Remodeling on adipocytic physiology of organophosphorus esters in mature adipocytes

Liu, Ying; Le, Yifei; Xu, Mengting; Wang, Wanyue; Chen, Hang; Zhang, Quan; Wang, Cui

doi:10.1016/j.envpol.2022.119287

Cited by 12 publications

(6 citation statements)

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“…The level of IL-6 has been shown to be negatively related with the lung function . Recent studies have reported that Cl-OPFRs could upregulate the level of IL-6 in zebrafish, steady-state bone marrow-derived dendritic cells, and mouse embryo fibroblast cells. ,, In this study, we observed a potential structural interaction between Cl-OPFRs/m-Cl-OPFRs and IL-6 using molecular docking analysis. These findings supported the involvement of IL-6 in the adverse effects induced by Cl-OPFR exposure.…”

Section: Discussionmentioning

confidence: 66%

“…Then, annotation of these genes showed that the induction of inflammatory cascades, predominantly activation of inflammatory cells, was the major biological process linking pulmonary dysfunction and Cl-OPFRs/m-Cl-OPFRs. Previous studies have revealed that Cl-OPFRs elevated the levels of CCL2/MCP1 and IL-6 in mouse embryo fibroblast cells and enhanced pulmonary inflammation in allergic asthmatic mice even at a dose less than or equal to a human-tolerable daily intake . Thus, we hypothesized that the inflammation-oriented AOP framework may explain the linkage between Cl-OPFR exposure and a decreased lung function to some extent.…”

Section: Discussionmentioning

confidence: 93%

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Chlorinated Organophosphate Flame Retardants Impair the Lung Function via the IL-6/JAK/STAT Signaling Pathway

Zhu

Zhang

Lü

et al. 2022

Environ. Sci. Technol.

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Toxicological studies have revealed the adverse impacts of organophosphate flame retardants (OPFRs) on the respiratory system, while there is a lack of epidemiological evidence, and information for risk assessment remains insufficient. Herein, we investigated the associations of urinary metabolites of OPFRs with the lung function in 987 adults participating in the U.S. National Health and Nutrition Examination Survey 2011–2012. The elevation of three primary metabolites of chlorinated OPFRs [bis(1,3-dichloro-2-propyl) phosphate (BDCIPP), bis(2-chloroethyl) phosphate (BCEP), and bis(1-chloro-2-propyl) phosphate (BCIPP)] was related to pulmonary dysfunction in a sample-weighted regression model. Each one-unit increase in the log-transformed levels of BDCIPP and BCEP was related to 91.52 and 79.34 mL reductions in the forced vital capacity (FVC). Each one-unit elevation in BCIPP was correlated with 130.86, 153.56, 302.26, and 148.24 mL reductions in forced expiratory volume 1st second (FEV1), FVC, peak expiratory flow rate (PEF), and forced expiratory flow at 25-75% of FVC (FEF25–75%), respectively. Then, an adverse outcome pathway (AOP) framework was constructed using the Comparative Toxicogenomics Database, the Toxicity Forecaster, and the GeneCards database. Based on the weight of the evidence, BDCIPP, BCEP, BCIPP, and their parent compounds (TDCIPP, TCEP, and TCIPP) may affect the IL-6/Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway, induce airway remodeling, and impair the lung function. Additionally, tobacco smoke exposure may modify the effects of BDCIPP on the lung function (P int < 0.05) and affect the IL-6-mediated AOP. These results suggested that chlorinated OPFRs were associated with pulmonary dysfunction via the IL-6/JAK/STAT pathway.

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Section: Discussionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 93%

Chlorinated Organophosphate Flame Retardants Impair the Lung Function via the IL-6/JAK/STAT Signaling Pathway

Zhu

Zhang

Lü

et al. 2022

Environ. Sci. Technol.

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“… 27 Likewise, numerous in vitro studies have confirmed the diabetogenic effects of TPHP and DPHP on 3T3-L1 adipose and HepG2 cells. 59 – 61 However, no previous studies have yet reported the relationships between exposure to TMPP, TiBP, and DBP and abnormal glucose metabolism. Thus, further health hazard assessments through epidemiological studies or in vivo and in vitro experiments are warranted.…”

Section: Discussionmentioning

confidence: 99%

Association between Organophosphate Ester Exposure and Insulin Resistance with Glycometabolic Disorders among Older Chinese Adults 60–69 Years of Age: Evidence from the China BAPE Study

