Table 8 Antioxidants: catalytic/enzymatic inactivation of free radicals.
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 |
Isoforms: |
(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 |
URIC ACID |
VITAMIN A, VITAMIN C, VITAMIN E |
THIOLS |
APOPROTEINS: Ceruloplasmin and transferrin. Bind copper and iron in forms which cannot participate in the Fenton reaction. [7, 8, 12] |