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Mitochondrial Activity after Cold Preservation of Pancreatic Islet Cellstreated with Pefloxacin (PFX)

Janusz Puc, Pawel Kwiatkowski, Jacek Pacanowski, Malgorzata Rotbart-Fiedor, Agata Wardawa, Aleksander P Mazurek, Wojciech Rowinski, Mark A Hardy, Piotr Fiedor

Ann Transplant 1998; 3(1): 38-41

ID: 497370

Mitochondrial energetic and oxidative dysfunctions caused by free radical production trigger release of proinflamnnatory cytokines involved in organ rejection. The aim of this study was to investigate the role of a fluoroquinolone drug. pefloxacin (PFX) and those of various cold preservation solutions on pancreatic f3 cell viability. Our data clearly demonstrate that islet cell viability, as determined by glucose-stimulated insulin secretion, is directly correlated with reduced expression of microsomal cytochrome P-4501llA. Moreover, IL-2, a known mediator of apoptosis was found to be downregulated, whereas TNF-a had been upregulated for the first 18 hours after pefloxacin administration.These results demonstrate that pefloxacin downregulates the expression of cytochrome P-4501l1A isozyme and regulates the production of TNF-a and IL-2. Thus, we postulate that the presence of pefloxacin in the pancreatic islet cells before organ preservation facilitates increased cell viability.

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