Mitochondrial toxicity and in vitro biological effects of ambient PM2.5 from an urban site in China. Issue 1 (20th April 2020)

• Record Type: Journal Article
• Authors: Lin, Zhipeng; Li, Jinzhuo; Zeng, Qianwen; Sun, Renshan
• Is Part Of: Toxicological and environmental chemistry. Volume 102:Issue 1/4(2020)
• Page Start: 170
• Page End: 185
• Publication Date: 2020-04-20
• Subjects: PM2.5 -- mast cells -- oxidative stress -- cell degranulation -- mitochondrial membrane potential -- complex III; Toxicology -- Periodicals; Environmental chemistry -- Periodicals; 571.95
• DOI: 10.1080/02772248.2020.1767780
• Languages: English
• ISSNs: 0277-2248

Abstract

Abstract: The roles of PM2.5 -induced mitochondrial damage and oxidative stress on mast cell degranulation were examined in vitro . Mast cells were treated with suspensions of PM2.5 in Dulbecco's modified Eagle's medium at concentrations from 25 to 200 mg/L in the absence or presence of 10 mmol/L N-acetyl-L-cysteine. Biological effects and mitochondrial function were assessed by determining cell viability, β-hexosaminidase release, interleukin-4 secretion, reactive oxygen species generation, adenosine triphosphate production, potential alteration of mitochondrial membrane, and activities of mitochondrial electron transport chain complexes I and III. Exposure of mast cells to PM2.5 induced reduction of adenosine triphosphate production, collapse of mitochondrial membrane potential, and inhibition of the activity of complex III. Co-treatment of mast cells exposed to PM2.5 with N-acetyl-L-cysteine attenuated cytotoxicity and the production of reactive oxygen species, and decreased the release of β-hexosaminidase and interleukin-4. Evidently, PM2.5 -induced oxidative stress plays an essential role in mitochondrial toxicity and mast cell activation.