1.6.5.2 additional information lack of NQO1 in male mice increases benzene-induced hematotoxicity but not genotoxicity or the DNA damage response. NQO1 appears critical in female mice for detoxifying the metabolites of benzene responsible for genotoxicity, hematotoxicity, and induction of the DNA damage response 1.6.5.2 additional information NQO1 activity colocalizes closely with Alzheimer‘s disease pathology supporting a presumed role as an antioxidant system upregulated in response to the oxidative stress of the Alzheimer‘s disease process 1.6.5.2 additional information plays one of the main roles in the bioactivation of quinoidal drugs 1.6.5.2 additional information regeneration of alpha-tocopherol may be one of the physiologic functions of this enzyme 1.6.5.2 additional information the enzyme is involved in the metabolic activation of carcinogenic aristolochic acid 1.6.5.2 additional information the main cytotoxicity mechanism of antitumour aziridinyl-benzoquinones is their two-electron reduction to alkylating products by NAD(P)H:quinone oxidoreductase. In addition to the activation of NQO1 the oxidative stress, presumably initiated by single-electron enzymatic reduction, plays an important role in the cytotoxicity of aziridinyl-substituted quinones 1.6.5.2 additional information enzyme contributes to the capacity of keratinocytes to protect epidermis against oxidant stress 1.6.5.2 additional information increased enzyme expression reflects an endogenous defense response against reactive oxygen species-mediated cellular toxicity 1.6.5.2 additional information role of enzyme in protecting against environmental stressors 1.6.5.2 additional information ChrR minimizes intracellular H2O2 stress 1.6.5.2 additional information TmQR2 could play a role in protecting the infected epidermis 1.6.5.2 additional information V5+ down-regulates Nqo1 at the transcriptional level, possibly through inhibiting the ATP-dependent activation of Nrf2 1.6.5.2 additional information the flavoprotein ferric reductase B, FerB, from Paracoccus denitrificans is one of two major enzymes able to reduce Fe(III)-ligand complexes when NADH is the electron donor. The protein is also active as a chromate reductase and, to a substantially greater extent, as a quinone reductase 1.6.5.2 NAD(P)H + H+ + a quinone the enzyme catalyzes a detoxification process. QR1 gene expression is induced in response to xenobiotics, oxidants, heavy metals, UV light, and ionisation radiation. The enzyme is part of an electrophilic-induced and/or oxidative stress-induced cellular defense mechanism that includes the induction of more than two dozen defensive genes 1.6.5.2 NADH + H+ + 17-(allylamino)-17-demethoxygeldanamycin NAD(P)H:quinone oxidoreductase 1 in pancreatic cell lines metabolizes the heat shock protein 90 inhibitor 17-(allylamino)-17-demethoxygeldanamycin to the corresponding hydroquinone 1.6.5.2 NADH + H+ + 2-methyl-1,4-naphthoquinone - 1.6.5.2 NADH + H+ + a quinone - 1.6.5.2 NADH + H+ + a quinone hydride transfer occurs from the 4-pro-S position of NADH to the solvent-accessible si side of the flavin ring 1.6.5.2 NADH + H+ + atovaquone atovaquone is 2-[4-(4-chlorophenyl)cyclohexyl]-3-hydroxynaphthalene-1,4-dione 1.6.5.2 NADH + H+ + duroquinone - 1.6.5.2 NADH + H+ + ubiquinone the enzyme plays an essential role in maintaining a reduced ubiquinone-pool during infection (Plasmodium falciparum is the causative agents of malaria). The enzyme is not only essential to parasite survival in vivo but may also contribute to the severity and outcome of disease. Type II NADH:quinone oxidoreductase the membrane-bound respiratory enzyme differs from the canonical NADH:dehydrogenase (complex I), because it is not involved in the vectorial transfer of protons across membranes. In the electron transport chain of Plasmodium, the canonical multimeric complex I (NADH:dehydrogenase) found in mammalian mitochondria is absent, and, instead, the parasite possesses five quinone-dependent oxidoreductases, namely a type II NADH:quinone oxidoreductase (PfNDH2), a malate: quinone oxidoreductase (MQO), a dihydroorotate dehydrogenase (DHOD), a glycerol-3-phosphate dehydrogenase (G3PDH), and a succinate: quinone oxidoreductase (SDH). These enzymes link cytosolic metabolism to mitochondrial metabolism, generating reducing power (ubiquinol) for the bc1 complex and an aa3-type cytochrome oxidase, enabling proton pumping and energy conservation 1.6.5.2 NADPH + H+ + 17-(allylamino)-17-demethoxygeldanamycin NAD(P)H:quinone oxidoreductase 1 in pancreatic cell lines metabolizes the heat shock protein 90 inhibitor 17-(allylamino)-17-demethoxygeldanamycin to the corresponding hydroquinone 1.6.5.2 NADPH + H+ + 2-methyl-1,4-naphthoquinone - 1.6.5.2 NADPH + H+ + a quinone - 1.6.5.2 NADPH + H+ + duroquinone - 1.6.5.2 quinone + NAD(P)H possible role in seed germination 1.6.5.2 quinone + NAD(P)H protection of cells against damage by reactive oxygen species generated during oxidative cycling of quinones and semiquinone radicals 1.6.5.2 vitamin K + NAD(P)H + H+ -