Acute hemorrhagic pancreatic necrosis in mice: alterations of serum complement.
Induction of acute hemorrhagic pancreatic necrosis by dietary means in mice produces alterations in the serum complement system. Total hemolytic complement, i.e., CH50, and native C3 levels fall during the development of pancreatitis while, at the same time, what could be immunoreactive C3 degradation products are demonstrable both in the circulation and in the urine. No evidence of renal deposition of C3 was obtained by immunofluorescence analysis, although marked alterations in proteinuria were observed, suggesting that renal dysfunction(s) is a feature of acute hemorrhagic pancreatic necrosis. Lack of renal complement deposition, together with our earlier negative findings with respect to pancreatic localization, suggests that serum complement alterations are side effects of the pancreatitis, attributable to intravascular, pancreatic enzyme-mediated degradation of serum complement components.
D000419:Albuminuria / Q000276:immunology; D000818:Animals; D002462:Cell Membrane / Q000276:immunology; D003176:Complement C3 / Q000032:analysis*; D005260:Female; D006470:Hemorrhage / Q000276:immunology; D007668:Kidney / Q000503:physiopathology; D051379:Mice; D009336:Necrosis; D010179:Pancreas / Q000473:pathology; D010195:Pancreatitis / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology
D003176:Complement C3