Cytotoxicity induced by fine particulate matter (PM2.5) via mitochondria-mediated apoptosis pathway in human cardiomyocytes.
TL;DR: It is demonstrated that mitochondria-mediated apoptosis pathway played a critical role in PM2.5-induced myocardial cytotoxicity in AC16, which suggested that PM1.7-induced cardiac dysfunction may contribute to cardiac dysfunction.
About: This article is published in Ecotoxicology and Environmental Safety.The article was published on 2018-10-15. It has received 69 citations till now. The article focuses on the topics: Reactive oxygen species & Superoxide dismutase.
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TL;DR: The epidemiological evidence for the cardiovascular effects of PM exposure is reviewed and current understanding about the biological mechanisms, by which PM exerts toxic effects on cardiovascular system to induce cardiovascular disease are discussed.
Abstract: Air pollution is a complex mixture of gaseous and particulate components, each of which has detrimental effects on human health. While the composition of air pollution varies greatly depending on the source, studies from across the world have consistently shown that air pollution is an important modifiable risk factor for significantly increased morbidity and mortality. Moreover, clinical studies have generally shown a greater impact of particulate matter (PM) air pollution on health than the gaseous components. PM has wide-ranging deleterious effects on human health, particularly on the cardiovascular system. Both acute and chronic exposure to PM air pollution is associated with increased risk of death from cardiovascular diseases including ischemic heart disease, heart failure, and ischemic/thrombotic stroke. Particulate matter has also been shown to be an important endocrine disrupter, contributing to the development of metabolic diseases such as obesity and diabetes mellitus, which themselves are risk factors for cardiovascular disease. While the epidemiological evidence for the deleterious effects of PM air pollution on health is increasingly accepted, newer studies are shedding light on the mechanisms by which PM exerts its toxic effects. A greater understanding of how PM exerts toxic effects on human health is required in order to prevent and minimize the deleterious health effects of this ubiquitous environmental hazard. Air pollution is a growing public health problem and mortality due to air pollution is expected to double by 2050. Here, we review the epidemiological evidence for the cardiovascular effects of PM exposure and discuss current understanding about the biological mechanisms, by which PM exerts toxic effects on cardiovascular system to induce cardiovascular disease.
325 citations
TL;DR: Results firstly revealed PM2.5 induced apoptosis in lung epithelial cells through a ROS-DRP1-mitochodrial fission axis-mediated mitochondrial apoptotic pathway, ultimately contributing to the onset and development of pulmonary diseases.
57 citations
TL;DR: It is suggested that the AD RB2 demethylation or ADRB2/β2AR activation may serve as a potential pathway to prevent cardiac dysfunction induced by PM2.5 exposure.
57 citations
Cites background or methods from "Cytotoxicity induced by fine partic..."
...%) in Tris-buffered saline (TBS) for a period of 1 h, then PVDF membranes was incubated using primary antibody (#4247 for PI3k 110α, #2870s for Bcl-2, #5023s for BAX, #9272s for AKT, #4060s for p-AKT, CST; ab182136 for β2AR,abcam; NB200-103 for p53, NOVUS) at 4 °C overnight, washed three times using TBST (10min each time), and incubated with anti-mouse or anti-rabbit Ig G secondary antibody (CST, USA) for 1 h at room temperature....
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...Compared with pEGFP-con group, relative protein expression in hADRB2 have no change, but PI3K/Bcl-2/BAX expression in PM2....
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...The protein expression levels of β2AR, PI3K, Akt, p-Akt, p53, Bcl-2, BAX were detected by western blot to analyze impact of PM2....
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...Compared with pEGFP-con group, relative mRNA expression in hADRB2 have no change, but PI3K/Bcl-2/BAX expression in PM2....
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...5-induced down-regulation of Bcl-2 and up-regulation of BAX (Yang et al., 2018)....
