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,