Adverse cardiovascular effects and potential molecular mechanisms of DEHP and its metabolites—A review

Wen, Zeng-Jin; Wang, Zhongyu; Zhang, Yinfeng

doi:10.1016/j.scitotenv.2022.157443

Cited by 38 publications

(15 citation statements)

References 128 publications

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“…The toxic effects of PAEs are causing increasing public concern, with several epidemiological studies revealing that PAEs can lead to oxidative stress (10)(11)(12)(13) and cardiovascular diseases (CVDs) (14)(15)(16)(17). Virani et al reported that high levels of triglycerides, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and lower levels of high-density lipoprotein cholesterol (HDL-C) are well-known CVD risk factors (18).…”

Section: Introductionmentioning

confidence: 99%

Phthalates and phthalate metabolites in urine from Tianjin and implications for platelet mitochondrial DNA methylation

Guo

Fang

et al. 2023

Front. Public Health

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BackgroundPhthalates (PAEs) are important synthetic substances in plastics, attracting much attention due to their potential effects on the cardiovascular system.MethodsIn this study, urine and blood samples from 39 individuals were collected in Tianjin, China. Phthalates and phthalate metabolites (mPAEs) were analyzed using gas chromatography-mass spectrometry (GC-MS) and high-performance liquid chromatography-mass spectrometry (HPLC-MS), respectively. The polymerase chain reaction (PCR) products from bisulfite-treated mitochondrial DNA (mtDNA) samples were analyzed using pyrosequencing technology.ResultsThe detection frequencies for 9 PAEs varied from 2.56 to 92.31%, and those for 10 mPAEs varied from 30.77 to 100%. The estimated daily intakes (EDIs) and cumulative risk of PAEs were calculated based on the experimental statistics of urinary PAEs and mPAEs. For PAEs, the HIRfD (hazard index corresponding to reference doses) values of 10.26% of participants and the HITDI (hazard index corresponding to tolerable daily intake) values of 30.77% of participants were estimated to exceed 1, suggesting a relatively high exposure risk. The mtDNA methylation levels in the MT-ATP8 and MT-ND5 were observed to be lower than in the MT-ATP6. Mono-ethyl phthalate (MEP) and MT-ATP8 were positively correlated with triglyceride levels (p < 0.05). Based on the association of PAEs, mtDNA methylation, and triglycerides, the mediating role of mtDNA methylation between PAEs and cardiovascular diseases (CVDs) was analyzed in this study, but no mediated effect was observed.ConclusionThe effects of PAE exposure on cardiovascular diseases (CVDs) should be investigated further.

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Section: Introductionmentioning

confidence: 99%

Phthalates and phthalate metabolites in urine from Tianjin and implications for platelet mitochondrial DNA methylation

Guo

Fang

et al. 2023

Front. Public Health

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“…5 Wen et al concluded that DEHP was recognized as a causative risk factor or indicator for causing and increasing cardiovascular disease (CVD). 6 DEHP exposure may impair placental development and function, as well as negatively affect fetal growth. 7 Considering the health concerns in relation to a growing number of products containing polyarylether (PAE)-derived plasticizers, it is important to evaluate the health effects of these plasticizers deeply.…”

Section: Introductionmentioning

confidence: 99%

“…), leading to several health problems . Wen et al concluded that DEHP was recognized as a causative risk factor or indicator for causing and increasing cardiovascular disease (CVD) . DEHP exposure may impair placental development and function, as well as negatively affect fetal growth .…”

Section: Introductionmentioning

confidence: 99%

Lycopene Attenuates Di(2-ethylhexyl) Phthalate-Induced Mitochondrial Damage and Inflammation in Kidney via cGAS–STING Signaling

Dai

Zhao

et al. 2022

J. Agric. Food Chem.

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Di(2-ethylhexyl) phthalate (DEHP) is a highly harmful and persistent environmental pollutant. Due to its unique chemical composition, it frequently dissolves and enters the environment to endanger human and animal health. Lycopene is a natural bioactive component that can potentially reduce the risk of environmental factor-induced chronic diseases. The present study sought to explore the role and underlying mechanism of lycopene (LYC) on DEHP-induced renal inflammatory response and apoptosis. In this study, mice were orally treated with LYC (5 mg/kg BW/day) and/or DEHP (500 or 1000 mg/kg BW/day) for 28 days. Our results indicated that LYC prevented DEHP-induced histopathological alterations and ultrastructural injuries, including decreased mitochondrial membrane potential (ΔΨm), PINK1/Parkin pathway-mediated mitophagy, and mitochondrial energetic deficit. When damaged mitochondria release mitochondrial DNA (mtDNA) into cytosol, LYC can alleviate inflammation and apoptosis caused by DEHP exposure by activating the cyclic GMP-AMP synthase-stimulator of interferon gene (cGAS–STING) signal pathway. Collectively, our data demonstrate that LYC can reduce mitophagy caused by DEHP exposure by activating the PINK1/Parkin pathway and then reduce renal inflammation and apoptosis through the cGAS–STING pathway.

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“…A study that followed 10,000 Americans for eight years found that higher levels of DEHP are associated with higher levels of infl ammation and oxidative stress [16]. DEHP metabolites that enter the body can disrupt mitochondrial function and produce excess Reactive Oxidants (ROS), reducing the activity of antioxidant enzymes, superoxide dismutase, catalase, and glutathione transferase.…”

Section: The Relationship Between Dehp and Bphmentioning

confidence: 99%

Diethylhexylphthalate-A Worthful to Pay Attention Risk Factor for Benign Prostate Hyperplasia

Tian

2022

J Biomed Res Environ Sci

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Adverse cardiovascular effects and potential molecular mechanisms of DEHP and its metabolites—A review

Cited by 38 publications

References 128 publications

Phthalates and phthalate metabolites in urine from Tianjin and implications for platelet mitochondrial DNA methylation

Phthalates and phthalate metabolites in urine from Tianjin and implications for platelet mitochondrial DNA methylation

Lycopene Attenuates Di(2-ethylhexyl) Phthalate-Induced Mitochondrial Damage and Inflammation in Kidney via cGAS–STING Signaling

Diethylhexylphthalate-A Worthful to Pay Attention Risk Factor for Benign Prostate Hyperplasia

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