The apoptotic pathways effect of fine particulate from cooking oil fumes in primary fetal alveolar type II epithelial cells

Che, Zhen; Liu, Ying; Chen, Yanyan; Cao, Jiyu; Liang, Chunmei; Wang, Lei; Ding, Rui

doi:10.1016/j.mrgentox.2014.01.004

Cited by 20 publications

(6 citation statements)

References 58 publications

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“…Elevated p-ERK/ERK ratios in the MAPK pathway indicated that increased concentrations of PM 2.5 can lead to lung inflammation. Additionally, IHC results indicated that PM 2.5 upregulated the expression of the pro-apoptotic protein, Bax, and downregulated the accumulation of the anti-apoptotic protein, Bcl-2, which eventually lead to enhanced expression of apoptosis proteins caspase-8 and caspase-3 (40).…”

Section: Discussionmentioning

confidence: 98%

Potential hazardous effects of printing room PM2.5 exposure include promotion of lung inflammation and subsequent injury

et al. 2020

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There have been few studies investigating the potential effects of indoor sources of particulate matter on human health. in this study, the effect of different concentrations of fine particulate matter (PM 2.5) collected from a printing room on lung health was examined using cultured cells and a mouse model. Further, the mechanism of lung injury was examined. The results indicated that PM 2.5 significantly enhanced malondialdehyde activity (P<0.05), decreased superoxide dismutase activity (P<0.05), upregulated the expression of pro-inflammatory factors including interleukin (IL)-1β, tumor necrosis factor-, il-6 and downregulated the expression of the inflammatory factor IL-2 (P<0.05). Western blot analysis indicated that PM 2.5 significantly enhanced expression of phosphorylated (p)-ERK relative to total ERK, cyclooxygenase-2, p-anti-nuclear-factor-κB (p-NF-κB) relative to nF-κB, transforming growth factor-β1 and Bax relative to Bcl-2 in inflammation (P<0.05), fibrosis and apoptosis signaling pathways. Furthermore, the results revealed that exposure was associated with an increased abundance of pathogens including Burkholderiales, Coriobacteriia, and Betaproteobacteria in in the lungs. in conclusion, exposure to PM 2.5 from a printing room significantly increased inflammation, fibrosis, apoptosis and the abundance of pathogenic bacteria, indicating that exposure is potential threat to individuals who spend a significant amount of time in printing rooms.

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Section: Discussionmentioning

confidence: 98%

Potential hazardous effects of printing room PM2.5 exposure include promotion of lung inflammation and subsequent injury

et al. 2020

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“…Che et al [42] also demonstrated exposure to CFs might lead to mitochondrial and death receptor pathways in AEC II cells, which would finally lead to apoptosis. Exposure to cooking oil fumes might increase the risk of lung adenocarcinoma in Chinese nonsmoking females (adjusted OR=1.58, 95%CI=1.11-2.25, P=0.011).…”

Section: B Cooking Fumes Effects On the Cellmentioning

confidence: 99%

Cooking Fumes and Relative Diseases

Wang¹,

Liu²,

He³

2017

Proceedings of the 2016 International Conference on Biological Engineering and Pharmacy (BEP 2016)

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Abstract-Cooking fumes are mixture of various toxic components such as aldehydes, heterocyclic amines (HCAs), polycyclic aromatic hydrocarbons (PAHs), fat aerosols and particulate matters (PM), which are mainly produced during or after cooking. Due to the toxic contents of CFs, CFs might cause lung toxicity, immune toxicity, hereditary toxicity, potential carcinogenicity and so on to organism. There were several studies investigated the toxicity impact of CFs. However, comprehensive review about the production, composition harm to the contacts and reduction methods of CFs is still lacking. In this review, the production, composition and effects on the contacts of cooking fumes were presented. In addition, reduction methods of cooking fumes were also presented. This review would provide references for the avoidance of CFs relative disease and the comprehensive disposal of CFs.

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“…directed through influence outside of the cells and the tissues; the second one is intrinsic and involves mitochondria; and the third one is intrinsic as well, predicated on cellular stressors that affect the endoplasmic reticulum (ER). Using primary fetal alveolar cells, Che et al (2014) [57] demonstrated that exposure of these cells to fine particulate matter, contained in cooking oil fumes, can upregulate pro-apoptotic signaling mediators and downregulate anti-apoptotic ones. Specifically, the extrinsic death receptor pathway and the intrinsic mitochondrial pathways were activated [57].…”

Section: Biological Plausibilitymentioning

confidence: 99%

“…Using primary fetal alveolar cells, Che et al (2014) [57] demonstrated that exposure of these cells to fine particulate matter, contained in cooking oil fumes, can upregulate pro-apoptotic signaling mediators and downregulate anti-apoptotic ones. Specifically, the extrinsic death receptor pathway and the intrinsic mitochondrial pathways were activated [57]. In another study, cultured rat embryos experienced growth retardation when exposed to PM2.5.…”

Section: Biological Plausibilitymentioning

confidence: 99%

Effects of Air Pollution on the Risk of Low Birth Weight in a Cold Climate

Balogun¹,

Rantala²,

Antikainen³

et al. 2020

Preprint

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There is accumulating evidence that prenatal exposure to air pollution disturbs fetal growth and development, but little is known about these effects in cold climates or their season-specific or joint effects. Our objective was to assess independent and joint effects of prenatal exposure to specific air pollutants on the risk of low birth weight (LBW). We utilized the 2568 children of the Espoo Cohort Study, born between 1984 and 1990, and living in the City of Espoo. We conducted stratified analyses for births during warm and cold seasons separately. We analyzed the effect estimates using multi-pollutant Poisson regression models with risk ratio (RR) as the measure of effect. The risk of LBW was related to exposure to CO and (adjusted RR 1.44, 95% CI: 1.04-2.00) and exposure to O3 in the spring-summer season (1.82, 1.11-2.96). There was also evidence of synergistic effects between CO and O3 (relative risk due to interaction, RERI, all year 1.08, 95% CI: 0.27-4.94, spring-summer 3.97, 2.17-25.85) and PM2.5 and O3 (all year 0.72, -0.07-3.60, spring-summer 2.80, 1.36-19.88). We present new evidence of both independent and joint effects of prenatal exposure in a cold climate on the risk of LBW at low levels of air pollution.

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The apoptotic pathways effect of fine particulate from cooking oil fumes in primary fetal alveolar type II epithelial cells

Cited by 20 publications

References 58 publications

Potential hazardous effects of printing room PM2.5 exposure include promotion of lung inflammation and subsequent injury

Potential hazardous effects of printing room PM2.5 exposure include promotion of lung inflammation and subsequent injury

Cooking Fumes and Relative Diseases

Effects of Air Pollution on the Risk of Low Birth Weight in a Cold Climate

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