|
| |
|
|
|
|
||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | ||||
|
Fig. 1. Ischemia/reperfusion presents numerous opportunities for formation of
reactive oxygen/nitrogen species and resultant tissue injury. Simultaneously,
numerous site-specific targets for therapeutic intervention are presented. It
quickly becomes clear that inhibition of a single pathway may be insufficient
to provide persistent protection against oxidative stress. (1) Inhibition of
lipid peroxidation; (2) inhibition of xanthine oxidase; (3) the superoxide
dismutases (SOD) and their mimetics; (4) catalase and glutathione peroxidase
(GSHPx); (5) glutathione (GSH) mimetics; (6) nitric oxide synthase (NOS)
inhibition; (7) metal chelators; (8) poly(ADP-ribose) polymerase (PARP)
inhibitors; (9) mitochondrial permeability transition inhibitors; (10) spin
traps and peroxynitrite scavengers. O2·–,
superoxide; CO3·–, carbonate radical;
H2O2, hydrogen peroxide; GSSG, glutathione disulfide;
·OH, hydroxyl radical; ·NO2, nitrogen dioxide;
·NO, nitric oxide; ONOO– nicotinamide adenine
dinucleotide. peroxynitrite; NAD,
|
