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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 PM 2.5 were investigated. Haze dosage PM 2.5 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 PM 2.5. In contrast, there was prominent augment of glycolytic markers at haze dosage PM 2.5 , 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 PM 2.5 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 PM 2.5 exposure led to the occurrence of lung tissue damage and reduction of ATP contents. • Winter PM 2.5 -reduced ATP production was slightly notable than that of summer PM 2.5. • The activity of TCA cycle in lung tissues was weakened by seasonal PM 2.5 exposure. • The level of glycolysis in lung tissues was strengthened in response to seasonal PM 2.5. [ABSTRACT FROM AUTHOR]

Fine particulate matter is one of the leading threats to cardiovascular health worldwide. The exploration of novel and sensitive biomarkers to detect damaging effect of fine particulate matter on cardiac tissues is of great importance in the better understanding of haze-caused myocardial injury. A link between heart failure and PPARα-regulated energy metabolism has been confirmed previously. Herein, the study intends to reveal the critical biomarkers of fine particulate matter induced myocardial damage from the PPARα-regulated energy metabolism. Ambient fine particulate matter induced severe pathological alterations in cultured cells, accompanied by the decrease in ATP content. Additionally, the expressions of CPT1/CPT2 and levels of CS and MDH, crucial members in β-oxidation and the TCA cycle, were significantly decreased. In direct contrast, fine particulate matter increased the biomarkers of glycolysis, as measured by the accumulation of pyruvate and lactate contents, and the enhanced activities of HK and PKM1/2. Importantly, fine particulate matter-exposed cardiomyocytes exhibited the reduced PPARα level, that increased when cardiomyocytes were co-incubation with WY-14643 and fine particulate matter. Simultaneously, the adverse impact of fine particulate matter on critical biomarkers were observed in β-oxidation, TCA cycle and glycolysis, associated with WY-14643 additional complement. Fine particulate matter caused the myocardial energy metabolism transformation through the regulation of PPARα expression and translation, which provided novel and critical biomarkers for haze particles-caused myocardial damage. Image 1 • Fine particulate matter contributed to the attenuation of myocardial ATP. • Fine particulate matter decreased the expressions of critical members in β-oxidation and TCA cycle. • Fine particulate matter increased the levels of biomarkers in glycolysis. • Fine particulate matter-caused transformation of energy metabolism was mediated by the regulation of PPARα. This study provided novel and critical biomarkers involved in myocardial energy metabolism for haze particles-caused myocardial damage. [ABSTRACT FROM AUTHOR]