Premium
Effects of a single intratracheal administration of phenanthraquinone on murine lung
Author(s) -
Hiyoshi Kyoko,
Takano Hirohisa,
Inoue Kenichiro,
Ichinose Takamichi,
Yanagisawa Rie,
Tomura Shigeo,
Cho Arthur K.,
Froines John R.,
Kumagai Yoshito
Publication year - 2005
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.1017
Subject(s) - chemistry , oxidative stress , bronchoalveolar lavage , pharmacology , eotaxin , reactive oxygen species , immunology , lung , biochemistry , medicine , chemokine , receptor
Abstract Although several studies have reported that diesel exhaust particles (DEP) affect cardiorespiratory health in animals and humans, the responsible components in DEP for the effects remain to be dened. Diesel exhaust particles contain quinones that can catalyse the generation of reactive oxygen species, resulting in the induction of oxidative stress. Oxidative stress can correlate with a variety of diseases and health effects. In the present study, we investigated the effects of phenanthraquinone — a relatively abundant quinone in DEP — on lung inammation and the local expression of cytokine proteins in mice as a measure of oxidative damage. The animals were randomized into two experimental groups that received vehicle or phenanthraquinone by intratracheal instillation. The cellular proles of bronchoalveolar lavage uid (BALF) and local expression of cytokines were evaluated 24 and 48 h after the instillation. Phenanthraquinone challenge revealed an increase in the numbers of neutrophils and eosinophils in BALF as compared to vehicle challenge ( P < 0.05 at 48 h post‐instillation). Phenanthraquinone induced the lung expression of interleukin (IL)‐5 and eotaxin 48 h and 24 h after the challenge, respectively. These results indicate that intratracheal exposure to phenanthraquinone induces recruitment of inammatory cells, at least partly, through the local expression of IL‐5 and eotaxin. Copyright © 2005 John Wiley & Sons, Ltd.