Antioxidant-dependent amelioration of brain injury: role of CuZn-superoxide dismutase.
Copper-zinc-superoxide dismutase (CuZn-SOD), a cytosolic antioxidant enzyme that is specific for scavenging superoxide radicals, is involved in neuroprotective mechanisms in brain injury following trauma and cerebral ischemia. Liposome-entrapped CuZn-SOD exhibit beneficial effects in vivo on cold-induced vasogenic edema and on blood-brain barrier disruption. The increased levels of edema and infarction following a focal cerebral ischemia also are decreased by the pretreatment of liposome-entrapped CuZn-SOD. The protective role of SOD on brain injury was further extended and confirmed in studies using transgenic mice overexpressing human CuZn-SOD. Our studies so far suggest that increased cerebral levels of SOD, either by means of external pharmacological application or by genetic manipulations, ameliorate brain edema and infarction induced by trauma and focal cerebral ischemia.
Chan
P H
PH
Department of Neurology, University of California School of Medicine, San Francisco.
D000818:Animals; D001929:Brain Edema / Q000188:drug therapy / Q000517:prevention & control*; D002540:Cerebral Cortex / Q000187:drug effects / Q000473:pathology; D002544:Cerebral Infarction / Q000188:drug therapy / Q000517:prevention & control*; D004337:Drug Carriers; D016166:Free Radical Scavengers; D006801:Humans; D002546:Ischemic Attack, Transient / Q000188:drug therapy*; D008081:Liposomes; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D008822:Mice, Transgenic; D051381:Rats; D011994:Recombinant Proteins / Q000008:administration & dosage / Q000627:therapeutic use; D013482:Superoxide Dismutase / Q000008:administration & dosage / Q000378:metabolism* / Q000627:therapeutic use*; D013481:Superoxides / Q000378:metabolism*
D004337:Drug Carriers; D016166:Free Radical Scavengers; D008081:Liposomes; D011994:Recombinant Proteins; D013481:Superoxides; D013482:Superoxide Dismutase