title: Mammalian peroxiredoxin isoforms can reduce hydrogen peroxide generated in response to growth factors and tumor necrosis factor-alpha.
abstract: Mammalian tissues express three immunologically distinct peroxiredoxin (Prx) proteins (Prx I, II, and III), which are the products of distinct genes. With the use of recombinant proteins Prx I, II, and III, all have now been shown to possess peroxidase activity and to rely on Trx as a source of reducing equivalents for the reduction of H2O2. Prx I and II are cytosolic proteins, whereas Prx III is localized in mitochondria. Transient overexpression of Prx I or II in cultured cells showed that they were able to eliminate the intracellular H2O2 generated in response to growth factors. Moreover, the activation of nuclear factor kappaB (NFkappaB) induced by extracellularly added H2O2 or tumor necrosis factor-alpha was blocked by overproduction of Prx II. These results suggest that, together with glutathione peroxidase and catalase, Prx enzymes likely play an important role in eliminating peroxides generated during metabolism. In addition, Prx I and II might participate in the signaling cascades of growth factors and tumor necrosis factor-alpha by regulating the intracellular concentration of H2O2.
authors.affiliation: Laboratory of Cell Signaling, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA.
authors.forename: S W
authors.initials: SW
authors.lastname: Kang
authors.forename: H Z
authors.initials: HZ
authors.lastname: Chae
authors.forename: M S
authors.initials: MS
authors.lastname: Seo
authors.forename: K
authors.initials: K
authors.lastname: Kim
authors.forename: I C
authors.initials: IC
authors.lastname: Baines
authors.forename: S G
authors.initials: SG
authors.lastname: Rhee
mesh_terms: D000818:Animals; D016207:Cytokines / Q000494:pharmacology*; D005980:Glutathione Reductase / Q000378:metabolism; D006133:Growth Substances / Q000494:pharmacology; D006367:HeLa Cells; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism*; D007527:Isoenzymes / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism; D009363:Neoplasm Proteins; D010084:Oxidation-Reduction; D010544:Peroxidases / Q000235:genetics / Q000378:metabolism*; D061105:Peroxiredoxin III; D054464:Peroxiredoxins; D011506:Proteins; D051381:Rats; D011994:Recombinant Proteins / Q000378:metabolism; D015398:Signal Transduction; D013045:Species Specificity; D013347:Subcellular Fractions / Q000201:enzymology; D013880:Thioredoxin-Disulfide Reductase / Q000378:metabolism; D013879:Thioredoxins / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D016207:Cytokines; D006133:Growth Substances; D007527:Isoenzymes; D016328:NF-kappa B; D009363:Neoplasm Proteins; C516116:Prdx3 protein, mouse; D011506:Proteins; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D013879:Thioredoxins; D006861:Hydrogen Peroxide; D010544:Peroxidases; C516115:PRDX3 protein, human; D061105:Peroxiredoxin III; D054464:Peroxiredoxins; D005980:Glutathione Reductase; D013880:Thioredoxin-Disulfide Reductase