Dataset Information

Phosphocholine-induced energy source shift alleviates mitochondrial dysfunction in lung cells caused by geospecific PM_2.5 components.

ABSTRACT: Fine particulate matter (PM_2.5) is globally recognized for its adverse implications on human health. Yet, remain limited the individual contribution of particular PM_2.5 components to its toxicity, especially considering regional disparities. Moreover, prevention solutions for PM_2.5-associated health effects are scarce. In the present study, we comprehensively characterized and compared the primary PM_2.5 constituents and their altered metabolites from two locations: Taiyuan and Guangzhou. Analysis of year-long PM_2.5 samples revealed 84 major components, encompassing organic carbon, elemental carbon, ions, metals, and organic chemicals. PM_2.5 from Taiyuan exhibited higher contamination, associated health risks, dithiothreitol activity, and cytotoxicities than Guangzhou's counterpart. Applying metabolomics, BEAS-2B lung cells exposed to PM_2.5 from both cities were screened for significant alterations. A correlation analysis revealed the metabolites altered by PM_2.5 and the critical toxic PM_2.5 components in both regions. Among the PM_2.5-down-regulated metabolites, phosphocholine emerged as a promising intervention for PM_2.5 cytotoxicities. Its supplementation effectively attenuated PM_2.5-induced energy metabolism disorder and cell death via activating fatty acid oxidation and inhibiting Phospho1 expression. The highlighted toxic chemicals displayed combined toxicities, potentially counteracted by phosphocholine. Our study offered a promising functional metabolite to alleviate PM_2.5-induced cellular disorder and provided insights into the geo-based variability in toxic PM_2.5 components.

SUBMITTER: Song Y

PROVIDER: S-EPMC10998597 | biostudies-literature | 2024 Apr

REPOSITORIES: biostudies-literature

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Phosphocholine-induced energy source shift alleviates mitochondrial dysfunction in lung cells caused by geospecific PM2.5 components.

Song Yuanyuan Y Zhang Yanhao Y Zhu Lin L Chen Yanyan Y Chen Yi-Jie YJ Zhu Zhitong Z Feng Jieqing J Qi Zenghua Z Yu Jian Zhen JZ Yang Zhu Z Cai Zongwei Z

Proceedings of the National Academy of Sciences of the United States of America 20240326 14

Fine particulate matter (PM2.5) is globally recognized for its adverse implications on human health. Yet, remain limited the individual contribution of particular PM2.5 components to its toxicity, especially considering regional disparities. Moreover, prevention solutions for PM2.5-associated health effects are scarce. In the present study, we comprehensively characterized and compared the primary PM2.5 constituents and their altered metabolites from t ...[more]

PMID: 38530899

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Project description:The Denver Aerosol Sources and Health (DASH) study was designed to evaluate associations between PM2.5 species and sources and adverse human health effects. The DASH study generated a five-year (2003-2007) time series of daily speciated PM2.5 concentration measurements from a single, special-purpose monitoring site in Denver, CO. To evaluate the ability of this site to adequately represent the short term temporal variability of PM2.5 concentrations in the five county Denver metropolitan area, a one year supplemental set of PM2.5 samples was collected every sixth day at the original DASH monitoring site and concurrently at three additional sites. Two of the four sites, including the original DASH site, were located in residential areas at least 1.9 km from interstate highways. The other two sites were located within 0.3 km of interstate highways. Concentrations of elemental carbon (EC), organic carbon (OC), and 58 organic molecular markers were measured at each site. To assess spatial variability, site pairs were compared using the Pearson correlation coefficient (r) and coefficient of divergence (COD), a statistic that provides information on the degree of uniformity between monitoring sites. Biweekly co-located samples collected from July 2004 to September 2005 were also analyzed and used to estimate the uncertainty associated with sampling and analytical measurement for each species. In general, the two near-highway sites exhibited higher concentrations of EC, OC, polycyclic aromatic hydrocarbons (PAHs), and steranes than did the more residential sites. Lower spatial heterogeneity based on r and COD was inferred for all carbonaceous species after considering their divergence and lack of perfect correlations in co-located samples. Ratio-ratio plots combined with available gasoline- and diesel-powered motor vehicle emissions profiles for the region suggested a greater impact to high molecular weight (HMW) PAHs from diesel-powered vehicles at the near-highway sites and a more uniformly distributed impact to ambient hopanes from gasoline-powered motor vehicles at all four sites.

