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Red blood cell lactate transport in sickle disease and sickle cell trait

¹School of Nursing and ²Department of Health and Human Performance, Auburn University, Auburn, Alabama

Submitted 28 February 2005 ; accepted in final form 9 May 2005

This study determined and compared rates and mechanisms of lactate transport in red blood cells (RBCs) of persons with 1) sickle cell disease (HbSS), 2) sickle cell trait (HbAS), and 3) a control group (HbAA). Blood samples were drawn from 30 African-American volunteers (10 HbSS, 10 HbAS, 10 HbAA). Lactate influx into RBCs was measured by using [¹⁴C]lactate at six (2, 5, 10, 15, 25, and 40 mM) unlabeled lactate concentrations. The monocarboxylate transporter pathway was blocked by p-chloromercuriphenylsulfonic acid to determine its percent contribution to total lactate influx. Generally, total lactate influx into RBCs from the HbSS group was significantly greater than influx into RBCs from HbAS or HbAA, with no difference between HbAS and HbAA. Faster influx into HbSS RBCs was attributed to increased monocarboxylate transporter activity [increased apparent V_max (V'_max)]. V'_max (4.7 ± 0.6 µmol·ml^–1·min^–1) for HbSS RBCs was significantly greater than V'_max of HbAS RBCs (2.9 ± 1.5 µmol·ml^–1·min^–1) and HbAA RBCs (2.0 ± 0.5 µmol·ml^–1·min^–1). K_m (42.8 ± 8 mM) for HbSS RBCs was significantly greater than K_m (27 ± 12 mM) for HbAA RBCs. We suspect that elevated erythropoietin levels in response to chronic anemia and/or pharmacological treatment (erythropoietin injections, hydroxyurea ingestion) is the underlying mechanism for increased lactate transport capacity in HbSS RBCs.

monocarboxylate transport; lactate influx; Michaelis-Menten kinetics

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				S. Fagnete, C. Philippe, H. Olivier, M.-H. Mona, E.-J. Maryse, and H.-D. Marie-Dominique Faster lactate transport across red blood cell membrane in sickle cell trait carriers J Appl Physiol, February 1, 2006; 100(2): 427 - 432. [Abstract] [Full Text] [PDF]