PMID- 30807911
OWN - NLM
STAT- MEDLINE
DCOM- 20190610
LR  - 20190613
IS  - 1879-1298 (Electronic)
IS  - 0045-6535 (Linking)
VI  - 224
DP  - 2019 Jun
TI  - Exposure to ambient fine particles causes abnormal energy metabolism and ATP 
      decrease in lung tissues.
PG  - 29-38
LID - S0045-6535(19)30341-8 [pii]
LID - 10.1016/j.chemosphere.2019.02.116 [doi]
AB  - 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.
CI  - Copyright (c) 2019 Elsevier Ltd. All rights reserved.
FAU - Jin, Xiaoting
AU  - Jin X
AD  - Institutes of Biomedical Sciences, Shanxi University, Taiyuan 030006, China.
FAU - Su, Huilan
AU  - Su H
AD  - Institutes of Biomedical Sciences, Shanxi University, Taiyuan 030006, China.
FAU - Ding, Guobin
AU  - Ding G
AD  - Institute of Biotechnology, Key Laboratory of Chemical Biology and Molecular 
      Engineering of National Ministry of Education, Shanxi University, Taiyuan 030006, 
      China.
FAU - Sun, Zhendong
AU  - Sun Z
AD  - State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research 
      Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 
      100085, China.
FAU - Li, Zhuoyu
AU  - Li Z
AD  - Institutes of Biomedical Sciences, Shanxi University, Taiyuan 030006, China; 
      Institute of Biotechnology, Key Laboratory of Chemical Biology and Molecular 
      Engineering of National Ministry of Education, Shanxi University, Taiyuan 030006, 
      China; School of Life Science, Shanxi University, Taiyuan 030006, China. 
      Electronic address: lzy@sxu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20190218
PL  - England
TA  - Chemosphere
JT  - Chemosphere
JID - 0320657
RN  - 0 (Particulate Matter)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
SB  - IM
MH  - Adenosine Triphosphate/*biosynthesis
MH  - Animals
MH  - Citric Acid Cycle/drug effects
MH  - Energy Metabolism/*drug effects
MH  - Glycolysis
MH  - Humans
MH  - Lung/metabolism
MH  - Particulate Matter/*pharmacology
MH  - Rats
OTO - NOTNLM
OT  - ATP
OT  - Glycolysis
OT  - Metabolic rewiring
OT  - PM(2.5)
OT  - TCA cycle
EDAT- 2019/02/27 06:00
MHDA- 2019/06/14 06:00
CRDT- 2019/02/27 06:00
PHST- 2018/11/06 00:00 [received]
PHST- 2019/01/15 00:00 [revised]
PHST- 2019/02/17 00:00 [accepted]
PHST- 2019/02/27 06:00 [pubmed]
PHST- 2019/06/14 06:00 [medline]
PHST- 2019/02/27 06:00 [entrez]
AID - S0045-6535(19)30341-8 [pii]
AID - 10.1016/j.chemosphere.2019.02.116 [doi]
PST - ppublish
SO  - Chemosphere. 2019 Jun;224:29-38. doi: 10.1016/j.chemosphere.2019.02.116. Epub 
      2019 Feb 18.