Oxidative stress indices induced by industrial and urban PM2.5-bound metals in A549 cells

Barzgar, Fatemeh; Sadeghi-Mohammadi, Sanam; Aftabi, Younes; Zarredar, Habib; Shakerkhatibi, Mohammad; Sarbakhsh, Parvin; Gholampour, Akbar

doi:10.1016/j.scitotenv.2023.162726

Cited by 16 publications

(4 citation statements)

References 103 publications

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“…According to the Pearson correlation analysis between the toxicity effect indicators ( Supporting Information, Table S7 ), ROS generation was strongly correlated with the cell survival rate, TNF–α, IL–6, cell apoptosis rate, and DNA damage. This suggested that ROS–mediated oxidative stress was an important mechanism for the PM 2.5 –induced toxicity effects, which was also consistent with the results of other studies [ 5 , 40 , 52 ].…”

Section: Resultssupporting

confidence: 92%

“…The trend of the DNA damage changes was consistent with the trend of the ROS level changes, which might be due to oxidative stress-induced DNA damage. It has been reported that PM 2.5 caused DNA strand breakage through the production of ROS, affecting the genetic toxicity of cells [ 38 , 39 , 40 ]. ROS could interact with DNA molecules, inducing DNA strand breaks and causing oxidative DNA damage [ 41 , 42 ].…”

Section: Resultsmentioning

confidence: 99%

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The Cytotoxic Effects of Fine Particulate Matter (PM2.5) from Different Sources at the Air–Liquid Interface Exposure on A549 Cells

Yan,

Ge,

et al. 2023

Toxics

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The health of humans has been negatively impacted by PM2.5 exposure, but the chemical composition and toxicity of PM2.5 might vary depending on its source. To investigate the toxic effects of particulate matter from different sources on lung epithelial cells (A549), PM2.5 samples were collected from residential, industrial, and transportation areas in Nanjing, China. The chemical composition of PM2.5 was analyzed, and toxicological experiments were conducted. The A549 cells were exposed using an air–liquid interface (ALI) exposure system, and the cytotoxic indicators of the cells were detected. The research results indicated that acute exposure to different sources of particulate matter at the air–liquid interface caused damage to the cells, induced the production of ROS, caused apoptosis, inflammatory damage, and DNA damage, with a dose–effect relationship. The content of heavy metals and PAHs in PM2.5 from the traffic source was relatively high, and the toxic effect of the traffic–source samples on the cells was higher than that of the industrial– and residential–source samples. The cytotoxicity of particulate matter was mostly associated with water–soluble ions, carbon components, heavy metals, PAHs, and endotoxin, based on the analysis of the Pearson correlation. Oxidative stress played an important role in PM2.5–induced biological toxicity.

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Section: Resultssupporting

confidence: 92%

Section: Resultsmentioning

confidence: 99%

The Cytotoxic Effects of Fine Particulate Matter (PM2.5) from Different Sources at the Air–Liquid Interface Exposure on A549 Cells

Yan,

Ge,

et al. 2023

Toxics

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“…It has been documented that the most toxic metals bound to PM 2.5 are mainly distributed in bioavailable fractions, which are water- or acid-soluble ( 31 ). Once solved, these metals are capable of producing ROS through Fenton-like reactions, leading to cytotoxic effects ( 32 ). Our DTT assay conducted on specific PM 2.5 components confirmed that many of these transition metals exhibited a high level of oxidative potential ( SI Appendix , Fig.…”

Section: Resultsmentioning

confidence: 99%

Phosphocholine-induced energy source shift alleviates mitochondrial dysfunction in lung cells caused by geospecific PM _2.5 components

Song,

Zhang,

Zhu

et al. 2024

Proc. Natl. Acad. Sci. U.S.A.

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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.

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“…The amino acid proline is yet another endogenous molecule that has recently been studied in the context of PM-induced oxidative stress, due to its inherent broad antioxidant profile. Proline supplementation prevented PM-induced DNA damage in epithelial cells, emphasizing that proline supplementation as an antioxidant approach merits further investigation in future works (Barzgar et al, 2023). The natural compound melatonin protected Cs-exposed human lung cells against ERstress-induced inflammasome activation and death, but it could only partially reverse the oxidative stress comparatively to NAC (Mahalanobish et al, 2020).…”

Section: Compounds With Antioxidant Activity Against Pm-induced Oxida...mentioning

confidence: 95%

Particulate Matter-Induced Oxidative Stress – Recent Mechanistic Insights from In Vitro Studies

Vilas-Boas,

Chatterjee,

Carvalho

et al. 2024

Preprint

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Inhaled particulate matter (PM) is a key player in the millions of yearly deaths worldwide related to air pollution. The oxidative potential of PM provides an indication of its ability to promote an oxidative environment. When the human lungs are exposed to PM, the reactive oxygen species (ROS) generated in such oxidative environment, if excessive, may lead to cell damage via oxidative stress. Inflammation, endoplasmic reticulum stress, airway remodeling, and many different cell death modes (apoptosis, ferroptosis, pyroptosis, among others) can be triggered by oxidative stress via complex molecular pathways, which also involve the adaptive cellular response. But ROS can also directly interact with macromolecules such as proteins and lipids, as well as nucleic acids, having been reported to induce DNA damage and epigenetic modifications, which jeopardizes homeostasis. These facts have been extensively studied in in vitro models and confirmed in in vivo models.In this review, we delve beyond conventional assessments of airborne particles, discussing their oxidative potential and the PM-induced ROS-mediated cellular damage observed in in vitro models. The close link between oxidative stress and inflammation, and the manifestation of different cell death modes is highlighted by reviewing the latest literature. The effects of ROS on the balance of DNA damage and repair, carcinogenicity and epigenetics interplay are then analyzed. Finally, we expand on the latest reports on the antioxidants’ potential to counteract the deleterious effects of ROS, and disclose future perspectives for the topic.

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Oxidative stress indices induced by industrial and urban PM2.5-bound metals in A549 cells

Cited by 16 publications

References 103 publications

The Cytotoxic Effects of Fine Particulate Matter (PM2.5) from Different Sources at the Air–Liquid Interface Exposure on A549 Cells

The Cytotoxic Effects of Fine Particulate Matter (PM2.5) from Different Sources at the Air–Liquid Interface Exposure on A549 Cells

Phosphocholine-induced energy source shift alleviates mitochondrial dysfunction in lung cells caused by geospecific PM _2.5 components

Particulate Matter-Induced Oxidative Stress – Recent Mechanistic Insights from In Vitro Studies

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Oxidative stress indices induced by industrial and urban PM2.5-bound metals in A549 cells

Cited by 16 publications

References 103 publications

The Cytotoxic Effects of Fine Particulate Matter (PM2.5) from Different Sources at the Air–Liquid Interface Exposure on A549 Cells

The Cytotoxic Effects of Fine Particulate Matter (PM2.5) from Different Sources at the Air–Liquid Interface Exposure on A549 Cells

Phosphocholine-induced energy source shift alleviates mitochondrial dysfunction in lung cells caused by geospecific PM 2.5 components

Particulate Matter-Induced Oxidative Stress – Recent Mechanistic Insights from In Vitro Studies

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Phosphocholine-induced energy source shift alleviates mitochondrial dysfunction in lung cells caused by geospecific PM _2.5 components