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Ischemic Preconditioning does not alter NADH supported state 3 respiration or complex I activity.
Author(s) -
TanakaEsposito Christine Chan,
Chen Qun,
Moghaddas Shadi,
Lesnefsky Edward J
Publication year - 2006
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.20.4.a319-a
Subject(s) - respiration , chemistry , ischemic preconditioning , cardiology , ischemia , medicine , biology , botany
Ischemic preconditioning (IPC) before sustained ischemia (ISC) decreases infarct size. We found that reversible chemical blockade of electron transport at complex I immediately before sustained ISC preserves mitochondrial respiration and decreases infarct size during ISC‐reperfusion. We proposed that IPC would decrease complex I activity and attenuate state 3 respiration through complex I as a potential mechanism of cardioprotection. Langendorff‐perfused rat hearts underwent IPC (3 cycles 5 min 37°C global ISC and 5 min reperfusion) or were perfused for 40 min without ISC as time controls. Subsarcolemmal (SSM) and interfibrillar (IFM) populations of mitochondria were isolated to measure respiration (natom O/min/mg protein) with complex I substrates (glutamate or pyruvate‐malate). Maximally‐expressed complex I activity (nmol NADH/min/mg) was measured as NADH:ubiquinone oxidoreductase in detergent‐solubilized mitochondria. IPC did not decrease state 3 respiration. Complex I activity was also unaffected by IPC. IPC increased state 4 respiration in IFM (59 ± 7, n=6 vs 41 ± 5, n=5, p<0.05) indicating decreased coupling of respiration. Thus, the protection of IPC does not occur via a decrease in complex I activity or a decrease in respiration through complex I during subsequent sustained ISC. Alternatively, IPC decreases the coupling of respiration as a potential mechanism of cardioprotection.