Oxidative Stress, Unfolded Protein Response, and Apoptosis in Developmental Toxicity

Kupsco, Allison; Schlenk, Daniel

doi:10.1016/bs.ircmb.2015.02.002

Cited by 81 publications

(57 citation statements)

References 312 publications

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“…Oxidative stress caused by reactive oxygen species (ROS) is an important part of cell apoptosis (29,30). Previous studies have demonstrated that oxidative stress injury is activated in vitiligo (25,31).…”

Section: Discussionmentioning

confidence: 99%

PM2.5 induces apoptosis, oxidative stress injury and melanin metabolic disorder in human melanocytes

et al. 2020

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Recent growing evidence suggested that particulate matter 2.5 (PM2.5) has strong toxic effects on skin systems. However, the possible effects and the mechanisms of PM2.5 on vitiligo remain poorly understood. Therefore, the present study aimed to further investigate the effects and possible mechanisms of PM2.5 on vitiligo. Human keratinocytes (HaCaT cells) and human melanocytes (PIG1 cells and PIG3V cells) were exposed to PM2.5 (0-200 µg/ml) for 24 h. The cell viability of the three cell lines was measured by a Cell Counting Kit-8 assay. The secretions of stem cell factor (SCF) and basic fibroblast growth factor (bFGF) in HaCaT cells were evaluated by ELISA. The melanin contents, cellular tyrosinase activity, apoptosis, cell migration, malondialdehyde (MDA) contents, superoxide dismutase (SOD) levels, glutathione peroxidase (GSH-Px) levels and related protein expressions in PIG1 cells and PIG3V cells were evaluated by a NaOH assay, DOPA assay, Annexin V-FITC/Propidium Iodide staining, MDA assay, SOD assay, GSH-Px assay and western blotting, respectively. It was demonstrated that PM2.5 exposure inhibited cell viability of all three cell lines (HaCaT, PIG1 and PIG3V cells). PM2.5 exposure attenuated the secretions of SCF and bFGF in HaCaT cells. Moreover, PM2.5 exposure attenuated the activation of tyrosinase and melanogenesis, inhibited cell migration, and induced apoptosis and oxidative stress injury in PIG1 cells and PIG3V cells. In addition, PM2.5 exposure caused upregulated cytosolic cytochrome C and activated caspase-3 in PIG1 cells and PIG3V cells. Furthermore, PM2.5 exposure activated the nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 signaling pathway. The present results suggested that PM2.5 exposure could inhibit the secretions of SCF and bFGF in keratinocytes, and cause oxidative stress injury and melanin metabolic disorder in melanocytes. Therefore, PM2.5 could be a new risk factor for vitiligo. PM2.5 induces apoptosis, oxidative stress injury and melanin metabolic disorder in human melanocytes

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Section: Discussionmentioning

confidence: 99%

PM2.5 induces apoptosis, oxidative stress injury and melanin metabolic disorder in human melanocytes

et al. 2020

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“…ERS and oxidative stress are closely related in many physiological and pathological conditions (21). Protein misfolding in ERS conditions results in reactive oxygen species production, and oxidative stress disturbs the ER redox state and promotes protein misfolding (22). Therefore, the authors hypothesized that ERS may also play an important role in the harmful effects of IS.…”

Section: Discussionmentioning

confidence: 99%

Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity

et al. 2018

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“…These reactive oxygen species can cause DNA strand breakage or fragmentation leading to cell mutation. The importance of oxidative stress as a mechanism of teratogenesis is suggested by several animal studies (Kupsco et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Maternal exposure to ozone and PM2.5 and the prevalence of orofacial clefts in four U.S. states

Zhou*¹,

Gilboa²,

Herdt³

et al. 2016

ISEE Conference Abstracts

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Background-While there is some evidence that maternal exposure to ambient air pollution is associated with orofacial clefts in offspring, the epidemiologic studies have been largely equivocal. We evaluated whether maternal exposure to elevated county-level ambient fine particulate matter with aerodynamic diameter ≤2.5 μm (PM 2.5 ) and ozone during early gestation was associated with a higher prevalence of orofacial clefts. * Corresponding author. yzhou2@cdc.gov (Y. Zhou). New York City), and Texas. The air pollution exposure assessment for gestational weeks 5-10 was based on county-level average concentrations of PM 2.5 and ozone data generated using a Bayesian fusion model available through CDC's Environmental Public Health Tracking Network. Two outcomes were analyzed separately: cleft lip with or without cleft palate, cleft palate alone. In logistic regression analyses, we adjusted for factors that were suspected confounders or modifiers of the association between the prevalence of orofacial clefts and air pollution, i.e., infant sex, race-ethnicity, maternal education, smoking status during pregnancy, whether this was mother's first baby, maternal age.Results-Each 10 μg/m 3 increase in PM 2.5 concentration was significantly associated with cleft palate alone (OR =1.43, 95% CI: 1.11-1.86). There was no significant association between PM 2.5 concentration and cleft lip with or without cleft palate. No associations were observed between ozone exposure and the two outcomes of orofacial clefts.Conclusions-Our study suggests that PM 2.5 significantly increased the risk of cleft palate alone, but did not change the incidence of cleft lip with or without palate. Ozone levels did not correlate with incidence of orofacial clefts.

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Oxidative Stress, Unfolded Protein Response, and Apoptosis in Developmental Toxicity

Cited by 81 publications

References 312 publications

PM2.5 induces apoptosis, oxidative stress injury and melanin metabolic disorder in human melanocytes

PM2.5 induces apoptosis, oxidative stress injury and melanin metabolic disorder in human melanocytes

Endoplasmic reticulum stress associated apoptosis as a novel mechanism in indoxyl sulfate‑induced cardiomyocyte toxicity

Maternal exposure to ozone and PM2.5 and the prevalence of orofacial clefts in four U.S. states

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