Heparin-induced release of extracellular-superoxide dismutase form (V) to plasma

• Published in: Journal of biochemistry (Tokyo) Vol. 117; no. 3; p. 586
• Main Authors: Adachi, T, Yamada, H, Futenma, A, Kato, K, Hirano, K
• Format: Journal Article
• Language: English
• Published: England 01-03-1995
• Subjects: Cell Line; Cell Membrane - drug effects; Endothelium, Vascular - cytology; Endothelium, Vascular - drug effects; Endothelium, Vascular - metabolism; Heparin - pharmacology; Humans; Isoenzymes - blood; Metabolic Clearance Rate; Sepharose; Superoxide Dismutase - blood; Superoxide Dismutase - pharmacokinetics
• ISSN: 0021-924X
• DOI: 10.1093/oxfordjournals.jbchem.a124748

Extracellular-superoxide dismutase [EC 1.15.1.1] (EC-SOD) is a secretory, tetrameric glycoprotein. A prominent feature of EC-SOD is its affinity for heparin. This enzyme in serum is heterogeneous with regard to heparin-affinity and can be divided into five fractions (I) to (V) by heparin-HPLC, whereas fibroblast-secreted EC-SOD consists mainly of form (V). An intravenous injection of 50 i.u. of heparin/kg body weight into two healthy volunteers led to an immediate rise of serum EC-SOD level by 2.4-2.8-fold. Only form (V), which was a minor component in pre-heparin serum, was increased by the intravenous injection. The half-life of serum EC-SOD after the prompt rise was about 90 min. The in vivo experiment using rats and an in vitro experiment strongly suggested the EC-SOD released into the plasma reconstituted the interaction with glycocalyx on the vascular endothelial cell surface in accordance with the elimination of heparin from the vascular system.