title: Reepithelialization of experimental scalds effected by topically applied superoxide dismutase: controlled animal studies.
abstract: Highly reactive metabolites, such as oxygen free radicals, initiate a cascade of inflammatory processes in thermally damaged skin, leading to enhanced tissue loss and delayed wound healing. The extent of tissue necrosis in the zone of stasis is of prognostic significance in the wound healing process. In this study, the effect of oxygen free radical removal by recombinant human-Cu/Zn-superoxide dismutase, given in three different formulations during the inflammatory postburn phase and wound repair, was examined. Recombinant human superoxide dismutase was either injected directly into the lesions, spread as enzyme-containing gel onto the burned tissue, or encapsulated into liposomes consisting of 1,2 dipalmitoy-sn-glycero-3-phosphocholine, cholesterol and stearylamine, suspended into a hydrophilic gel and administered to burned animals immediately after trauma. Controls were treated with plain gel or kept untreated. Edema formation, size of lesions, deepening of necrosis, and reepithelialization were examined. Results indicate that superoxide dismutase treatment resulted in reduced and faster recruitment of edema formation, smaller wound sizes, and minor tissue necrosis compared to the controls, thus resulting in significantly faster reepithelialization after 3 weeks. These animal studies on the efficacy of liposomal oxygen free radical scavenger showed accelerated wound healing in all parameters tested.
authors.affiliation: Institute of Applied Microbiology, University of Agricultural Sciences, Vienna, Austria. K.Vorauer@iam.boku.ac.at
authors.forename: Karola
authors.initials: K
authors.lastname: Vorauer-Uhl
authors.forename: Eckhard
authors.initials: E
authors.lastname: Fürnschlief
authors.forename: Andreas
authors.initials: A
authors.lastname: Wagner
authors.forename: Boris
authors.initials: B
authors.lastname: Ferko
authors.forename: Hermann
authors.initials: H
authors.lastname: Katinger
mesh_terms: D000287:Administration, Topical; D000818:Animals; D002056:Burns / Q000150:complications* / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D004487:Edema / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology*; D004848:Epithelium / Q000187:drug effects* / Q000503:physiopathology*; D005110:Extracellular Space / Q000502:physiology; D016166:Free Radical Scavengers / Q000008:administration & dosage* / Q000494:pharmacology*; D006801:Humans; D009336:Necrosis; D011817:Rabbits; D051381:Rats; D017208:Rats, Wistar; D011994:Recombinant Proteins / Q000008:administration & dosage* / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000008:administration & dosage* / Q000494:pharmacology*; D013997:Time Factors; D014945:Wound Healing / Q000187:drug effects* / Q000502:physiology*
chemical_list: D016166:Free Radical Scavengers; D011994:Recombinant Proteins; D013482:Superoxide Dismutase