Exposure to ambient fine particles causes abnormal energy metabolism and ATP decrease in lung tissues. (June 2019)

• Record Type: Journal Article
• Authors: Jin, Xiaoting; Su, Huilan; Ding, Guobin; Sun, Zhendong; Li, Zhuoyu
• Is Part Of: Chemosphere. Volume 224(2019)
• Page Start: 29
• Page End: 38
• Publication Date: 2019-06
• Subjects: PM2.5 -- ATP -- TCA cycle -- Glycolysis -- Metabolic rewiring; PM2.5 fine particulate matter -- ATP adenosine triphosphate -- QFFs quartz fiber filters -- SEM scanning electron microscopy -- TCA cycle tricarboxylic acid cycle -- MDA malondialdehyde -- CS citrate synthase -- MDH malate dehydrogenase -- Glut1 glucose transporter 1 -- HK hexokinase -- PKM pyruvate kinase -- LDH lactate dehydrogenase -- qRT-PCR quantitative real time PCR; Pollution -- Periodicals; Pollution -- Physiological effect -- Periodicals; Environmental sciences -- Periodicals; Atmospheric chemistry -- Periodicals; 551.511
• DOI: 10.1016/j.chemosphere.2019.02.116
• Languages: English
• ISSNs: 0045-6535

Abstract

Abstract: Airborne fine particles, generating from human activities, have drawn increasing attention due to their potential lung health hazards. The currently available toxicological data on fine particles is still not sufficient to explain their cause-and-effect. Based on well reported critical role of ATP on maintaining lung structure and function, the alterations of ATP production and energy metabolism in lungs of rats exposed to different dosages of seasonal PM2.5 were investigated. Haze dosage PM2.5 exposure was demonstrated to reduce the ATP production. Activity of critical enzymes in TCA cycle, such as malate dehydrogenase (MDH) and citrate synthase (CS), and expression of mitochondrial respiration chain genes were attenuated in groups exposed to haze dosage PM2.5 . In contrast, there was prominent augment of glycolytic markers at haze dosage PM2.5, including metabolite contents (pyruvate and lactic acid), enzyme activities (hexokinase (HK) and pyruvate kinase (PKM)), along with mRNA levels of PKM and LDH. Consequently, sub-chronic exposure to seasonal haze PM2.5 caused reduction in ATP generation and metabolic rewiring from TCA cycle to glycolysis. Our findings can help better understand the toxicological mechanism of lung disease caused by particulate air pollution. Highlights: Haze dosage PM2.5 exposure led to the occurrence of lung tissue damage and reduction of ATP contents. Winter PM2.5 -reduced ATP production was slightly notable than that of summer PM2.5 . The activity of TCA cycle in lung tissues was weakened by seasonal PM2.5 exposure. The level of glycolysis in lung tissues was strengthened in response to seasonal PM2.5 .