the susceptibility to infections by virtue of acting as a pro-inflammatory molecule [ 51 ]. Long-term exposure to BPA-induced TLR4-dependent hypothalamic inflammation exacerbates diet-induced prediabetes [ 52 ].…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Selenium Nanoparticles against Bisphenol A-Induced Toxicity in Porcine Intestinal Epithelial Cells

Pan

Huang

et al. 2023

IJMS

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Bisphenol A (BPA) is widely used to harden plastics and polycarbonates and causes serious toxic effects in multiple organs, including the intestines. Selenium, as an essential nutrient element for humans and animals, exhibits a predominant effect in various physiological processes. Selenium nanoparticles have attracted more and more attention due to their outstanding biological activity and biosafety. We prepared chitosan-coated selenium nanoparticles (SeNPs) and further compared the protective effects, and investigated the underlying mechanism of SeNPs and inorganic selenium (Na2SeO3) on BPA-induced toxicity in porcine intestinal epithelial cells (IPEC-J2). The particle size, zeta potential, and microstructure of SeNPs were detected by using a nano-selenium particle size meter and a transmission electron microscope. IPEC-J2 cells were exposed to BPA alone or simultaneously exposed to BPA and SeNPs or Na2SeO3. The CCK8 assay was performed to screen the optimal concentration of BPA exposure and the optimal concentration of SeNPs and Na2SeO3 treatment. The apoptosis rate was detected by flow cytometry. Real-time PCR and Western blot methods were used to analyze the mRNA and protein expression of factors related to tight junctions, apoptosis, inflammatory responses and endoplasmic reticulum stress. Increased death and morphological damage were observed after BPA exposure, and these increases were attenuated by SeNPs and Na2SeO3 treatment. BPA exposure disturbed the tight junction function involved with decreased expression of tight junction protein Zonula occludens 1 (ZO-1), occludin, and claudin-1 proteins. Proinflammatory response mediated by the transcription factor nuclear factor-k-gene binding (NF-κB), such as elevated levels of interleukin-1β(IL-1β), interleukin-6 (IL-6), interferon-γ (IFN-γ), interleukin-17 (IL-17), and tumor necrosis factor-α (TNF-α) expression was induced at 6 and 24 h after BPA exposure. BPA exposure also disturbed the oxidant/antioxidant status and led to oxidative stress. IPEC-J2 cell apoptosis was induced by BPA exposure, as indicated by increased BCL-2-associated X protein (Bax), caspase 3, caspase 8, and caspase 9 expression and decreased B-cell lymphoma-2 (Bcl-2) and Bcl-xl expression. BPA exposure activated the endoplasmic reticulum stress (ERS) mediated by the receptor protein kinase receptor-like endoplasmic reticulum kinase (PERK), Inositol requiring enzyme 1 (IRE1α), and activating transcription factor 6 (ATF6). We found that treatment with SeNPs and Na2SeO3 can alleviate the intestinal damage caused by BPA. SeNPs were superior to Na2SeO3 and counteracted BPA-induced tight junction function injury, proinflammatory response, oxidative stress, apoptosis, and ERS stress. Our findings suggest that SeNPs protect intestinal epithelial cells from BPA-induced damage, partly through inhibiting ER stress activation and subsequently attenuating proinflammatory responses and oxidative stress and suppressing apoptosis, thus enhancing the intestinal epithelial barrier function. Our data indicate that selenium nanoparticles may represent an effective and reliable tool for preventing BPA toxicity in animals and humans.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of Selenium Nanoparticles against Bisphenol A-Induced Toxicity in Porcine Intestinal Epithelial Cells

Pan

Huang

et al. 2023

IJMS

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“…Thus, it appears that BPA …..can worsen the prognosis of diseases that are adversely affected by inflammation." Del Rio Araiza et al (2021) endocrine-disruptor; estrogenic activity; endocrine modulating; immune system; immune response; immune cell populations; infections; pro-inflammatory; inflammation. IIC “An extended time was observed in BPA-treated but not BPS-treated animals in bleeding time; … Taken together, these data show BPA and BPS as capable of interfering with the coagulation process via FVIIa."…”

Section: Appendix 2cf Linkage Mechanisms and Biomarkersmentioning

confidence: 99%

Modifiable contributing factors to COVID-19: A comprehensive review

Kostoff

Briggs²,

Kanduc

et al. 2023

Food and Chemical Toxicology

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“…BPA promotes the expression and release of certain proinflammatory cytokines, resulting in a constant low-grade inflammatory state at local and systemic levels [56]. Additionally, BPA has been reported to interfere with adipogenic processes [57]; therefore, it is important to establish the existence of a possible association between inflammatory events during adipocyte differentiation and BPA's influence.…”

Section: Influence Of Bpa On Inflammatory Signals In Adipose Tissuementioning

confidence: 99%

New Evidence on BPA’s Role in Adipose Tissue Development of Proinflammatory Processes and Its Relationship with Obesity

Casanova

Bermúdez

Fuentes

et al. 2023

IJMS

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Bisphenol A (BPA) is a xenobiotic with endocrine disruptor properties which interacts with various receptors, eliciting a cellular response. In the plastic industry, BPA is widely used in the production of polycarbonate and epoxy-phenolic resins to provide elastic properties. It can be found in the lining of canned foods, certain plastic containers, thermal printing papers, composite dental fillings, and medical devices, among other things. Therefore, it is a compound that, directly or indirectly, is in daily contact with the human organism. BPA is postulated to be a factor responsible for the global epidemic of obesity and non-communicable chronic diseases, belonging to the obesogenic and diabetogenic group of compounds. Hence, this endocrine disruptor may be responsible for the development of metabolic disorders, promoting in fat cells an increase in proinflammatory pathways and upregulating the expression and release of certain cytokines, such as IL6, IL1β, and TNFα. These, in turn, at a systemic and local level, are associated with a chronic low-grade inflammatory state, which allows the perpetuation of the typical physiological complications of obesity.

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Bisphenol A, an endocrine-disruptor compund, that modulates the immune response to infections

Cited by 20 publications

References 14 publications

Protective Effects of Selenium Nanoparticles against Bisphenol A-Induced Toxicity in Porcine Intestinal Epithelial Cells

Protective Effects of Selenium Nanoparticles against Bisphenol A-Induced Toxicity in Porcine Intestinal Epithelial Cells

Modifiable contributing factors to COVID-19: A comprehensive review

New Evidence on BPA’s Role in Adipose Tissue Development of Proinflammatory Processes and Its Relationship with Obesity

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