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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

Published: 1998-03-13


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.

Keywords: pefloxacin (PFX), Cytokines, cytochrome P-450



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