EC Number |
Natural Substrates |
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1.6.5.2 | more |
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 | more |
NQO1 activity colocalizes closely with Alzheimers disease pathology supporting a presumed role as an antioxidant system upregulated in response to the oxidative stress of the Alzheimers disease process |
1.6.5.2 | more |
plays one of the main roles in the bioactivation of quinoidal drugs |
1.6.5.2 | more |
regeneration of alpha-tocopherol may be one of the physiologic functions of this enzyme |
1.6.5.2 | more |
the enzyme is involved in the metabolic activation of carcinogenic aristolochic acid |
1.6.5.2 | more |
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 | more |
enzyme contributes to the capacity of keratinocytes to protect epidermis against oxidant stress |
1.6.5.2 | more |
increased enzyme expression reflects an endogenous defense response against reactive oxygen species-mediated cellular toxicity |
1.6.5.2 | more |
role of enzyme in protecting against environmental stressors |
1.6.5.2 | more |
ChrR minimizes intracellular H2O2 stress |