Neutrophil-endothelial cell interaction. Evidence for and mechanisms of the self-protection of bovine microvascular endothelial cells from hydrogen peroxide-induced oxidative stress.
Bovine microvascular endothelial cells (MEC) were able to degrade the H2O2 generated by phorbol myristate acetate-activated bovine neutrophils or by glucose oxidase with a maximal capacity of 4.0 +/- 1.2 (SD) nmol/10(6) cells/min, corresponding to the H2O2 released by about 3 X 10(6) neutrophils. H2O2 degradation occurred via the glutathione redox cycle and catalase. Degradation via the glutathione redox cycle was coupled with a marked stimulation of the hexose monophosphate shunt activity. The effect of H2O2 on ethidium bromide exclusion and on succinate oxidation was studied. Neither parameter was altered when MEC were exposed to H2O2 produced at rates within their degradative capacity. As soon as this was exceeded, impairment of both functions occurred. It is concluded that endothelial cells can protect themselves from H2O2-induced injury in a well-defined range of environmental H2O2 concentrations by actively degrading the peroxide.
D000818:Animals; D002374:Catalase / Q000502:physiology; D002417:Cattle; D002450:Cell Communication; D002470:Cell Survival / Q000187:drug effects; D004727:Endothelium / Q000201:enzymology / Q000378:metabolism / Q000502:physiology*; D005978:Glutathione / Q000502:physiology; D006861:Hydrogen Peroxide / Q000378:metabolism / Q000494:pharmacology*; D008297:Male; D008833:Microcirculation / Q000201:enzymology / Q000378:metabolism / Q000502:physiology; D009504:Neutrophils / Q000201:enzymology / Q000502:physiology*; D010084:Oxidation-Reduction; D010101:Oxygen Consumption / Q000187:drug effects*; D010413:Penis / Q000098:blood supply; D010427:Pentose Phosphate Pathway / Q000187:drug effects
D006861:Hydrogen Peroxide; D002374:Catalase; D005978:Glutathione