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TL;DR: Investigation of the toxic effects and possible mechanism of PM2.5 on the formation of macrophage foam cells induced by oxidized low density lipoprotein showed that it induced cytotoxicity by decreasing the cell viability and increasing the LDH level in macrophages foam cells, suggesting that PM 2.5 was a risk factor of atherosclerosis progression.
56 citations
TL;DR: Findings demonstrated PM2.5 might induce apoptosis via the mitochondrial apoptosis pathway through causing DNA damage resulting from oxidative stress, and finally caused spermatogenesis disorder.
44 citations
References
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TL;DR: Attention is focussed on the ROS/RNS-linked pathogenesis of cancer, cardiovascular disease, atherosclerosis, hypertension, ischemia/reperfusion injury, diabetes mellitus, neurodegenerative diseases, rheumatoid arthritis, and ageing.
12,240 citations
Icahn School of Medicine at Mount Sinai1, Pure Earth2, World Bank3, University of Arizona4, McGill University5, Indian Ministry of Environment and Forests6, Qatar Airways7, University of Health Sciences Antigua8, Ludwig Maximilian University of Munich9, Johns Hopkins University10, Boston College11, Chulabhorn Research Institute12, University of Maryland, College Park13, University of Ghana14, Centro Nacional de Investigaciones Cardiovasculares15, University of Chicago16, University of London17, University of Oxford18, Indian Institute of Technology Delhi19, Simon Fraser University20, Consortium of Universities for Global Health21, University of Ottawa22, Columbia University23, Stockholm Resilience Centre24, Massachusetts Institute of Technology25, University of Queensland26, University of California, Berkeley27, New York University28, National Institutes of Health29, Public Health Research Institute30, United Nations Industrial Development Organization31, Renmin University of China32
TL;DR: This book is dedicated to the memory of those who have served in the armed forces and their families during the conflicts of the twentieth century.
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TL;DR: The role of important factors such as solution ionic strength, pH, and particle surface chemistry that control nanoparticle dispersion was examined in this article, where the size and zeta potential of four TiO2 and three quantum dot samples dispersed in different solutions (including one physiological medium) were characterized.
Abstract: Characterizing the state of nanoparticles (such as size, surface charge, and degree of agglomeration) in aqueous suspensions and understanding the parameters that affect this state are imperative for toxicity investigations. In this study, the role of important factors such as solution ionic strength, pH, and particle surface chemistry that control nanoparticle dispersion was examined. The size and zeta potential of four TiO2 and three quantum dot samples dispersed in different solutions (including one physiological medium) were characterized. For 15 nm TiO2 dispersions, the increase of ionic strength from 0.001 M to 0.1 M led to a 50-fold increase in the hydrodynamic diameter, and the variation of pH resulted in significant change of particle surface charge and the hydrodynamic size. It was shown that both adsorbing multiply charged ions (e.g., pyrophosphate ions) onto the TiO2 nanoparticle surface and coating quantum dot nanocrystals with polymers (e.g., polyethylene glycol) suppressed agglomeration and stabilized the dispersions. DLVO theory was used to qualitatively understand nanoparticle dispersion stability. A methodology using different ultrasonication techniques (bath and probe) was developed to distinguish agglomerates from aggregates (strong bonds), and to estimate the extent of particle agglomeration. Probe ultrasonication performed better than bath ultrasonication in dispersing TiO2 agglomerates when the stabilizing agent sodium pyrophosphate was used. Commercially available Degussa P25 and in-house synthesized TiO2 nanoparticles were used to demonstrate identification of aggregated and agglomerated samples.
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TL;DR: Different sensitivity was observed for each assay with the neutral red and the MTT assay being the most sensitive in detecting cytotoxic events compared to the LDH leakage and the protein assay.
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TL;DR: A robust approach is described that couples chromatin immunoprecipitation (ChIP) with the paired-end ditag (PET) sequencing strategy for unbiased and precise global localization of transcription-factor binding sites (TFBS).
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