PMID- 20025942
OWN - NLM
STAT- MEDLINE
DCOM- 20100302
LR  - 20100215
IS  - 1879-3169 (Electronic)
IS  - 0378-4274 (Linking)
VI  - 193
IP  - 1
DP  - 2010 Mar 1
TI  - Acute effects of fine particles on cardiovascular system: differences between the 
      spontaneously hypertensive rats and wistar kyoto rats.
PG  - 50-60
LID - 10.1016/j.toxlet.2009.12.002 [doi]
AB  - The study is to explore the potential mechanisms linking fine particles and 
      cardiovascular toxicity. Spontaneous hypertensive rats (SHR) and age-matched 
      wistar kyoto (WKY) rats were exposed by intratracheal instillation to fine 
      particles with the doses of 0.0, 1.6, 8.0 and 40.0mg/kg b.w., respectively. The 
      exposure was conducted once a day, for three continuous days. Twenty-four hours 
      after the last exposure, the rats were killed and the levels of high sensitive 
      C-reactive proteins (hsCRPs), nitrous oxide (NO), D-dimer and endothelin-1 (ET-1) 
      were measured in blood. Reverse transcriptase polymerase chain reaction (RT-PCR) 
      assay assessed the expression of interleukin-1 beta (IL-1beta), intercellular 
      adhesion molecule-1 (ICAM-1), ET-1, Bax and Bcl-2 in left ventricle of rats. 
      Meanwhile, cardiac histological lesions were assessed. The expression 
      transforming growth factor-beta 1 (TGF-beta(1)) in left ventricle was measured by 
      immunohistochemical staining. The results showed that the levels of hsCRP, 
      D-dimer, ET-1 and the expression of IL-1beta, ICAM-1, ET-1, Bax and TGF-beta(1) 
      increased in a dose-dependent manner, but NO and Bcl-2 decreased. Cardiac 
      histology demonstrated exacerbated cardiac lesions in SHR when compared to WKY 
      rats. Meanwhile, at the same dose exposed, the levels of hsCRP, d-dimer, ET-1 and 
      the expression of IL-1beta, ICAM-1, ET-1, Bax and TGF-beta(1) were higher in SHR 
      than those in WKY rats. The results indicated that ambient fine particles which 
      entered into lungs could influence the cardiovascular system. When exposed to 
      fine particles, SHR exhibited more severe cardiovascular injury in comparison to 
      WKY rats. The results indicated that the inflammation, endothelial dysfunction, 
      coagulation disorders and imbalance of apoptosis/anti-apoptosis might be the 
      mechanisms of cardiovascular injury induced by fine particles. Different response 
      between SHR and WKY rats after exposed to fine particles indicated that SHR was 
      more susceptible than WKY rats to acute cardiac impairments from fine particle 
      exposure.
CI  - Copyright 2009 Elsevier Ireland Ltd. All rights reserved.
FAU - Zhao, Jinzhuo
AU  - Zhao J
AD  - Department of Environment Health, School of Public Health, Fudan University, 
      Shanghai, China.
FAU - Xie, Yuquan
AU  - Xie Y
FAU - Qian, Xiaolin
AU  - Qian X
FAU - Jiang, Rongfang
AU  - Jiang R
FAU - Song, Weimin
AU  - Song W
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20091216
PL  - Netherlands
TA  - Toxicol Lett
JT  - Toxicology letters
JID - 7709027
RN  - 0 (Blood Coagulation Factors)
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Animals
MH  - Blood Cell Count
MH  - Blood Coagulation Factors/metabolism
MH  - C-Reactive Protein/analysis/metabolism
MH  - Cardiovascular System/*drug effects
MH  - Cytokines/biosynthesis
MH  - Endothelium, Vascular/drug effects
MH  - Immunohistochemistry
MH  - Inflammation/chemically induced/pathology
MH  - Inflammation Mediators/metabolism
MH  - Nanoparticles/*toxicity
MH  - Particle Size
MH  - RNA, Messenger/biosynthesis
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Species Specificity
MH  - Transforming Growth Factor beta1/biosynthesis
EDAT- 2009/12/23 06:00
MHDA- 2010/03/03 06:00
CRDT- 2009/12/23 06:00
PHST- 2009/07/28 00:00 [received]
PHST- 2009/12/01 00:00 [revised]
PHST- 2009/12/06 00:00 [accepted]
PHST- 2009/12/23 06:00 [entrez]
PHST- 2009/12/23 06:00 [pubmed]
PHST- 2010/03/03 06:00 [medline]
AID - S0378-4274(09)01539-2 [pii]
AID - 10.1016/j.toxlet.2009.12.002 [doi]
PST - ppublish
SO  - Toxicol Lett. 2010 Mar 1;193(1):50-60. doi: 10.1016/j.toxlet.2009.12.002. Epub 
      2009 Dec 16.