Project description:Rapid urbanization and consuming lifestyles have intensified air pollution in urban areas. Air pollution in megacities has imposed severe environmental damages to human health. Proper management of the issue necessitates identification of the share of emission sources. Therefore, numerous research works have studied the apportionment of the total emissions and observed concentrations among different emissions sources. In this research, a comprehensive review is conducted to compare the source apportioning results for ambient air PM2.5 in the megacity of Tehran, the capital of Iran. One hundred seventy-seven pieces of scientific literatures, published between 2005 and 2021, were reviewed. The reviewed research are categorized according to the source apportioning methods: emission inventory (EI), source apportionment (SA), and sensitivity analysis of the concentration to the emission sources (SNA). The possible reasons for inconsistency among the results are discussed according to the scope of the studies and the implemented methods. Although 85% of the reviewed original estimates identify that mobile sources contribute to more thant 60% of Tehran air pollution, the distribution of vehicle types and modes are clearly inconsistent among the EI studies. Our review suggests that consistent results in the SA studies in different locations in central Tehran may indicate the reliability of this method for the identification of the type and share of the emission sources. In contrast, differences among the geographical and sectoral coverage of the EI studies and the disparities among the emission factors and activity data have caused significant deviations among the reviewed EI studies. Also, it is shown that the results of the SNA studies are highly dependent on the categorization type, model capabilities and EI presumptions and data input to the pollutant dispersion modelings. As a result, integrated source apportioning in which the three methods complement each other's results is necessary for consistent air pollution management in megacities.Supplementary informationThe online version contains supplementary material available at 10.1007/s40201-023-00855-0.

Project description:BackgroundPM2.5 is a well-known harmful air pollutant that can lead to acute exacerbation and aggravation of respiratory diseases. Although ferroptosis is involves in the pathological process of pulmonary disease, the potential mechanism of ferroptosis in PM2.5-caused lung inflammation and fibrosis need to be further clarified. Quercetin is a phenolic compound that can inhibit ferroptosis in various diseases. Hence, this study explores the role of ferroptosis in lung injury induced by PM2.5 in order to further elucidate the beneficial effect of quercetin and its underlying mechanism.MethodsC57BL/6J mice were treated with either saline or PM2.5 by intratracheal instillation 20 times (once every two days). Additionally, PM2.5-treated mice were supplemented with two doses of quercetin. Lung injury, lipid peroxidation, iron content and ferroptosis marker protein expression and the Nrf2 signaling pathway were evaluated. In vitro, cell experiments were applied to verify the mechanisms underlying the links between Nrf2 signaling pathway activation and ferroptosis as well as between ferroptosis and inflammation.ResultsIn vivo, PM2.5 increased lung inflammation and caused lung fibrosis and increased lipid peroxidation contents, iron contents and ferroptosis markers in lung tissues; these effects were significantly reversed by quercetin. Additionally, quercetin upregulated the nuclear Nrf2 expression and downregulated Keap1 expression in lung tissues of PM2.5-exposed mice. Quercetin decreased lipid peroxidation products, iron contents and ferroptosis levels and increased the nuclear translocation of Nrf2 and the degradation of Keap1 in PM2.5-exposed BEAS-2B cells. Moreover, we found that quercetin and dimethyl fumarate markedly decreased lipid peroxidation production and ferroptosis by activating the Nrf2-Keap1 pathway in PM2.5-exposed cells. Furthermore, quercetin reduced inflammatory cytokines and TGF-β1 in PM2.5-exposed cells.ConclusionOur data suggested that Nrf2 is involved in ferroptosis in PM2.5-induced lung injury, and quercetin can alleviate these adverse effects via activating Nrf2-Keap1 signaling pathway.

Dataset Information

Phosphocholine-induced energy source shift alleviates mitochondrial dysfunction in lung cells caused by geospecific PM_2.5 components.

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Phosphocholine-induced energy source shift alleviates mitochondrial dysfunction in lung cells caused by geospecific PM<sub>2.5</sub> components.

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