PMID- 33197790
OWN - NLM
STAT- MEDLINE
DCOM- 20210421
LR  - 20231213
IS  - 1873-6750 (Electronic)
IS  - 0160-4120 (Linking)
VI  - 146
DP  - 2021 Jan
TI  - Unravelling the metabolic alterations of liver damage induced by thirdhand smoke.
PG  - 106242
LID - S0160-4120(20)32197-8 [pii]
LID - 10.1016/j.envint.2020.106242 [doi]
AB  - BACKGROUND: Thirdhand smoke (THS) is the accumulation of tobacco smoke gases and 
      particles that become embedded in materials. Previous studies concluded that THS 
      exposure induces oxidative stress and hepatic steatosis in liver. Despite the 
      knowledge of the increasing danger of THS exposure, the metabolic disorders 
      caused in liver are still not well defined. OBJECTIVES: The aim of this study is 
      to investigate the metabolic disorders caused by THS exposure in liver of male 
      mice and to evaluate the effects of an antioxidant treatment in the exposed mice. 
      METHODS: We investigated liver from three mice groups: non-exposed mice, exposed 
      to THS in conditions that mimic human exposure and THS-exposed treated with 
      antioxidants. Liver samples were analyzed using a multiplatform untargeted 
      metabolomics approach including nuclear magnetic resonance ((1)H NMR), liquid 
      chromatography coupled to high-resolution mass spectrometry (LC-HRMS) and laser 
      desorption/ionization mass spectrometry imaging (MSI), able to map lipids in 
      liver tissues. RESULTS: Our multiplatform approach allowed the annotation of 
      eighty-eight metabolites altered by THS exposure, including amino acids, 
      nucleotides and several types of lipids. The main dysregulated pathways by THS 
      exposure were D-glutamine and D-glutamate metabolism, glycerophospholipid 
      metabolism and oxidative phosphorylation and glutathione metabolism, being the 
      last two related to oxidative stress. THS-exposed mice also presented higher 
      lipid accumulation and decrease of metabolites involved in the phosphocholine 
      synthesis, as well as choline deficiency, which is related to Non-Alcoholic Fatty 
      Liver Disease and steatohepatitis. Interestingly, the antioxidant treatment of 
      THS-exposed mice reduced the accumulation of some lipids, but could not revert 
      all the metabolic alterations, including some related to the impairment of the 
      mitochondrial function. CONCLUSIONS: THS alters liver function at a molecular 
      level, dysregulating many metabolic pathways. The molecular evidences provided 
      here confirm that THS is a new factor for liver steatosis and provide the basis 
      for future research in this respect.
CI  - Copyright (c) 2020 The Author(s). Published by Elsevier Ltd.. All rights reserved.
FAU - Torres, Sonia
AU  - Torres S
AD  - Department of Electronic Engineering, Universitat Rovira i Virgili, Tarragona, 
      Catalonia, Spain; Institut d'Investigacio Sanitaria Pere Virgili, Tarragona, 
      Catalonia, Spain.
FAU - Samino, Sara
AU  - Samino S
AD  - Department of Electronic Engineering, Universitat Rovira i Virgili, Tarragona, 
      Catalonia, Spain; CIBERDEM, Spanish Biomedical Research Centre in Diabetes and 
      Associated Metabolic Disorders, Barcelona, Catalonia, Spain.
FAU - Rafols, Pere
AU  - Rafols P
AD  - Department of Electronic Engineering, Universitat Rovira i Virgili, Tarragona, 
      Catalonia, Spain; CIBERDEM, Spanish Biomedical Research Centre in Diabetes and 
      Associated Metabolic Disorders, Barcelona, Catalonia, Spain.
FAU - Martins-Green, Manuela
AU  - Martins-Green M
AD  - Department of Molecular, Cell and Systems Biology, University of California, 
      Riverside CA 92521, USA.
FAU - Correig, Xavier
AU  - Correig X
AD  - Department of Electronic Engineering, Universitat Rovira i Virgili, Tarragona, 
      Catalonia, Spain; Institut d'Investigacio Sanitaria Pere Virgili, Tarragona, 
      Catalonia, Spain; CIBERDEM, Spanish Biomedical Research Centre in Diabetes and 
      Associated Metabolic Disorders, Barcelona, Catalonia, Spain.
FAU - Ramirez, Noelia
AU  - Ramirez N
AD  - Department of Electronic Engineering, Universitat Rovira i Virgili, Tarragona, 
      Catalonia, Spain; Institut d'Investigacio Sanitaria Pere Virgili, Tarragona, 
      Catalonia, Spain; CIBERDEM, Spanish Biomedical Research Centre in Diabetes and 
      Associated Metabolic Disorders, Barcelona, Catalonia, Spain. Electronic address: 
      noelia.ramirez@urv.cat.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20201113
PL  - Netherlands
TA  - Environ Int
JT  - Environment international
JID - 7807270
RN  - 0 (Smoke)
RN  - 0 (Tobacco Smoke Pollution)
SB  - IM
MH  - Animals
MH  - Liver/chemistry
MH  - Male
MH  - Mice
MH  - Oxidative Stress
MH  - *Smoke/adverse effects
MH  - Nicotiana
MH  - *Tobacco Smoke Pollution/adverse effects/analysis
OTO - NOTNLM
OT  - LC-based metabolomics
OT  - Liver damage
OT  - Mass Spectrometry Imaging
OT  - NAFLD
OT  - NMR-based metabolomics
OT  - Thirdhand smoke
EDAT- 2020/11/17 06:00
MHDA- 2021/04/22 06:00
CRDT- 2020/11/16 20:14
PHST- 2020/05/12 00:00 [received]
PHST- 2020/08/16 00:00 [revised]
PHST- 2020/10/22 00:00 [accepted]
PHST- 2020/11/17 06:00 [pubmed]
PHST- 2021/04/22 06:00 [medline]
PHST- 2020/11/16 20:14 [entrez]
AID - S0160-4120(20)32197-8 [pii]
AID - 10.1016/j.envint.2020.106242 [doi]
PST - ppublish
SO  - Environ Int. 2021 Jan;146:106242. doi: 10.1016/j.envint.2020.106242. Epub 2020 
      Nov 13.