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Inhibition of carrageenin-induced paw edema by a superoxide dismutase derivative that circulates bound to albumin

Authors
Journal
Biochimica et Biophysica Acta (BBA) - General Subjects
0304-4165
Publisher
Elsevier
Publication Date
Volume
1073
Issue
2
Identifiers
DOI: 10.1016/0304-4165(91)90145-7
Keywords
  • Paw Edema
  • Oxygen Toxicity
  • Polymorphonuclear Leukocyte
  • Diamine Oxidase
  • Superoxide Dismutase
Disciplines
  • Biology

Abstract

Abstract Although the possible involvement of superoxide radical and its metabolite(s) in the pathogenesis of various types of edema have been suggested, direct evidence supporting this concept is lacking. Since intravenously administered Cu 2+Zn 2+-type superoxide dismutase (SOD) rapidly disappeared from the circulation with a half-life of 4 min, the enzyme could not be used to test whether superoxide radicals played a critical role in the modulation of vascular permeability. We previously synthesized a SOD derivative (SM-SOD) by linking poly(styrene co-maleic acid butyl ester) (SM) to the enzyme (Ogino, T., Inoue, M., Ando, Y., Awai, M., Maeda, H. and Morino Y. (1988) Int. J. Pept. Protein Res. 32, 1583–1588); SM-SOD circulates bound to albumin with a half-life of 6 h. To test whether superoxide radicals play an important role in the regulation of vascular permeability, the effect of SM-SOD on experimental paw edema was studied in the rat. Subcutaneous injections of carrageenin to the paw rapidly induced local edema by increasing vascular permeability. Intravenous administration of SM-SOD markedly inhibited the carrageenin-induced increase in vascular permeability and suppressed the development of paw edema. In contrast, the same dose of SOD showed no such inhibitory effect. These results suggested that superoxide radical and/or its metabolite(s) might play a critical role in the pathogenesis of carrageenin-induced vasogenic edema.

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