Copper dependent control of the enzymic and phagocyte induced degradation of some biopolymers, a possible link to systemic inflammation

Clin Chim Acta. 1985 Oct 31;152(1-2):95-103. doi: 10.1016/0009-8981(85)90180-9.

Abstract

The role of copper during inflammation is unknown. An attempt was made to examine the reactivity of copper on the oxygen free radical induced depolymerization of hyaluronic acid and synovial fluid. Thionein-copper and CuSO4 at 2 mumol/l concentrations inhibited the degradation of this biopolymer successfully. Translation of the enzymically generated excited oxygen species onto a cellular level was performed. Activated PMN cells were used to decompose hyaluronic acid in the presence of CuSO4, Cu-thionein and ceruloplasmin not exceeding physiological levels. All employed copper compounds inhibited the depolymerizing process. Furthermore, PMN cell induced bleaching of cytochrome c was also affected in the presence of both CuSO4 and thionein-copper.

MeSH terms

  • Animals
  • Biopolymers / metabolism*
  • Cattle
  • Ceruloplasmin / pharmacology
  • Copper / pharmacology
  • Copper / physiology*
  • Copper Sulfate
  • Cytochrome c Group / metabolism
  • Hyaluronic Acid / metabolism
  • Hypoxanthine
  • Hypoxanthines / metabolism
  • Inflammation / physiopathology*
  • Macromolecular Substances / metabolism*
  • Metallothionein / pharmacology
  • Neutrophils / immunology
  • Phagocytosis*
  • Synovial Fluid / metabolism
  • Viscosity
  • Xanthine Oxidase / antagonists & inhibitors

Substances

  • Biopolymers
  • Cytochrome c Group
  • Hypoxanthines
  • Macromolecular Substances
  • copper thionein
  • Hypoxanthine
  • Copper
  • Hyaluronic Acid
  • Metallothionein
  • Ceruloplasmin
  • Xanthine Oxidase
  • Copper Sulfate