Pulmonary Inflammation Impacts on CYP1A1-Mediated Respiratory Tract DNA Damage Induced by the Carcinogenic Air Pollutant Benzo[a]pyrene

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F15%3A10297926" target="_blank" >RIV/00216208:11310/15:10297926 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1093/toxsci/kfv086" target="_blank" >http://dx.doi.org/10.1093/toxsci/kfv086</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1093/toxsci/kfv086" target="_blank" >10.1093/toxsci/kfv086</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Pulmonary Inflammation Impacts on CYP1A1-Mediated Respiratory Tract DNA Damage Induced by the Carcinogenic Air Pollutant Benzo[a]pyrene

Popis výsledku v původním jazyce

Pulmonary inflammation can contribute to the development of lung cancer in humans. We investigated whether pulmonary inflammation alters the genotoxicity of polycyclic aromatic hydrocarbons (PAHs) in the lungs of mice and what mechanisms are involved. Tomodel nonallergic acute inflammation, mice were exposed intranasally to lipopolysaccharide (LPS; 20 mg/mouse) and then instilled intratracheally with benzo[ a] pyrene (BaP; 0.5mg/mouse). BaP-DNA adduct levels, measured by 32P-postlabeling analysis, wereapproximately 3-fold higher in the lungs of LPS/BaP-treated mice than in mice treated with BaP alone. Pulmonary Cyp1a1 enzyme activity was decreased in LPS/BaP-treated mice relative to BaP-treated mice suggesting that pulmonary inflammation impacted onBaP-induced Cyp1a1 activity in the lung. Our results showed that Cyp1a1 appears to be important for BaP detoxification in vivo and that the decrease of pulmonary Cyp1a1 activity in LPS/BaP-treated mice results in a decrease of pulmonary B

Název v anglickém jazyce

Pulmonary Inflammation Impacts on CYP1A1-Mediated Respiratory Tract DNA Damage Induced by the Carcinogenic Air Pollutant Benzo[a]pyrene

Popis výsledku anglicky

Pulmonary inflammation can contribute to the development of lung cancer in humans. We investigated whether pulmonary inflammation alters the genotoxicity of polycyclic aromatic hydrocarbons (PAHs) in the lungs of mice and what mechanisms are involved. Tomodel nonallergic acute inflammation, mice were exposed intranasally to lipopolysaccharide (LPS; 20 mg/mouse) and then instilled intratracheally with benzo[ a] pyrene (BaP; 0.5mg/mouse). BaP-DNA adduct levels, measured by 32P-postlabeling analysis, wereapproximately 3-fold higher in the lungs of LPS/BaP-treated mice than in mice treated with BaP alone. Pulmonary Cyp1a1 enzyme activity was decreased in LPS/BaP-treated mice relative to BaP-treated mice suggesting that pulmonary inflammation impacted onBaP-induced Cyp1a1 activity in the lung. Our results showed that Cyp1a1 appears to be important for BaP detoxification in vivo and that the decrease of pulmonary Cyp1a1 activity in LPS/BaP-treated mice results in a decrease of pulmonary B

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

CE - Biochemie

OECD FORD obor

—

Projekt

<a href="/cs/project/GA15-02328S" target="_blank" >GA15-02328S: Organismy a mechanismy určující osud endokrinních disruptorů v životním prostředí</a><br>

Návaznosti

S - Specificky vyzkum na vysokych skolach<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2015

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Toxicological Sciences

ISSN

1096-6080

e-ISSN

—

Svazek periodika

146

Číslo periodika v rámci svazku

2

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

13

Strana od-do

213-225

Kód UT WoS článku

000359630300002

EID výsledku v databázi Scopus

2-s2.0-84939614563