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Am J Physiol Lung Cell Mol Physiol (October 12, 2001). doi:10.1152/ajplung.00283.2001
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Articles in PresS, published online ahead of print October 12, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00283.2001
Submitted on July 24, 2001
Accepted on October 2, 2001

INTRACELLULAR REDOX STATUS AFFECTS TRANSPLASMA MEMBRANE ELECTRON TRANSPORT IN PULMONARY ARTERIAL ENDOTHELIAL CELLS

Marilyn P Merker1*, Robert D Bongard2, Nicholas J Kettenhofen3, Yoshiyuki Okamoto4, and Christopher A Dawson2

1 Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA; Pharmacology/Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA; Research Service, VA Medical Center, Milwaukee, WI, USA
2 Physiology, Medical College of Wisconsin, Milwaukee, WI, USA; Research Service, VA Medical Center, Milwaukee, WI, USA
3 Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA; Research Service, VA Medical Center, Milwaukee, WI, USA
4 Chemistry, Polytechnic University, New York, NY, USA

* To whom correspondence should be addressed. E-mail: mmerker{at}mcw.edu.

Pulmonary arterial endothelial cells possess transplasma membrane electron transport (TPMET) systems that transfer intracellular reducing equivalents to extracellular electron acceptors. As one aspect of determining cellular mechanisms involved in one such TPMET system in pulmonary arterial endothelial cells in culture, glycolysis was inhibited by treatment with iodoacetate (IOA) or by replacing the glucose in the cell medium with 2-deoxyglucose (2-DOG). TPMET activity was measured as the rate of reduction of the extracellular electron acceptor polymer, toluidine blue O-polyacrylamide (TBOP). Intracellular concentrations of NADH, NAD+, NADPH and NADP+ were determined by high performance liquid chromatography of KOH cell extracts. IOA decreased TPMET activity to 47% of control activity concomitant with a decrease in the NADH/NAD+ ratio to 34% of the control level, without a significant change in the NADPH/NADP+ ratio. 2-DOG decreased TPMET activity to 53% of control and decreased both NADH/NAD+ and NADPH/NADP+ ratios to 51% and 55%, respectively, of control levels. When lactate was included in the medium along with the inhibitors, the effects of IOA and 2-DOG on both TPMET activity and the NADPH/NADP+ ratios were prevented. The results suggest that cellular redox status is a determinant of pulmonary arterial endothelial cell TPMET activity, with TPMET activity more highly correlated with the poise of the NADH/NAD+ redox pair.




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