Table 7 |
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Courtesy [9] Antioxidants: catalytic/enzymatic inactivation of free radicals |
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Enzymatic antioxidants |
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SUPER OXIDE DISMUTASE (SOD) – Location: mitochondrion |
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[O2- + SOD → H2O2 + O2] |
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ecSOD (extracellular) |
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MnSOD (mitochondrial) |
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CuZnSOD (intracellular) |
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CATALASE – Location: peroxisome |
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[2H2O2 + catalase → 2 H2O + O2] |
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GLUTATHIONE PEROXIDASE – Location: mitochondrion/cytosol |
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(Glutamyl-cysteinyl-glycine tripeptide) glutathione reduced -SH to the oxidized disulfide GSSG. |
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(Glutathione peroxidase) [GSH + 2H2O2 → GSSG + H2O + O2] |
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(Glutathione reductase) [GSSG → GSH] at the expense of [NADH → NAD+] and/or [NAD(P)H → NAD(P)+] |
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*NOS (nitric oxide synthase). – Location: membrane |
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Isoforms: |
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(e) NOS (endothelial): good (importance of eNOS uncoupling) LDL native and oxidized. |
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(n)NOS (neuronal): good |
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(i)NOS (inducible-inflammatory): good in host defense. BAD in chronic inflammation. |
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O2- and nitric oxide (NO) are consumed in this process with the creation of reactive nitrogen species (RNS). |
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O2- + NO → ONOO- (peroxynitrite) + tyrosine → nitrotyrosine. (also causes eNOS uncoupling) |
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Nitrotyrosine reflects redox stress and leaves a measurable footprint. |
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NO: the good; O2-: the bad; ONOO-: the ugly [122] |
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eNOS uncoupling causes the generation of O2' instead of NO induced by LDL-C, Glucose, O2', and ONOO'. |
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Nonenzymatic antioxidants |
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URIC ACID |
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VITAMIN A |
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VITAMIN C |
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VITAMIN E |
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THIOLS |
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APOPROTEINS: Ceruloplasmin and transferrin. Bind copper and iron in forms which cannot participate in the Fenton reaction. [9] |
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Hayden and Tyagi Cardiovascular Diabetology 2002 1:3 doi:10.1186/1475-2840-1-3 |
