Literature DB >> 8068952

Human HL-60 myeloid leukemia cells transport dehydroascorbic acid via the glucose transporters and accumulate reduced ascorbic acid.

J C Vera1, C I Rivas, R H Zhang, C M Farber, D W Golde.   

Abstract

The cellular accumulation of vitamin C, a substance critical to human physiology, is mediated by transporters located at the cell membrane, and is regulated in a cell-specific manner. Neoplastic cells may have special needs for vitamin C. Therefore, we investigated the transport of vitamin C in a human myeloid leukemia cell line (HL-60). The HL-60 cells lacked the capacity to transport the reduced form of vitamin C, ascorbic acid, but they showed a remarkable ability to transport the oxidized form of vitamin C, dehydroascorbic acid (DHA). Uptake-accumulation studies indicated that the HL-60 cells accumulated ascorbic acid when provided with DHA. Kinetic analysis showed the presence of two functional activities involved in the uptake of DHA, one with low affinity and one with high affinity. Cytochalasin B and phloretin, which inhibit the passage of glucose through the facilitative glucose transporters, also inhibited the transport of DHA by HL-60 cells. Transport of DHA was completed by D- but not L-hexoses, and was sensitive to D-hexose-dependent counter transport acceleration. These data support the concept that HL-60 myeloid leukemic cells transport DHA through the facilitative hexose transporters (glucose transporters) and accumulate the reduced form of ascorbic acid.

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Year:  1994        PMID: 8068952

Source DB:  PubMed          Journal:  Blood        ISSN: 0006-4971            Impact factor:   22.113


  22 in total

1.  Moderately controlled transport of ascorbate into aortic endothelial cells against slowdown of the cell cycle, decreasing of the concentration or increasing of coexistent glucose as compared with dehydroascorbate.

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Journal:  Mol Cell Biochem       Date:  1997-08       Impact factor: 3.396

2.  Ascorbate enhances the toxicity of the photodynamic action of Verteporfin in HL-60 cells.

Authors:  Galina G Kramarenko; Werner W Wilke; Disha Dayal; Garry R Buettner; Freya Q Schafer
Journal:  Free Radic Biol Med       Date:  2006-01-19       Impact factor: 7.376

Review 3.  Targeting cancer vulnerabilities with high-dose vitamin C.

Authors:  Bryan Ngo; Justin M Van Riper; Lewis C Cantley; Jihye Yun
Journal:  Nat Rev Cancer       Date:  2019-05       Impact factor: 60.716

4.  Interaction of respiratory burst and uptake of dehydroascorbic acid in differentiated HL-60 cells.

Authors:  H Laggner; H Goldenberg
Journal:  Biochem J       Date:  2000-01-15       Impact factor: 3.857

5.  Efflux of hepatic ascorbate: a potential contributor to the maintenance of plasma vitamin C.

Authors:  J M Upston; A Karjalainen; F L Bygrave; R Stocker
Journal:  Biochem J       Date:  1999-08-15       Impact factor: 3.857

6.  Two distinct uptake mechanisms for ascorbate and dehydroascorbate in human lymphoblasts and their interaction with glucose.

Authors:  F C Ngkeekwong; L L Ng
Journal:  Biochem J       Date:  1997-05-15       Impact factor: 3.857

7.  Vitamin C crosses the blood-brain barrier in the oxidized form through the glucose transporters.

Authors:  D B Agus; S S Gambhir; W M Pardridge; C Spielholz; J Baselga; J C Vera; D W Golde
Journal:  J Clin Invest       Date:  1997-12-01       Impact factor: 14.808

8.  Vitamin C antagonizes the cytotoxic effects of antineoplastic drugs.

Authors:  Mark L Heaney; Jeffrey R Gardner; Nicos Karasavvas; David W Golde; David A Scheinberg; Emily A Smith; Owen A O'Connor
Journal:  Cancer Res       Date:  2008-10-01       Impact factor: 12.701

9.  The prospects of vitamin C in cancer therapy.

Authors:  Wang-Jae Lee
Journal:  Immune Netw       Date:  2009-10-30       Impact factor: 6.303

10.  A human sodium-dependent vitamin C transporter 2 isoform acts as a dominant-negative inhibitor of ascorbic acid transport.

Authors:  Eugene A Lutsenko; Juan M Carcamo; David W Golde
Journal:  Mol Cell Biol       Date:  2004-04       Impact factor: 4.272

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