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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, ischemia – ischemia reperfusion injury, acute and chronic as in autoimmunity – T1DM.
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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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eNO : A chain breaking antioxidant see (table 2) item 6.
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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, VITAMIN C, 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. [7, 8, 12]
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