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Increase of urinary extracellular‐superoxide dismutase level correlated with cyclic adenosine monophosphate
Author(s) -
Adachi Tetsuo,
Yamada Harutaka,
Hara Hirokazu,
Futenma Arao,
Kakumu Shinichi
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)01185-0
Subject(s) - superoxide dismutase , endocrinology , medicine , urinary system , chemistry , adenylate kinase , extracellular , isozyme , cyclic adenosine monophosphate , adenosine , cyclase , kidney , biochemistry , enzyme , biology , receptor
Extracellular superoxide dismutase (EC‐SOD) is a secretory protein that is the major SOD isozyme in extracellular fluids. Plasma EC‐SOD levels are distributed in two discrete groups with the rare group having an enzyme with glycine instead of arginine‐213, which causes a 10‐fold higher serum level. Within the common phenotype group, the urinary EC‐SOD level was significantly correlated with the urinary excretion of N ‐acetyl‐β‐ D ‐glucosaminidase (NAG), but not with serum EC‐SOD. EC‐SOD appears not to be leaked from the plasma by glomerular filtration, but rather to be secreted from the renal tubule or its surrounding tissues. The urinary EC‐SOD level was also significantly correlated with the urinary cyclic adenosine monophosphate (cAMP) level. cAMP analogues and adenylate cyclase modulators significantly stimulated the expression of EC‐SOD but not other SOD isozymes in cultured fibroblast cell lines. Moreover, injection of parathyroid hormone, in Ellsworth‐Howard tests, increased urinary EC‐SOD accompanied with the elevations of urinary cAMP and NAG. Together these observations suggest that factor(s) that stimulate the adenylate cyclase‐cAMP system regulate the urinary EC‐SOD level.