Bisphenol S-induced chronic inflammatory stress in liver via peroxisome proliferator-activated receptor γ using fish in vivo and in vitro models

Zheng, Yan; Yang, Ming; Liu, Jingyu; Xu, Hai; Luo, Shusheng; Wong, Ming Hung; Chen, Kewei

doi:10.1016/j.envpol.2018.11.039

Cited by 51 publications

(23 citation statements)

References 55 publications

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“…Acetate constitutes about 60% of total SCFAs in humans, making it an important part of metabolic systems. A decrease in acetate by BPS may lead to decrease in immune-regulatory effects as acetate has been linked to the increase of interferon gamma level (Graham et al, 2015), and BPS is known to produce chronic inflammation (Qiu et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Early Life Exposure to Environmental Contaminants (BDE-47, TBBPA, and BPS) Produced Persistent Alterations in Fecal Microbiome in Adult Male Mice

Gomez

Dutta

Suvorov

et al. 2020

Toxicological Sciences

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The gut microbiome is a pivotal player in toxicological responses. We investigated the effects of maternal exposure to 3 human health-relevant toxicants (BDE-47, TBBPA, and BPS) on the composition and metabolite levels (bile acids [BAs] and short chain fatty acids [SCFAs]) of the gut microbiome in adult pups. CD-1 mouse dams were orally exposed to vehicle (corn oil, 10ml/kg), BDE-47 (0.2 mg/kg), TBBPA (0.2 mg/kg), or BPS (0.2 mg/kg) once daily from gestational day 8 to the end of lactation (postnatal day 21). 16S rRNA sequencing and targeted metabolomics were performed in feces of 20-week-old adult male pups (n = 14-23/group). Host gene expression and BA levels were quantified in liver. BPS had the most prominent effect on the beta-diversity of the fecal microbiome compared to TBPPA and BDE-47 (QIIME). Seventy-three taxa were persistently altered by at least 1 chemical, and 12 taxa were commonly regulated by all chemicals (most of which were from the Clostridia class and were decreased). The most distinct microbial biomarkers were S24-7 for BDE-47, Rikenellaceae for TBBPA, and Lactobacillus for BPS (LefSe). The community-wide contributions to the shift in microbial pathways were predicted using FishTaco. Consistent with FishTaco predictions, BDE-47 persistently increased fecal and hepatic BAs within the 12α hydroxylation pathway, corresponding to an up-regulation with the hepatic BA-synthetic enzyme Cyp7a1. Fecal BAs were also persistently up-regulated by TBBPA and BPS (LC-MS). TBBPA increased propionic acid and succinate, whereas BPS decreased acetic acid (GC-MS). There was a general trend in the hepatic down-regulation of pro-inflammatory cytokines and the oxidative stress sensor target gene (Nqo1), and a decrease in G6Pdx (the deficiency of which leads to dyslipidemia). In conclusion, maternal exposure to these toxicants persistently modified the gut-liver axis, which may produce an immune-suppressive and dyslipidemia-prone signature later in life.

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Section: Discussionmentioning

confidence: 99%

Early Life Exposure to Environmental Contaminants (BDE-47, TBBPA, and BPS) Produced Persistent Alterations in Fecal Microbiome in Adult Male Mice

Gomez

Dutta

Suvorov

et al. 2020

Toxicological Sciences

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“…Bisphenol S (BPS) is a structural analogue and substitute for Bisphenol A (BPA) commercially used to manufacture BPA free products such as plastics, thermal receipts, epoxy resins, infant feeding bottles, canned food items, medical equipment and recycled paper 1‐3 . BPS has emerged as a persistent worldwide environmental contaminant present in water, food and air and has even been detected in human urine and proved as detrimental for health 4‐6 …”

Section: Introductionmentioning

confidence: 99%

Melatonin ameliorates Bisphenol S induced testicular damages by modulating Nrf‐2/HO‐1 and SIRT‐1/FOXO‐1 expressions

