Oxidative/nitrosative stress Reactive oxygen species

In general, oxidative and nitrosative stress result from an imbalance between an overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) on one side and a deficiency of enzymatic and... 

Fig. 2.5 Diagram showing effect of oxidative and nitrosative stress on neuronal injury. Plasma membrane (PM) Af-methyl-D-aspartate receptor (NMDA-R) glutamate (Glu) phosphatidylcholine (PtdCho) lyso-phosphatidylcholine (lyso-PtdCho) cytosolic phospholipase A2 (CPLA2) secretory phosphohpase A2 (SPLA2) cyclooxygenase (COX-2) arachidonic acid (ARA) reactive oxygen species (ROS) nuclear factor kappaB (NF-kB) nuclear factor kappaB response element (NF-kB-RE) inhibitory subunit of NFkB (IkB) inducible nitric oxide synthase (iNOS) perox-ynitrite (ONOO ) Superoxide ( O2) matrix metalloproteinases (MMPs) vascular cell adhesion molecule-1 (VCAM-1) poly(ADP-ribose) polymerase (PARP) nicotinamide (Nam) nicotineunide adenine dinucleotide (NAD) positive sign (+) represents upregulation...

Inflammatory reactions, oxidative stress (increase in production of reactive oxygen species, ROS), and nitrosative stress (increased generation of reactive nitrogen species, RNS) are major components of secondary injury. All these processes play a major role in regulating the pathogenesis of acute and chronic TBI (Fig. 6.1). 

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