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1 Institute for Applied Physiology, University of Freiburg, D-79104 Freiburg/Breisgau, Germany; and 2 Department of Physiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814-4799
Myocardial
ischemia-reperfusion is associated with bursts of reactive oxygen
species (ROS) such as superoxide radicals (O2
·).
Membrane-associated NADH oxidase (NADHox) activity is a hypothetical source of O2·, implying the NADH
concentration-to-NAD+ concentration ratio
([NADH]/[NAD+]) as a determinant of ROS. To test this
hypothesis, cardiac NADHox and ROS formation were measured as
influenced by pyruvate or L-lactate. Pre- and postischemic
Langendorff guinea pig hearts were perfused at different
pyruvate/L-lactate concentrations to alter cytosolic [NADH]/[NAD+]. NADHox and ROS were measured with the
use of lucigenin chemiluminescence and electron spin resonance,
respectively. In myocardial homogenates, pyruvate (0.05, 0.5 mM) and
the NADHox blocker hydralazine markedly inhibited NADHox (16 ± 2%, 58 ± 9%). In postischemic hearts, pyruvate (0.1-5.0
mM) dose dependently inhibited ROS up to 80%. However, L-lactate (1.0-15.0 mM) stimulated both basal and
postischemic ROS severalfold. Furthermore,
L-lactate-induced basal ROS was dose dependently inhibited
by pyruvate (0.1-5.0 mM) and not the xanthine oxidase inhibitor
oxypurinol. Pyruvate did not inhibit ROS from xanthine oxidase. The
data suggest a substantial influence of cytosolic NADH on cardiac
O2· formation that can be inhibited by
submillimolar pyruvate. Thus cytotoxicities due to cardiac
ischemia-reperfusion ROS may be alleviated by redox reactants such as pyruvate.
reduced nicotinamide adenine dinucleotide oxidase; heart; ischemia-reperfusion
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