Ding

Deng

Fang

et al. 2023

Environ Health Perspect

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Background: Organophosphate esters (OPEs) are common endocrine-disrupting chemicals, and OPE exposure may be associated with type 2 diabetes (T2D). However, greater knowledge regarding the biomolecular intermediators underlying the impact of OPEs on T2D in humans are needed to understand biological etiology. Objectives: We explored the associations between OPE exposure and glycometabolic markers among older Chinese adults 60–69 years of age to elucidate the underlying mechanisms using a multi-omics approach. Methods: This was a longitudinal panel study comprising 76 healthy participants 60–69 years of age who lived in Jinan city of northern China. The study was conducted once every month for 5 months, from September 2018 to January 2019. We measured a total of 17 OPEs in the blood, 11 OPE metabolites in urine, and 4 glycometabolic markers (fasting plasma glucose, glycated serum protein, fasting insulin, and homeostatic model assessment for insulin resistance). The blood transcriptome and serum/urine metabolome were also evaluated. The associations between individual OPEs and glycometabolic markers were explored. An adverse outcome pathway (AOP) was established to determine the biomolecules mediating the associations. Results: Exposure to five OPEs and OPE metabolites (trimethylolpropane phosphate, triphenyl phosphate, tri-iso-butyl phosphate, dibutyl phosphate, and diphenyl phosphate) was associated with increased levels of glycometabolic markers. The mixture effect analysis further indicated the adverse effect of OPE mixtures. Multi-omics analyses revealed that the endogenous changes in the transcriptional and metabolic levels were associated with OPE exposure. The putative AOPs model suggested that triggers of molecular initiation events (e.g., insulin receptor and glucose transporter type 4) with subsequent key events, including disruptions in signal transduction pathways (e.g., phosphatidylinositol 3-kinase/protein kinase B and insulin secretion signaling) and biological functions (glucose uptake and insulin secretion), may constitute the diabetogenic effects of OPEs. Discussion: OPEs are associated with the elevated risk of T2D among older Chinese adults 60–69 years of age. Implementing OPE exposure reduction strategies may help reduce the T2D burden among these individuals, if the relationship is causal. https://doi.org/10.1289/EHP11896

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“…Furthermore, OPEs can cause an inflammatory environment and oxidative stress. Higher quantities of proinflammatory cytokines have been linked to higher OPE levels ( 41 , 42 ).…”

Section: Discussionmentioning

confidence: 99%

Environmental exposure to organophosphate esters and suspected non-alcoholic fatty liver disease among US adults: A mixture analysis

Chai

Hu²,

Dai³

et al. 2022

Front. Public Health

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ObjectivesNon-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide. We evaluated NAFLD using the US FLI to determine whether there is an association between urinary organophosphorus (OPE) levels and the “prevalence” of NAFLD in US individuals.MethodsThe current study included 1,102 people aged 20 years and older with information from the 2011–2014 U.S. National Health and Nutrition Examination Survey. NAFLD was assessed using the U.S. FLI. Individual OPE metabolites and OPE combinations were linked to NAFLD using logistic regression and weighted quantile sum (WQS) regression. All analyzes were carried out separately on males and females. The possible impacts of age, serum total testosterone (TT), and menopausal state, as well as the importance of the interaction term with exposure, were investigated using stratified analysis.ResultsBis (2-chloroethyl) phosphate and bis (1,3-dichloro-2-propyl) phosphate were associated with NAFLD in all males after adjusting for covariates (P < 0.05). A combination of OPEs (OPE index) was positively linked with NAFLD in the WQS analysis of all males (odds ratio for OPE index: 1.52; 95% CI: 1.06, 2.19). Stratified analyzes for males revealed that considerable connections were largely confined to individuals over 60 years old or with low total testosterone. In women, the connection was limited and inconsistent, except for the OPE index, which was positively linked with NAFLD in post-menopausal women.ConclusionsIn this study, environmental exposure to OPE was linked to an elevated risk of NAFLD in males, particularly those over 60 years old or with low TT levels. Aside from the continuous positive connection of a combination of OPEs with NAFLD risk in post-menopausal women, these correlations were weaker in women. However, these findings should be taken with caution and verified in future investigations by collecting numerous urine samples in advance to strengthen OPE exposure estimates.

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Remodeling on adipocytic physiology of organophosphorus esters in mature adipocytes

Cited by 12 publications

References 50 publications

Chlorinated Organophosphate Flame Retardants Impair the Lung Function via the IL-6/JAK/STAT Signaling Pathway

Chlorinated Organophosphate Flame Retardants Impair the Lung Function via the IL-6/JAK/STAT Signaling Pathway

Association between Organophosphate Ester Exposure and Insulin Resistance with Glycometabolic Disorders among Older Chinese Adults 60–69 Years of Age: Evidence from the China BAPE Study

Environmental exposure to organophosphate esters and suspected non-alcoholic fatty liver disease among US adults: A mixture analysis

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