Water soluble and insoluble components of PM2.5 and their functional cardiotoxicities on neonatal rat cardiomyocytes in vitro

Qi, Zenghua; Song, Yuanyuan; Ding, Qianqian; Liao, Xiaoliang; Li, Ruijin; Liu, Guoguang; Tsang, Suk Ying; Cai, Zongwei

doi:10.1016/j.ecoenv.2018.10.107

Cited by 50 publications

(21 citation statements)

References 46 publications

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“…Particulate matter shows oxidative potential, and many studies note that exposure to the constituents of PM 2.5 or PM 0.1 has deleterious effects on the liver via reactive oxygen species (ROS) production 51 ; black carbon nanoparticles 52,53 , graphene oxide 54 , TiO nanoparticles 55 , nickel 56 and even the PM 2.5 mixture 57,58 , have been shown to promote liver damage via ROS. In addition, previous studies showed that acute exposure to PM 2.5 increased ROS in cells and decreased levels of GSH in the liver with similar results obtained for chronic exposure 33,59,60 . Therefore, our studies support compromised GSH synthesis as potentially an additional mechanism for the increase in oxidative stress following chronic exposure to PM 2.5 .…”

Section: Discussionsupporting

confidence: 77%

Air pollution-derived particulate matter dysregulates hepatic Krebs cycle, glucose and lipid metabolism in mice

Reyes-Caballero

Rao

Sun

et al. 2019

Sci Rep

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Exposure to ambient air particulate matter (PM2.5) is well established as a risk factor for cardiovascular and pulmonary disease. Both epidemiologic and controlled exposure studies in humans and animals have demonstrated an association between air pollution exposure and metabolic disorders such as diabetes. Given the central role of the liver in peripheral glucose homeostasis, we exposed mice to filtered air or PM2.5 for 16 weeks and examined its effect on hepatic metabolic pathways using stable isotope resolved metabolomics (SIRM) following a bolus of 13C6-glucose. Livers were analyzed for the incorporation of 13C into different metabolic pools by IC-FTMS or GC-MS. The relative abundance of 13C-glycolytic intermediates was reduced, suggesting attenuated glycolysis, a feature found in diabetes. Decreased 13C-Krebs cycle intermediates suggested that PM2.5 exposure led to a reduction in the Krebs cycle capacity. In contrast to decreased glycolysis, we observed an increase in the oxidative branch of the pentose phosphate pathway and 13C incorporations suggestive of enhanced capacity for the de novo synthesis of fatty acids. To our knowledge, this is one of the first studies to examine 13C6-glucose utilization in the liver following PM2.5 exposure, prior to the onset of insulin resistance (IR).

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Section: Discussionsupporting

confidence: 77%

Air pollution-derived particulate matter dysregulates hepatic Krebs cycle, glucose and lipid metabolism in mice

Reyes-Caballero

Rao

Sun

et al. 2019

Sci Rep

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“…This will subsequently modify the ionic conformation of the active site of the enzyme, thereby reducing the activity of soil enzymes [17]. Furthermore, these WSII-PM 2.5 may also inhibit microbial activity through cytotoxicity [46][47][48]. For example, among the multiple chemical components in WSII-PM 2.5 , one of the primary components is SO 4 2-, which contains the sulfur necessary for specific amino-acids (e.g., methionine and cysteine) that participate in the biosynthesis of proteins in organisms [49].…”

Section: Discussionmentioning

confidence: 99%

The Impact of Water-Soluble Inorganic Ions in Particulate Matter (PM2.5) on Litter Decomposition in Chinese Subtropical Forests

