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Research Article Free access | 10.1172/JCI106372

Chromate transport in human leukocytes

David L. Lilien, Jerry L. Spivak, and I. David Goldman

1Human Tumor Cell Biology Branch and Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014

Find articles by Lilien, D. in: PubMed | Google Scholar

1Human Tumor Cell Biology Branch and Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014

Find articles by Spivak, J. in: PubMed | Google Scholar

1Human Tumor Cell Biology Branch and Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014

Find articles by Goldman, I. in: PubMed | Google Scholar

Published August 1, 1970 - More info

Published in Volume 49, Issue 8 on August 1, 1970
J Clin Invest. 1970;49(8):1551–1557. https://doi.org/10.1172/JCI106372.
© 1970 The American Society for Clinical Investigation
Published August 1, 1970 - Version history
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Abstract

Chromium is a trace metal of importance in human physiology and, in addition, as 51-chromate, has been extensively used as a label in the study of blood cell pool sizes and intravascular kinetics. The transport characteristics of 51-chromate were investigated in normal human leukocytes. Chromate uptake is unidirectional over a 1 hr incubation with extracellular chromate concentrations up to 200 μmoles/liter. Under these conditions, intracellular 51-chromium is in a form in which it is nonexchangeable. Influx is temperature sensitive with a Q10 of approximately 2 and may be energy dependent since a variety of metabolic poisons strongly inhibit uptake. The unidirectional influx of chromate follows Michaelis-Menten kinetics; the maximum velocity is 52 mμmoles/g dry weight of cells per min and the chromate concentration at which influx velocity is half maximal is 87 μmoles/liter. This transport mechanism is highly specific for chromate; other divalent tetrahedral anions only slightly inhibit influx at concentrations up to 10 times that of chromate. Metavanadate, however, competitively inhibits chromate influx at equimolar concentrations. Exposure of cells to unlabeled chromate leads to inhibition of subsequent influx of 51-chromate. It is suggested that this is due to a primary inhibitory effect of chromate on cellular energy metabolism.

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