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Table 2 Courtesy [9] Origins of reactive oxygen species (ROS) and cellular location

From: Intimal redox stress: Accelerated atherosclerosis in metabolic syndrome and type 2 diabetes mellitus. Atheroscleropathy

Nicotinamide adenine dinucleotide reduced (NADH)

NADH Oxidase NADH / NAD + (mitochondrion, cytosol)

NADH + 2O2 → NAD+ + H+ + 2O 2 - (Super Oxide)

Nicotinamide adenine dinucleotide phosphate reduced (NAD(P)H)

NAD(P)H Oxidase NAD(P)H / NAD(P) + (membrane)

NAD(P)H + 2O2 → NAD(P)+ + H+ + 2O 2 - (Super Oxide)

Super oxide dismutase (SOD):

MnSOD = Mitochondrial SOD

CuZnSOD = Intracellular (cytosolic) SOD

EcSOD = Extracellular SOD

O2- + SOD → H2O2 (hydrogen peroxide)

Fenton Reaction: H2O2 + Fe++-OH' (the hydroxyl radical) * + Fe+++ + OH-

Haber-Weiss Reaction: H2O2 + O2--OH- (the hydroxyl radical) + O2 +OH-

Peroxynitrite: origins of reactive nitrogen species (RNS)

O2- is consumed. Nitric oxide (NO) is also consumed in this process with the creation of reactive nitrogen species (RNS).

O2- +NO → ONOO- (peroxynitrite) + tyrosine → nitrotyrosine

O2- +NO → ONOO- (peroxynitrite) + arginine → nitroarginine

Nitroarginine competes for arginine in the formation of eNO.

Nitrotyrosine reflects redox stress and leaves an indelible measurable footprint.

NO: the good; O2-: the bad; ONOO-: the ugly [122, 9]