Mitochondrial redox state as a potential detector of liver dysoxia in vivo |
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Authors: | Dishart, Michael K. Schlichtig, Robert Tonnessen, Tor Inge Rozenfeld, Ranna A. Simplaceanu, Elena Williams, Donald Gayowski, Timothy J.P. |
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Abstract: | Dysoxia canbe defined as ATP flux decreasing in proportion toO2 availability with preserved ATPdemand. Hepatic venous -hydroxybutyrate-to-acetoacetate ratio(-OHB/AcAc) estimates liver mitochondrial NADH/NAD and may detectthe onset of dysoxia. During partial dysoxia (as opposed to anoxia),however, flow may be adequate in some liver regions, diluting effluentfrom dysoxic regions, thereby rendering venous -OHB/AcAc unreliable.To address this concern, we estimated tissue ATP whilegradually reducing liver blood flow of swine to zero in a nuclearmagnetic resonance spectrometer. ATP flux decreasing withO2 availability was taken asO2 uptake(O2) decreasing inproportion to O2 delivery(O2);and preserved ATP demand was taken as increasingPi/ATP.O2, tissuePi/ATP, and venous -OHB/AcAcwere plotted againstO2to identify critical inflection points. Tissue dysoxia required meanO2for the group to be critical for bothO2 and forPi/ATP. CriticalO2values for O2 andPi/ATP of 4.07 ± 1.07 and 2.39 ± 1.18 (SE) ml · 100 g1 · min1,respectively, were not statistically significantly different but notclearly the same, suggesting the possibility that dysoxia might havecommenced after O2 begandecreasing, i.e., that there could have been"O2 conformity." CriticalO2for venous -OHB/AcAc was 2.44 ± 0.46 ml · 100 g1 · min1(P = NS), nearly the same as that forPi/ATP, supporting venous -OHB/AcAc as a detector of dysoxia. All issues considered, tissue mitochondrial redox state seems to be an appropriate detector ofdysoxia in liver. |
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