PMID- 11498801
OWN - NLM
STAT- MEDLINE
DCOM- 20011004
LR  - 20191025
IS  - 0895-8378 (Print)
IS  - 0895-8378 (Linking)
VI  - 13
IP  - 8
DP  - 2001 Aug
TI  - Recovery from oxidant-mediated lung injury: response of metallothionein, MIP-2, 
      and MCP-1 to nitrogen dioxide, oxygen, and ozone exposures.
PG  - 689-702
AB  - Oxidant-induced lung injury is believed to be mediated by reactive oxygen 
      species. Recovery from oxidant exposure has been associated with pulmonary 
      inflammation. Inflammatory cell accumulation involves the synthesis of 
      chemokines, including neutrophil chemoattractants such as macrophage inflammatory 
      protein-2 (MIP-2) and monocyte chemoattractants such as monocyte chemoattractant 
      protein-1 (MCP-1). Antioxidants are the first line of defense of lung cells 
      against inhaled oxidants. Metallothionein (MT) can act as an antioxidant and 
      free-radical scavenger. To better understand the pulmonary response associated 
      with recovery from oxidant-mediated injury, we exposed mice to either 15 ppm 
      nitrogen dioxide for 24 h, >99% oxygen for 72 h, or 1 ppm ozone for 24 h. Mice 
      were examined at the end of exposure or after recovering in room air for 4 or 24 
      h. Neutrophils were elevated at the end of exposure and remained elevated through 
      the postexposure period, whereas macrophage numbers were decreased at the end of 
      exposure and remained below control levels at 4 and 24 h postexposure. MT, MIP-2, 
      and MCP-1 mRNA levels were elevated at 4 h postexposure; however, after 24 h of 
      recovery only MCP-1 remained elevated. These results indicate that MT, MIP-2, and 
      MCP-1 mRNA levels responded similarly to recovery from nitrogen dioxide, oxygen, 
      and ozone exposure. Monocyte accumulation was delayed as compared to neutrophils 
      and was consistent with the timing of MIP-2 and MCP-1 expression. Peak expression 
      of MT and MIP-2 preceded peak neutrophil accumulation. Consequently, the timing 
      of MT, MIP-2, and MCP-1 expression may be important biological markers in 
      assessing the state of injury and recovery associated with oxidant-mediated 
      injury.
FAU - Johnston, C J
AU  - Johnston CJ
AD  - Department of Environmental Medicine, University of Rochester, 601 Elmwood 
      Avenue, Box 777, Rochester, NY 14642, USA.
FAU - Oberdorster, G
AU  - Oberdorster G
FAU - Finkelstein, J N
AU  - Finkelstein JN
LA  - eng
GR  - ESO1247/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Inhal Toxicol
JT  - Inhalation toxicology
JID - 8910739
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CXCL2)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Monokines)
RN  - 0 (Oxidants, Photochemical)
RN  - 0 (RNA, Messenger)
RN  - 66H7ZZK23N (Ozone)
RN  - 9038-94-2 (Metallothionein)
RN  - S7G510RUBH (Nitrogen Dioxide)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Administration, Inhalation
MH  - Animals
MH  - Bronchoalveolar Lavage
MH  - Bronchoalveolar Lavage Fluid/chemistry/cytology
MH  - Chemokine CCL2/*metabolism
MH  - Chemokine CXCL2
MH  - Chemotactic Factors/*metabolism
MH  - In Situ Hybridization
MH  - Lung Diseases/*chemically induced/*metabolism/pathology
MH  - Male
MH  - Metallothionein/*metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Monokines/*metabolism
MH  - Nitrogen Dioxide/*toxicity
MH  - Nuclease Protection Assays
MH  - Oxidants, Photochemical/*toxicity
MH  - Oxygen/*toxicity
MH  - Ozone/*toxicity
MH  - RNA, Messenger/biosynthesis
EDAT- 2001/08/11 10:00
MHDA- 2001/10/05 10:01
CRDT- 2001/08/11 10:00
PHST- 2001/08/11 10:00 [pubmed]
PHST- 2001/10/05 10:01 [medline]
PHST- 2001/08/11 10:00 [entrez]
AID - 10.1080/08958370126867 [doi]
PST - ppublish
SO  - Inhal Toxicol. 2001 Aug;13(8):689-702. doi: 10.1080/08958370126867.