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Use of genetically modified mouse models to assess pathways of benzene-induced bone marrow cytotoxicity and genotoxicity.
Recio, Leslie; Bauer, Alison; Faiola, Brenda.
Afiliación
  • Recio L; Integrated Laboratory Systems Inc., Genetic Toxicology Program, P.O. Box 13501, Research Triangle Park, NC 27709, USA.
Chem Biol Interact ; 153-154: 159-64, 2005 May 30.
Article en En | MEDLINE | ID: mdl-15935812
ABSTRACT
Benzene induces bone marrow cytotoxicity and chromosomal breaks as a primary mode of action for the induction of bone marrow toxicity. Our research group has used genetically modified mouse models to examine metabolic and genomic response pathways involved in benzene induced cytotoxicity and genotoxicity in bone marrow and in hematopoietic stem cells (HSC). We review our studies using NQO1-/- mice and mEH-/- mice to examine the roles of these enzymes, NAD(P)Hquinone oxidoreductase-1 (NQO1) and microsomal epoxide hydrolase (mEH) in mediating benzene-induced toxicity. NQO1 catalyzes the detoxication of benzene quinone metabolites and mEH catalyzes the hydrolysis of benzene oxide. Our studies using gene expression profiling of bone marrow and enriched HSC populations isolated from the bone marrow of benzene-exposed mice demonstrate differential gene expression responses of key genes induced by inhaled benzene. These studies show that benzene toxicity is regulated by a number of genetic pathways that affect the production of reactive metabolites and DNA damage response pathways in a target tissue.
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Benceno / Médula Ósea / Células Madre Hematopoyéticas / Perfilación de la Expresión Génica Límite: Animals Idioma: En Revista: Chem Biol Interact Año: 2005 Tipo del documento: Article País de afiliación: Estados Unidos
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Benceno / Médula Ósea / Células Madre Hematopoyéticas / Perfilación de la Expresión Génica Límite: Animals Idioma: En Revista: Chem Biol Interact Año: 2005 Tipo del documento: Article País de afiliación: Estados Unidos