PMID- 22465845
OWN - NLM
STAT- MEDLINE
DCOM- 20120612
LR  - 20231213
IS  - 1879-3185 (Electronic)
IS  - 0300-483X (Linking)
VI  - 296
IP  - 1-3
DP  - 2012 Jun 14
TI  - In vivo hydroquinone exposure impairs MCP-1 secretion and monocyte recruitment 
      into the inflamed lung.
PG  - 20-6
LID - 10.1016/j.tox.2012.02.012 [doi]
AB  - Alveolar macrophages (AMs) are important cells in the resolution of the 
      inflammatory process and they come into direct contact with inhaled pollutants. 
      Hydroquinone (HQ) is an environmental pollutant and a component of cigarette 
      smoke that causes immunosuppressive effects. In the present work, we showed that 
      mice exposed to low levels of aerosolized HQ (25 ppm; 1 h/day/5 days) presented 
      impaired mononuclear cell migration to the lipopolysaccharide (LPS)-inflamed 
      lung. This may have been due to reduced monocyte chemoattractant protein-1 
      (MCP-1) secretion into bronchoalveolar lavage fluid (BALF), and it was not 
      related to alterations to mononuclear cell mobilization into the blood or 
      adhesion molecules expression on mononuclear cell membranes. Corroborating the 
      actions of HQ on MCP-1 secretion, reduced MCP-1 concentrations were also found in 
      the supernatant of ex vivo AM and tracheal tissue collected from HQ-exposed mice. 
      A direct action of HQ on MCP-1 secretion, resulting from impaired gene synthesis, 
      was verified by in vitro incubation of naive AMs or tracheal tissue with HQ. The 
      role of reduced levels of MCP-1 in the BALF on monocyte migration was analysed in 
      the human monocytic lineage THP-1 in in vitro chemotaxis assays, which showed 
      that the reduced concentrations of MCP-1 found in the BALF or cell supernatants 
      from HQ-exposed mice impaired cell migration. Considering the fact that MCP-1 
      presents a broad spectrum of actions on pathophysiological conditions and that 
      resident mononuclear cells are involved in lung tissue homeostasis and in immune 
      host defence, the mechanism of HQ toxicity presented herein might be relevant to 
      the genesis of infectious lung diseases in smokers and in inhabitants of polluted 
      areas.
CI  - Copyright (c) 2012 Elsevier Ireland Ltd. All rights reserved.
FAU - Shimada, Ana Lucia Borges
AU  - Shimada AL
AD  - Laboratory of Experimental Toxicology, Department of Clinical and Toxicological 
      Analyses, School of Pharmaceutical Sciences, University of Sao Paulo, Brazil.
FAU - Ribeiro, Andre Luiz Teroso
AU  - Ribeiro AL
FAU - Bolonheis, Simone Marques
AU  - Bolonheis SM
FAU - Ferraz-de-Paula, Viviane
AU  - Ferraz-de-Paula V
FAU - Hebeda, Cristina Bichels
AU  - Hebeda CB
FAU - Farsky, Sandra Helena Poliselli
AU  - Farsky SH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120323
PL  - Ireland
TA  - Toxicology
JT  - Toxicology
JID - 0361055
RN  - 0 (Chemokine CCL2)
RN  - 0 (Environmental Pollutants)
RN  - 0 (Hydroquinones)
RN  - 0 (Immunosuppressive Agents)
RN  - 0 (Smoke)
RN  - XV74C1N1AE (hydroquinone)
SB  - IM
MH  - Animals
MH  - Bronchoalveolar Lavage Fluid/cytology
MH  - Cell Count
MH  - Cell Line, Tumor
MH  - Cell Movement/drug effects
MH  - Chemokine CCL2/*metabolism
MH  - Environmental Pollutants/toxicity
MH  - Humans
MH  - Hydroquinones/*toxicity
MH  - Immunosuppressive Agents/*toxicity
MH  - Macrophages, Alveolar/cytology
MH  - Male
MH  - Mice
MH  - Monocytes/*drug effects/immunology
MH  - Pneumonia/*immunology/pathology
MH  - Smoke
MH  - Nicotiana
EDAT- 2012/04/03 06:00
MHDA- 2012/06/13 06:00
CRDT- 2012/04/03 06:00
PHST- 2011/10/04 00:00 [received]
PHST- 2012/02/04 00:00 [revised]
PHST- 2012/02/24 00:00 [accepted]
PHST- 2012/04/03 06:00 [entrez]
PHST- 2012/04/03 06:00 [pubmed]
PHST- 2012/06/13 06:00 [medline]
AID - S0300-483X(12)00065-0 [pii]
AID - 10.1016/j.tox.2012.02.012 [doi]
PST - ppublish
SO  - Toxicology. 2012 Jun 14;296(1-3):20-6. doi: 10.1016/j.tox.2012.02.012. Epub 2012 
      Mar 23.