et al. 2020

Forests

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Although numerous studies have demonstrated the toxic effects of fine particulates less than 2.5 µm (PM2.5) on the health of humans, little information is available on the ecotoxicity of PM2.5. Water-soluble inorganic ions (WSII, including Na+, NH4+, K+, Mg2+, Ca2+, Cl−, NO3−, and SO42−) can compose more than 60% of PM2.5. To better understand the possible impacts of WSII-PM2.5 on leaf litter decomposition, we conducted an experiment in which two leaf litters from oak (Quercus variabilis) and pine (Pinus massoniana) dominant forests in subtropical China were incubated in microcosms containing their respective forest soils and treated with WSII-PM2.5. Our results showed that, after six-months of decomposition, the WSII-PM2.5 treatments inhibited leaf litter decomposition rates, carbon and nitrogen loss, microbial biomass, and enzyme activities in the two forests. In addition, higher WSII-PM2.5 concentration led to stronger negative effects. Comparative analysis showed that the negative effects of WSII-PM2.5 on oak forest were greater than on pine forest, relating to the higher susceptibility to changes of soil microenvironment in oak forests. WSII-PM2.5 may influence decomposition through soil acidification and salinization, which could also cause a sub-lethal depression in soil isopod activity. However, in the first month of decomposition, mass loss of the oak and pine leaf litters under the low concentration WSII-PM2.5 were 21.63% and 35.64% higher than that under the control, respectively. This suggests that transitory low concentrations of WSII-PM2.5 have a promoting effect on decomposition. Long-term PM2.5 exposure, therefore, may have profound ecosystem consequences by altering the balance of ecosystem carbon flux, nutrient cycling, and humus formation in the future.

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“…Long-term exposure to PM2.5 (the air polluted particles with a diameter less than 2.5 μm) affects the health of billions of people around the world [1], many of whom, especially the people in developing countries, are in very dangerous concentrations of PM2.5 [2]. Although PM2.5 exposure have been confirmed to play crucial roles in promoting respiratory and cardiovescular diseases [3][4][5][6][7], neurodegenerative diseases, like AD, are attracting more and more researchers' attention [8][9][10][11]. Numerous epidemiological and toxicology studies recently demonstrated that PM2.5 can cross the Blood Brain Barrier (BBB) and bring about abnormal expression and deposition of Aβ proteins, neuronal damage, chronic inflammation and even AD-like changes [8] in the brain [12][13][14].…”

Section: Introductionmentioning

confidence: 99%

PM2.5 can Promote the Alzheimer's Disease-like Changes through Microglia Related Mechanism in Mice

Wang

et al. 2020

Preprint

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Background: PM2.5, the main particulate air pollutant, poses serious hazard to human health. Alzheimer's disease (AD) is a major neurodegenerative disease characterized by amyloid plaques and neurofibrillary tangles. Recent studies reported that PM could promote AD-like pathologies in human brain. However, the mechanism of PM2.5-induced AD-like changes is still unclear and more investigations are needed for further understanding.Methods: In this study, we established experimental model of long-term PM2.5 exposure with young/old wildtype C57BL/6 and APP/PS transgenic mice. Behavior assessments were monitored after four weeks of exposure. The changes of blood cells were detected by Complete Blood Count and splenic macrophages were detected by flow cytometry. Immunohistochemical staining was used to observe the damage of PM2.5 on neurons, the deposition of Aβ and the changes of microglia. RNA-seq was used to analyze the whole genome changes of hippocampus after PM2.5 exposure. In addition, microglia related genes were analyzed via Real-time PCR. Results: After mice were exposed to PM2.5 for a month, some AD-like behavioral changes, such as learning and memory impairment were detected especially in old and transgenic mice. The histopathological changes, such as β-amyloid (Aβ) deposition, morphological changes of microglia, as well as great impairments of hippocampus neurons but not cortex neurons were observed. The analyze of whole-genome expression in the hippocampus suggested long term PM2.5 exposure changed the expression of genes related with AD process (mouse behavior and microglia differentiation). Furthermore, the mRNA level, which related to microglia, of CD86, CD22, IL-1β was upregulated and CD206, TREM2, TGF-β2 was downregulated. Conclusions: Aged population were more susceptible to long-term PM2.5 exposure and PM2.5 could promote AD-like phenotype through microglia related mechanism.

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Water soluble and insoluble components of PM2.5 and their functional cardiotoxicities on neonatal rat cardiomyocytes in vitro

Cited by 50 publications

References 46 publications

Air pollution-derived particulate matter dysregulates hepatic Krebs cycle, glucose and lipid metabolism in mice

Air pollution-derived particulate matter dysregulates hepatic Krebs cycle, glucose and lipid metabolism in mice

The Impact of Water-Soluble Inorganic Ions in Particulate Matter (PM2.5) on Litter Decomposition in Chinese Subtropical Forests

PM2.5 can Promote the Alzheimer's Disease-like Changes through Microglia Related Mechanism in Mice

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