The role of oxidative stress in DNA damage in pancreatic β cells induced by di-(2-ethylhexyl) phthalate

She, Yan; Jiang, Liping; Zheng, Lulin; Zuo, Heming; Chen, Min; Sun, Xiance; Li, Qiujuan; Chen, Geng; Yang, Guang; Jiang, Lijie; Liu, Xiaofang

doi:10.1016/j.cbi.2017.01.015

Cited by 47 publications

(38 citation statements)

References 49 publications

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“…Indeed, several compounds have been shown to increase oxidative stress in cell lines and animal models. These compounds include cadmium [65], lead [66], mercury [67–69], bisphenol A [64], diethylhexyl phthalate [70, 71], perfluorooctanoic acid [72], and tributyl tin [73]. Expression of proteins regulating oxidative stress was also shown to be modulated by polychlorinated biphenyl exposure [74].…”

Section: Broader Implications For Metabolic Toxicitymentioning

confidence: 99%

Environmental toxicant exposures and type 2 diabetes mellitus: Two interrelated public health problems on the rise

Bonini¹,

Sargis²

2018

Current Opinion in Toxicology

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Rates of type 2 diabetes mellitus (T2DM) are rising rapidly across the globe and the impact of this devastating disease threatens to plague the 21 century. While some contributing factors are well-recognized (e.g. sedentary lifestyles and caloric excess), others diabetes-promoting risk factors are less established or poorly appreciated. The latter category includes environmental exposures to diabetogenic contaminants. Herein we review some of the latest concepts and mechanisms by which environmental exposures may contribute to rising rates of T2DM with a particular focus on mechanisms involving mitochondrial dysfunction and imbalances in reactive oxygen species (ROS). Furthermore, while the pathogenesis of diabetes includes impairments in insulin sensitivity as well as insulin secretion, we will specifically delve into the links between environmental exposures to toxicants such as arsenic and disruptions in insulin release from pancreatic β-cells. Since β-cell death or dysfunction lies at the heart of both T2DM as well as type 1 diabetes mellitus (T1DM), environmental endocrine disrupting chemicals (EDCs) that disrupt the production or regulated release of the glucose-lowering hormone insulin are likely contributors to diabetes risk. Importantly, understanding the contribution of toxicants to diabetes risk as well as improved understanding of their mechanisms of action offer unique opportunities to modulate diabetes risk via targeted therapeutics or public policy interventions to reduce and remediate exposures.

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Section: Broader Implications For Metabolic Toxicitymentioning

confidence: 99%

Environmental toxicant exposures and type 2 diabetes mellitus: Two interrelated public health problems on the rise

Bonini¹,

Sargis²

2018

Current Opinion in Toxicology

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Section: Introductionmentioning

confidence: 99%

“…Previous researches have demonstrated, in vitro and in vivo, that DEHP induces cytotoxicity through reactive oxygen species (ROS) generation leading to lipid peroxidation, DNA damage, decrease in the GSH, and significant increase in the activities of superoxide dismutase (SOD), catalase (CAT), and GPx. [13][14][15][16] To reduce ROS formation or to detoxify ROS, physiological systems have involved several adaptive mechanisms that employed antioxidant enzymes or antioxidant compounds. 17 The master cellular sensor for oxidative stress is the nuclear factor (erythroid-derived 2)like 2 (Nrf2).…”

Section: Introductionmentioning

confidence: 99%

Di (2‐ethylhexyl) phthalate induces cytotoxicity in HEK‐293 cell line, implication of the Nrf‐2/HO‐1 antioxidant pathway

