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A more recent version of this article appeared on November 22, 2002
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M208675200v1
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Papers In Press, published online ahead of print September 25, 2002
J. Biol. Chem, 10.1074/jbc.M208675200
Submitted on August 23, 2002
Revised on September 19, 2002
Accepted on September 25, 2002

Disruption of NRH:Quinone oxidoreductase2 (NQO2) leads to myeloid hyperplasia of bone marrow and decreased sensitivity to menadione toxicity

Delwin J. LongII, Karim Iskander, Amos Gaikwad, Meral Arin, Dennis R. Roop, Richard Knox, Roberto Barrios, and Anil K. Jaiswal

Pharmacology Dept., Baylor College of Medicine, Houston, TX 77030

Corresponding Author: ajaiswal{at}bcm.tmc.edu

NRH:quinone oxidoreductase 2 (NQO2) is a flavoenzyme that catalyzes reductive metabolism of quinones. To examine the in vivo role of NQO2, NQO2-null mice were generated using targeted gene disruption. Mice lacking NQO2 gene expression showed no detectable developmental abnormalities and were indistinguishable from wild-type mice. However, NQO2-null mice exhibited myeloid hyperplasia of the bone marrow and increased neutrophils, basophils, eosinophils and platelets in the peripheral blood. Decreased apoptosis of bone marrow cells and circulating granulocytes contributed to myeloid hyperplasia and hyperactivity of bone marrow in NQO2-null mice. The hematological changes in NQO2-/- mice were specifically associated with loss of the NQO2 gene, since histological analysis of various tissues including spleen, thymus, blood cultures and urine analysis did not demonstrate any sign of infection. NQO2-null mice also demonstrated decreased toxicity when exposed to menadione, or menadione with NRH. These results establish a role for NQO2 in protection against myelogenous hyperplasia and in metabolic activation of menadione, leading to hepatic toxicity. The NQO2-null mice are a model for NQO2 deficiency in humans and can be used to determine the role of this enzyme in sensitivities to toxicity and carcinogenesis.


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