Bisphenol A induces oxidative stress-associated DNA damage in INS-1 cells

Xin, Fei; Jiang, Liping; Liu, Xiaofang; Chen, Geng; Wang, Wenbin; Zhong, Laifu; Yang, Guang; Chen, Min

doi:10.1016/j.mrgentox.2014.04.019

Cited by 109 publications

(71 citation statements)

References 36 publications

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“…In our study, Cd or BPA alone treatments did not show genotoxicity and cytotoxicity, with the exception of BPA exposure at 50 μM. Our results are consistent with previous data showing that BPA exposure at 25 μM does not cause oxidative stress-associated DNA damage in INS-1 cells according to the comet assay [18]. Moreover, no significant changes in cell viability or DNA damage levels have been observed in GM00637 or HeLa S3 cells when exposed to 5 μM or 10 μM Cd [14].…”

Section: Discussionsupporting

confidence: 93%

“…Considering that oxidative stress is one of the mechanisms thought to be involved in both Cd-and BPA-induced cytotoxicity [18,29], we examined the levels of ROS in Cd-treated, BPA-treated or combined treatment groups. The results demonstrated that Cd exposure at 5 or 10 μM did not increase levels of ROS, whereas BPA treatment alone elevated ROS production only at the 50 μM dose.…”

Section: Resultsmentioning

confidence: 99%

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Cadmium Exposure Enhances Bisphenol A-Induced Genotoxicity through 8-Oxoguanine-DNA Glycosylase-1 OGG1 Inhibition in NIH3T3 Fibroblast Cells

Chen

Liu²,

Lu³

et al. 2016

Cell Physiol Biochem

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Background: Both cadmium (Cd) and bisphenol A (BPA) are commonly encountered in humans' daily activities, but their combined genotoxic effects remain unclear. Methods: In the present study, we exposed a mouse embryonic fibroblast cell line (NIH3T3) to Cd for 24 h, followed by a 24 h BPA exposure to evaluate toxicity. The cytotoxicity was evaluated by viability with CCK-8 assay and lactate dehydrogenase (LDH) release. Reactive oxygen species (ROS) production was measured by 2′,7′-dichlorofluorescein diacetate (DCFH-DA). And DNA damage was measured by 8-hydroxydeoxyguanosine (8-OHdG), phosphorylated H2AX (γH2AX) and the comet assay. The flow cytometry was used to detect cell cycle distribution, and apoptosis was determined by TUNEL assay and western blot against poly-ADP-ribose polymerase (PARP). Results: The results showed that Cd or BPA treatments alone (with the exception of BPA exposure at 50 μM) did not alter cell viability. However, pre-treatment with Cd aggravated the BPA-induced reduction in cell viability; increased BPA-induced LDH release, ROS production, DNA damage and G2 phase arrest; and elevated BPA-induced TUNEL-positive cells and the expression levels of cleaved PARP. Cd exposure concurrently decreased the expression of 8-oxoguanine-DNA glycosylase-1 (OGG1), whereas OGG1 over-expression abolished the enhancement of Cd on BPA-induced genotoxicity and cytotoxicity. Conclusion: These findings indicate that Cd exposure aggravates BPA-induced genotoxicity and cytotoxicity through OGG1 inhibition.

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Section: Discussionsupporting

confidence: 93%

Section: Resultsmentioning

confidence: 99%

Cadmium Exposure Enhances Bisphenol A-Induced Genotoxicity through 8-Oxoguanine-DNA Glycosylase-1 OGG1 Inhibition in NIH3T3 Fibroblast Cells

Chen

Liu²,

Lu³

et al. 2016

Cell Physiol Biochem

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“…Mitochondria are critical regulators of the cellular redox balance, responsible for both ROS and antioxidant production; thus perturbations to mitochondrial integrity leads to increased cellular stress. Several MDCs promote oxidative stress in β-cells, including BPA [19,29], arsenic [30,31], and diethylhexylphthalate (DEHP) [32]. For example, rat islets exposed to the phenolic compounds octylphenol, nonylphenol, and BPA exhibited disruptions in islet mitochondrial architecture with alterations in mitochondrial gene expression [19].…”

