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1.
J Toxicol Sci ; 31(2): 99-109, 2006 May.
Artigo em Inglês | MEDLINE | ID: mdl-16772700

RESUMO

Airway epithelium is exposed to inhaled exogenous sources. Injury of the alveolar epithelium by cigarette smoking is presumed to be an important process in the pathogenesis of smoking-related pulmonary diseases. Current mechanistic assays that measure the toxicity of cigarette smoke focus on carcinogenesis. However, there is a need to design assays relevant to other disease processes. Oxidative stress is implicated in the pathogenesis of many respiratory diseases including chronic obstructive pulmonary disease. Therefore, we evaluated whether in vitro studies of cigarette smoking are appropriate to examine HO-1 mRNA expression. The human lung epithelial cell line A549 was exposed to the particulate fraction of cigarette smoke (Cigarette Smoke Condensate; CSC) and examined for the induction of HO-1 mRNA. HO-1 gene expression by CSC is increased dose-dependently. In comparison of the induction of HO-1 mRNA by CSC prepared from flue-cured or Burley tobacco, CSC from flue-cured tobacco seems to tend to induce an mRNA of HO-1 higher than CSC from Burley tobacco. The adaptation of HO-1 mRNA expression assay as a biologically relevant indicator of cigarette smoke-induced stress may be exemplified in this study whereby CSC derived from cigarette smoke positively correlated with an increase in HO-1 expression and the difference of the type of tobacco can be detected.


Assuntos
Células Epiteliais/enzimologia , Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos , Heme Oxigenase-1/genética , Alvéolos Pulmonares/citologia , Fumaça/efeitos adversos , Auranofina/farmacologia , Northern Blotting , Linhagem Celular , Relação Dose-Resposta a Droga , Humanos , Estresse Oxidativo , RNA Mensageiro/metabolismo , Nicotiana/química
2.
FEBS Lett ; 579(17): 3560-4, 2005 Jul 04.
Artigo em Inglês | MEDLINE | ID: mdl-15953603

RESUMO

Phenobarbital (PB) induction of CYP2B, a representative target gene of constitutive androstane receptor (CAR), has been observed to be attenuated in preneoplastic lesions of rat liver; however, molecular basis for this attenuation is poorly understood. In this report, we provide evidence indicating that the CAR expressed in the hepatic preneoplastic lesions of rats and mice was resistant to nuclear translocation and transactivation of the PB-responsive enhancer module upon PB treatment. These observations suggest that the attenuation of the induction of CYP2B by PB in hepatic preneoplastic lesions is evidently a consequence of impaired nuclear translocation of CAR.


Assuntos
Núcleo Celular/metabolismo , Citocromo P-450 CYP2B1/metabolismo , Neoplasias Hepáticas/metabolismo , Fígado/efeitos dos fármacos , Fenobarbital/farmacologia , Lesões Pré-Cancerosas/metabolismo , Receptores Citoplasmáticos e Nucleares/metabolismo , Fatores de Transcrição/metabolismo , Transporte Ativo do Núcleo Celular/efeitos dos fármacos , Animais , Núcleo Celular/química , Receptor Constitutivo de Androstano , Citocromo P-450 CYP2B1/genética , Regulação para Baixo , Fígado/patologia , Masculino , Camundongos , Ratos , Receptores Citoplasmáticos e Nucleares/análise , Receptores Citoplasmáticos e Nucleares/genética , Fatores de Transcrição/análise , Fatores de Transcrição/genética , Ativação Transcricional/efeitos dos fármacos
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