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Table 8 Antioxidants: catalytic/enzymatic inactivation of free radicals.

From: Is type 2 diabetes mellitus a vascular disease (atheroscleropathy) with hyperglycemia a late manifestation? The role of NOS, NO, and redox stress.

Enzymatic antioxidants
SUPER OXIDE DISMUTASE (SOD)– Location: mitochondrion
[O2- + SOD → H2O2 + O2]
ecSOD (extracellular)
MnSOD (mitochondrial)
CuZnSOD (intracellular)
CATALASE– Location: peroxisome
[2H2O2 + catalase → 2 H2O + O2]
GLUTATHIONE PEROXIDASE– Location: mitochondrion/cytosol
(Glutamyl-cysteinyl-glycine tripeptide) glutathione reduced -SH to the oxidized disulfide GSSG.
(Glutathione peroxidase) [GSH + 2H2O2 → GSSG + H2O + O2]
(Glutathione reductase) [GSSG → GSH] at the expense of [NADH → NAD+] and/or [NAD(P)H → NAD(P)+]
* NOS (nitric oxide synthase). – Location: membrane
(e) NOS (endothelial): good (importance of eNOS uncoupling) LDL native and oxidized.
(n) NOS (neuronal): good
(i) NOS (inducible-inflammatory): GOOD in host defense. BAD in chronic inflammation, ischemia – ischemia reperfusion injury, acute and chronic as in autoimmunity – T1DM.
O2- and nitric oxide (NO) are consumed in this process with the creation of reactive nitrogen species (RNS).
O2- + NO → ONOO- (peroxynitrite) + tyrosine → nitrotyrosine. (also causes eNOS uncoupling)
Nitrotyrosine reflects redox stress and leaves a measurable footprint.
NO: the good; O2-: the bad; ONOO-: the ugly [122]
eNO : A chain breaking antioxidant see (table 2) item 6.
eNOS uncoupling causes the generation of O2' instead of NO induced by LDL-C, Glucose, O2', and ONOO'.
Nonenzymatic antioxidants
APOPROTEINS: Ceruloplasmin and transferrin. Bind copper and iron in forms which cannot participate in the Fenton reaction. [7, 8, 12]