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MitoQ protects against cold ischemic injury in renal cells and rat kidneys
Author(s) -
Mitchell Tanecia,
Rotaru Dumitru,
Saba Hamida,
Murphy Michael,
MacMillanCrow Lee Ann
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1059.8
Subject(s) - cold storage , transplantation , mitochondrion , chemistry , viability assay , membrane potential , pharmacology , depolarization , apoptosis , medicine , biology , biochemistry , horticulture
Cold preservation is a beneficial and necessary procedure used to preserve deceased donor kidneys prior to transplantation. However, extended preservation periods result in injury that can lead to poor graft function following transplantation. Thus, this study's purpose was to evaluate the early effects of cold storage (CS) alone and to determine if MitoQ, a mitochondrial targeted antioxidant, could offer protection during this stage. We hypothesize that CS increases oxidant production and mitochondrial dysfunction, and that adding MitoQ to cold preservation solutions will attenuate injury. Renal cells and rat kidneys were exposed to CS (UW‐Viaspan solution; 4°C) with or without MitoQ (1μM; 100μM respectively) and monitored for oxidants (O 2 ·− , NO, ONOO − ), mitochondrial function (respiratory complexes, mitochondrial membrane potential), and cell viability. Our cell model results suggest that CS first causes mitochondrial membrane depolarization, followed by oxidant production, then mitochondrial dysfunction, and modest cell death. MitoQ reduced oxidant production and protected against mitochondrial complex inactivation using both cellular and isolated rat kidney models. Excitingly, we have identified a potential therapeutic reagent that could be added to existing preservation solutions to reduce CS damage and possibly improve renal function following transplantation.