Kumar

Verma

Haldar

2020

Environmental Toxicology

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BPS has detrimental effects on human reproductive health and emerged as an environmental contaminant for global health concern. This study deals with the adverse impact of BPS exposure on testicular oxidative stress, inflammation and apoptosis in adult male golden hamster, Mesocricetus auratus and its amelioration by melatonin. BPS (75 mg/kg BW/day) exposure caused testicular impairment as evident by histological degenerative changes, declined sperm quality (viability and motility), serum levels of testosterone and melatonin with a concomitant decrease in testicular androgen receptor (AR) and melatonin receptor (MT1) expression. The BPS exposure caused marked increase in testicular oxidative load, inflammation (NF‐kB/COX‐2) and apoptosis (caspase‐3). Melatonin (10 mg/kg BW/alternate day) pretreatment to BPS exposed hamsters resumed normal testicular histoarchitecture, sperm quality and decreased testicular oxidative load as evident by enhanced antioxidant enzymes (SOD and catalase) activities and decreased lipid peroxidation (LPO) level. Further, melatonin also stimulated the testicular antioxidant proteins Nrf‐2/HO‐1, SIRT‐1/FOXO‐1 and reduced inflammatory proteins NF‐kB/COX‐2 expression to counteract BPS induced testicular damages. Melatonin administration to the BPS treated hamsters resulted in increased testicular cell proliferation (PCNA), survival (Bcl‐2), gap junction (connexin‐43) and decreased apoptosis (caspase‐3). In conclusion, our study documented the detrimental effects of BPS on testes that compromises male fertility. Further, melatonin was found as a potent molecule that rescued the BPS induced testicular damages in male golden hamster Mesocricetus auratus.

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“…Based on the data of the population included in our study, the average exposure concentration of BPS in the offspring, increase lysozyme activity, change oxidative stress and in ammatory cytokines, and lead to decreased immune defense in zebra sh (Qiu et al 2019). The study found that immune system pathways were also affected by exposure to BPS in zebra sh embryos (Dong et al 2018).…”

Section: Discussionmentioning

confidence: 99%

The Bisphenol F and Bisphenol S and Cardiovascular disease: results from NHANES 2013-2016

wang¹,

Fei²,

Liu³

et al. 2021

Preprint

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Background Bisphenol F (BPF) and bisphenol S (BPS) are replacing bisphenol A (BPA) in the manufacturing of products containing polycarbonates and epoxy resins, however, the effects of these substitutes on the risk of cardiovascular disease (CVD) have not been assessed. Objective To examine the association of urinary BPS and BPF with the CVD risk in a U.S. representative population. Method A cross-sectional data with 1,266 participants aged 20 to 80 years from the 2013–2016 National Health and Nutrition Examination Survey (NHANES) was analyzed. The logistic regression was used to assess the association between BPF, BPS and CVD. The Bayesian kernel machine regression (BKMR) model was applied to assess the mixed effect. Results A total of 138 patients with CVD were identified. After adjusting for potential confounding factors, T3 concentration of BPS increased the risk of total CVD (OR: 1.98, 95%CI: 1.20–3.28). When stratified by age, we found that BPS increased the risk of CVD in the 50–80 age groups (OR:1.40, 95%CI: 1.05–1.87). BPS was positively associated with the risk of stroke and T3 of BPS increased the stroke risk by 3.46 times (95%CI: 1.09–10.95). No significant association was observed between BPF and CVD. Although BKMR model did not identify the mixed exposure effect of BPS, the risk of CVD increased, with the increase of compound concentration. Conclusion Our results suggest that BPS may increase the risk of total CVD and stroke in the U.S population, and prospective studies are needed to confirm the results.

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Bisphenol S-induced chronic inflammatory stress in liver via peroxisome proliferator-activated receptor γ using fish in vivo and in vitro models

Cited by 51 publications

References 55 publications

Early Life Exposure to Environmental Contaminants (BDE-47, TBBPA, and BPS) Produced Persistent Alterations in Fecal Microbiome in Adult Male Mice

Early Life Exposure to Environmental Contaminants (BDE-47, TBBPA, and BPS) Produced Persistent Alterations in Fecal Microbiome in Adult Male Mice

Melatonin ameliorates Bisphenol S induced testicular damages by modulating Nrf‐2/HO‐1 and SIRT‐1/FOXO‐1 expressions

The Bisphenol F and Bisphenol S and Cardiovascular disease: results from NHANES 2013-2016

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