Section: Endoplasmic Reticulum and Oxidative Stress In MDC Actionmentioning

confidence: 99%

“…For example, rat islets exposed to the phenolic compounds octylphenol, nonylphenol, and BPA exhibited disruptions in islet mitochondrial architecture with alterations in mitochondrial gene expression [19]. Micromolar concentrations of BPA also induced reactive oxygen species (ROS) in INS-1 cells, causing glutathione depletion, DNA damage, and p53 induction, which was partially rescued by pretreatment with the antioxidant N-acetylcysteine (NAC) [29]. In INS-1 cells treatment with 0.25-1 μM sodium arsenite for 96 hours reduced thioredoxin reductase activity, increased pro-apoptotic gene expression, and reduced viability, possibly via a c-Jun-N-terminal kinase (JNK)-mediated pathway [31].…”

Section: Endoplasmic Reticulum and Oxidative Stress In MDC Actionmentioning

confidence: 99%

“…Where oxidative stress is implicated in MDC action, investigations into the utility of antioxidants are warranted. This approach is supported by studies showing that pre-treatment with NAC mitigates some of the β-cell toxicity induced by arsenic [30,124] and BPA [29]. As our appreciation of MDCs as metabolic risk factors increases, future work mandates investigations into the specific disease-promoting mechanisms by which these toxicants work in order to devise targeted interventions to stem the global tide of metabolic deterioration.…”

Section: Conclusion: From Mechanisms To Interventionsmentioning

confidence: 99%

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Polluted Pathways: Mechanisms of Metabolic Disruption by Endocrine Disrupting Chemicals

Mimoto

Nadal

Sargis

2017

Curr Envir Health Rpt

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Purpose of review Environmental toxicants are increasingly implicated in the global decline in metabolic health. Focusing on diabetes, herein the molecular and cellular mechanisms by which metabolism disrupting chemicals (MDCs) impair energy homeostasis are discussed. Recent findings Emerging data implicate MDC perturbations in a variety of pathways as contributors to metabolic disease pathogenesis, with effects in diverse tissues regulating fuel utilization. Potentiation of traditional metabolic risk factors, such as caloric excess, and emerging threats to metabolism, such as disruptions in circadian rhythms, are important areas of current and future MDC research. Increasing evidence also implicates deleterious effects of MDCs on metabolic programming that occur during vulnerable developmental windows, such as in utero and early post-natal life as well as pregnancy. Summary Recent insights into the mechanisms by which MDCs alter energy homeostasis will advance the field’s ability to predict interactions with classical metabolic disease risk factors and empower studies utilizing targeted therapeutics to treat MDC-mediated diabetes.

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Increased ROS levels in mitochondrial outer membrane protein Mul1‐deficient oocytes result in abnormal preimplantation embryogenesis

Nakai,

Fukushima,

Yamamoto

et al. 2024

FEBS Letters

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Reactive oxygen species (ROS) are associated with oocyte maturation inhibition, and N‐acetyl‐l‐cysteine (NAC) partially reduces their harmful effects. Mitochondrial E3 ubiquitin ligase 1 (Mul1) localizes to the mitochondrial outer membrane. We found that female Mul1‐deficient mice are infertile, and their oocytes contain high ROS concentrations. After fertilization, Mul1‐deficient embryos showed a DNA damage response (DDR) and abnormal preimplantation embryogenesis, which was rescued by NAC addition and ROS depletion. These observations clearly demonstrate that loss of Mul1 in oocytes increases ROS concentrations and triggers DDR, resulting in abnormal preimplantation embryogenesis. We conclude that manipulating the mitochondrial ROS levels in oocytes may be a potential therapeutic approach to target infertility.

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Bisphenol A induces oxidative stress-associated DNA damage in INS-1 cells

Cited by 109 publications

References 36 publications

Cadmium Exposure Enhances Bisphenol A-Induced Genotoxicity through 8-Oxoguanine-DNA Glycosylase-1 OGG1 Inhibition in NIH3T3 Fibroblast Cells

Cadmium Exposure Enhances Bisphenol A-Induced Genotoxicity through 8-Oxoguanine-DNA Glycosylase-1 OGG1 Inhibition in NIH3T3 Fibroblast Cells

Polluted Pathways: Mechanisms of Metabolic Disruption by Endocrine Disrupting Chemicals

Increased ROS levels in mitochondrial outer membrane protein Mul1‐deficient oocytes result in abnormal preimplantation embryogenesis

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