Amara

Timoumi

Graiet

et al. 2019

Environmental Toxicology

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The di (2‐ethylhexyl) phthalate (DEHP) is a plasticizer used in the polyvinyl chloride industry. Human exposure to this plasticizer is inevitable and contributes to several side effects. In this study, we examined whether DEHP induces apoptosis and oxidative stress in embryonic kidney cells (HEK‐293) and whether the nuclear factor E2‐related factor 2 (Nrf‐2)/heme oxygenase‐1 (HO‐1) antioxidant pathway is involved in the pathogenesis of this process. We demonstrated that DEHP is cytotoxic to HEK‐293 cells. It causes oxidative damage through the generation of free radicals, induces lipid peroxidation, and alters superoxide dismutase and catalase activities. Simultaneously, DEHP treatment decreases the expression and the protein level of Nrf‐2 and HO‐1. Inhibition of the Nrf‐2/HO‐1 pathway is related to the mitochondrial pathway of apoptosis. This apoptotic process is characterized by a loss of mitochondrial transmembrane potential (ΔΨm) and upregulation of the expression of caspase‐3 mRNA as well as its protein level.

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“…People with high insulin resistance indices along with altered metabolism are highly sensitive to DEHP exposure [32]. Evidences from various studies confirmed that DEHP cause pancreatic dysfunction through the induction of oxidative stress (MDA); alterations in the enzymatic and non-enzymatic antioxidant defense (SOD, catalase, and glutathione peroxidase) accompanied by elevated ROS production and DNA damages in the pancreatic tissue [33][34][35]. Our results showed high levels of lipid peroxidation and significant decrease in enzymatic antioxidant levels in the DEHP-exposed RIN-5F cell line.…”

Section: Resultsmentioning

confidence: 99%

Antidiabetic Activity of Gold Nanoparticles Synthesized Using Wedelolactone in RIN-5F Cell Line

et al. 2019

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We synthesized the gold nanoparticles (AuNPs) using wedelolactone (WDL) and characterized them using UV-visible spectroscopy, fourier transform infrared spectroscopy (FTIR), X-ray diffraction (XRD), scanning electron microscopic (SEM), transmission electron microscopic (TEM), energy dispersive X-ray diffraction, and atomic force microscopic (AFM) studies. The electronic spectrum exhibited an absorption peak at 535 nm. The FT-IR results proved that WDL was stabilized on the surface of AuNPs by acting as a capping or reducing agent. The crystalline structure was affirmed by XRD pattern and the spherical shape of WDL-AuNPs was evidenced by SEM, TEM, and AFM. The synthesized WDL-AuNPS were evaluated for anti-diabetic activity in pancreatic RIN-5F cell lines. In vitro results showed that WDL-AuNPs did not only improve the insulin secretion affected by di-(2-ethylhexyl) phthalate (DEHP), but also the cell viability in RIN5F cells. WDL-AuNPs treatment modulates the pro-apoptotic proteins and anti-apoptotic proteins expression to prevent the cells undergoing apoptosis in DEHP-exposed RIN-5F cells. The exposure of DEHP causes an increase in ROS production and lipid peroxidation levels. The free radical scavenging and antioxidant properties of WDL-AuNPs increase the deleterious effect caused by DEHP. On the other side, WDL-AuNPs increase mRNA expressions of insulin-signaling proteins in RIN-5F cells. This study concludes that WDL-AuNPs can be successfully used to regulate the expression of Bcl-2 family proteins, reduce lipid peroxidation, and to improve the secretion of antioxidants and insulin through the GLUT2 pathway in RIN-5F cell lines.

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The role of oxidative stress in DNA damage in pancreatic β cells induced by di-(2-ethylhexyl) phthalate

Cited by 47 publications

References 49 publications

Environmental toxicant exposures and type 2 diabetes mellitus: Two interrelated public health problems on the rise

Environmental toxicant exposures and type 2 diabetes mellitus: Two interrelated public health problems on the rise

Di (2‐ethylhexyl) phthalate induces cytotoxicity in HEK‐293 cell line, implication of the Nrf‐2/HO‐1 antioxidant pathway

Antidiabetic Activity of Gold Nanoparticles Synthesized Using Wedelolactone in RIN-5F Cell Line

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