Journal
BIOFACTORS
Volume 12, Issue 1-4, Pages 5-11Publisher
IOS PRESS
DOI: 10.1002/biof.5520120102
Keywords
glutathione transferase; glutathione; NAD(P)H : quinone reductase; heme oxygenase; gamma-glutamylcysteine synthetase; epoxide hydrolase; ferritin; electrophile toxicity; redox cycling; antioxidants; reactive oxygen species
Funding
- NCI NIH HHS [CA44530] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P01CA044530] Funding Source: NIH RePORTER
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Induction of Phase 2 enzymes is an effective and sufficient strategy for achieving protection against the toxic and neoplastic effects cf many carcinogens. It is proposed that the concept of Phase 2 enzymes as being responsible only for the conjugation of functionalized xenobiotics with endogenous cellular ligands such as glutathione (glutathione S-transferases) and glucuronic acid (UDP-glucuronosyltransferases) be expanded to include proteins with the following common characteristics: (a) coordinate induction by a broad range of chemical agents that all have the capacity to react with sulfhydryl groups; (b) possible regulation by common promoter elements; and (c) catalysis of reactions that lead to comprehensive protection against electrophile and reactive oxygen toxicities, by a wide variety of mechanisms. These mechanisms include: conjugation with endogenous ligands, chemical modification of reactive features of molecules that can damage DNA and other macromolecules, and generation or augementation of cellular antioxidants. In addition to the above conjugating enzymes, a provisional and partial list of Phase 2 proteins might include: NAD(P)H:quinone reductase, epoxide hydrolase, dihydrodiol dehydrogenase, gamma -glutamylcysteine synthetase, heme oxygenase-1, leukotriene B1 dehydrogenase, aflatoxin B-4 dehydrogenase, and ferritin.
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