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Exposure to ambient fine particles causes abnormal energy metabolism and ATP decrease in lung tissues

Jin, Xiaoting, Su, Huilan, Ding, Guobin, Sun, Zhendong, Li, Zhuoyu
Chemosphere 2019 v.224 pp. 29-38
adenosine triphosphate, air pollution, citrate (si)-synthase, energy metabolism, enzyme activity, genes, glycolysis, health hazards, hexokinase, lactic acid, lung function, lungs, malate dehydrogenase, messenger RNA, metabolites, mitochondria, particulates, pyruvate kinase, pyruvic acid, rats, respiratory tract diseases, subchronic exposure, tricarboxylic acid cycle
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.