Ascorbate recycling in human neutrophils: Induction by bacteria

Yaohui Wang, Thomas A. Russo, Oran Kwon, Stephen Chanock, Steven C. Rumsey, Mark Levine

Research output: Contribution to journalArticle

Abstract

Ascorbate (vitamin C) recycling occurs when extracellular ascorbate is oxidized, transported as dehydroascorbic acid, and reduced intracellularly to ascorbate. We investigated microorganism induction of ascorbate recycling in human neutrophils and in microorganisms themselves. Ascorbate recycling was determined by measuring intracellular ascorbate accumulation. Ascorbate recycling in neutrophils was induced by both Gram-positive and Gram-negative pathogenic bacteria, and the fungal pathogen Candida albicans. Induction of recycling resulted in as high as a 30-fold increase in intracellular ascorbate compared with neutrophils not exposed to microorganisms. Recycling occurred at physiologic concentrations of extracellular ascorbate within 20 min, occurred over a 100-fold range of effector/target ratios, and depended on oxidation of extracellular ascorbate to dehydroascorbic acid. Ascorbate recycling did not occur in bacteria nor in C. albicans. Ascorbate did not enter microorganisms, and dehydroascorbic acid entry was less than could be accounted for by diffusion. Because microorganism lysates reduced dehydroascorbic acid to ascorbate, ascorbate recycling was absent because of negligible entry of the substrate dehydroascorbic acid. Because ascorbate recycling occurs in human neutrophils but not in microorganisms, it may represent a eukaryotic defense mechanism against oxidants with possible clinical implications.

Original languageEnglish (US)
Pages (from-to)13816-13819
Number of pages4
JournalProceedings of the National Academy of Sciences of the United States of America
Volume94
Issue number25
DOIs
StatePublished - Dec 9 1997
Externally publishedYes

Fingerprint

Recycling
Dehydroascorbic Acid
Neutrophils
Bacteria
Candida albicans
Gram-Negative Bacteria
Oxidants
Ascorbic Acid

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

Ascorbate recycling in human neutrophils : Induction by bacteria. / Wang, Yaohui; Russo, Thomas A.; Kwon, Oran; Chanock, Stephen; Rumsey, Steven C.; Levine, Mark.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 94, No. 25, 09.12.1997, p. 13816-13819.

Research output: Contribution to journalArticle

Wang, Yaohui ; Russo, Thomas A. ; Kwon, Oran ; Chanock, Stephen ; Rumsey, Steven C. ; Levine, Mark. / Ascorbate recycling in human neutrophils : Induction by bacteria. In: Proceedings of the National Academy of Sciences of the United States of America. 1997 ; Vol. 94, No. 25. pp. 13816-13819.
@article{d35d3d33f6d34dffa5c9c14188d83ff8,
title = "Ascorbate recycling in human neutrophils: Induction by bacteria",
abstract = "Ascorbate (vitamin C) recycling occurs when extracellular ascorbate is oxidized, transported as dehydroascorbic acid, and reduced intracellularly to ascorbate. We investigated microorganism induction of ascorbate recycling in human neutrophils and in microorganisms themselves. Ascorbate recycling was determined by measuring intracellular ascorbate accumulation. Ascorbate recycling in neutrophils was induced by both Gram-positive and Gram-negative pathogenic bacteria, and the fungal pathogen Candida albicans. Induction of recycling resulted in as high as a 30-fold increase in intracellular ascorbate compared with neutrophils not exposed to microorganisms. Recycling occurred at physiologic concentrations of extracellular ascorbate within 20 min, occurred over a 100-fold range of effector/target ratios, and depended on oxidation of extracellular ascorbate to dehydroascorbic acid. Ascorbate recycling did not occur in bacteria nor in C. albicans. Ascorbate did not enter microorganisms, and dehydroascorbic acid entry was less than could be accounted for by diffusion. Because microorganism lysates reduced dehydroascorbic acid to ascorbate, ascorbate recycling was absent because of negligible entry of the substrate dehydroascorbic acid. Because ascorbate recycling occurs in human neutrophils but not in microorganisms, it may represent a eukaryotic defense mechanism against oxidants with possible clinical implications.",
author = "Yaohui Wang and Russo, {Thomas A.} and Oran Kwon and Stephen Chanock and Rumsey, {Steven C.} and Mark Levine",
year = "1997",
month = "12",
day = "9",
doi = "10.1073/pnas.94.25.13816",
language = "English (US)",
volume = "94",
pages = "13816--13819",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
number = "25",

}

TY - JOUR

T1 - Ascorbate recycling in human neutrophils

T2 - Induction by bacteria

AU - Wang, Yaohui

AU - Russo, Thomas A.

AU - Kwon, Oran

AU - Chanock, Stephen

AU - Rumsey, Steven C.

AU - Levine, Mark

PY - 1997/12/9

Y1 - 1997/12/9

N2 - Ascorbate (vitamin C) recycling occurs when extracellular ascorbate is oxidized, transported as dehydroascorbic acid, and reduced intracellularly to ascorbate. We investigated microorganism induction of ascorbate recycling in human neutrophils and in microorganisms themselves. Ascorbate recycling was determined by measuring intracellular ascorbate accumulation. Ascorbate recycling in neutrophils was induced by both Gram-positive and Gram-negative pathogenic bacteria, and the fungal pathogen Candida albicans. Induction of recycling resulted in as high as a 30-fold increase in intracellular ascorbate compared with neutrophils not exposed to microorganisms. Recycling occurred at physiologic concentrations of extracellular ascorbate within 20 min, occurred over a 100-fold range of effector/target ratios, and depended on oxidation of extracellular ascorbate to dehydroascorbic acid. Ascorbate recycling did not occur in bacteria nor in C. albicans. Ascorbate did not enter microorganisms, and dehydroascorbic acid entry was less than could be accounted for by diffusion. Because microorganism lysates reduced dehydroascorbic acid to ascorbate, ascorbate recycling was absent because of negligible entry of the substrate dehydroascorbic acid. Because ascorbate recycling occurs in human neutrophils but not in microorganisms, it may represent a eukaryotic defense mechanism against oxidants with possible clinical implications.

AB - Ascorbate (vitamin C) recycling occurs when extracellular ascorbate is oxidized, transported as dehydroascorbic acid, and reduced intracellularly to ascorbate. We investigated microorganism induction of ascorbate recycling in human neutrophils and in microorganisms themselves. Ascorbate recycling was determined by measuring intracellular ascorbate accumulation. Ascorbate recycling in neutrophils was induced by both Gram-positive and Gram-negative pathogenic bacteria, and the fungal pathogen Candida albicans. Induction of recycling resulted in as high as a 30-fold increase in intracellular ascorbate compared with neutrophils not exposed to microorganisms. Recycling occurred at physiologic concentrations of extracellular ascorbate within 20 min, occurred over a 100-fold range of effector/target ratios, and depended on oxidation of extracellular ascorbate to dehydroascorbic acid. Ascorbate recycling did not occur in bacteria nor in C. albicans. Ascorbate did not enter microorganisms, and dehydroascorbic acid entry was less than could be accounted for by diffusion. Because microorganism lysates reduced dehydroascorbic acid to ascorbate, ascorbate recycling was absent because of negligible entry of the substrate dehydroascorbic acid. Because ascorbate recycling occurs in human neutrophils but not in microorganisms, it may represent a eukaryotic defense mechanism against oxidants with possible clinical implications.

UR - http://www.scopus.com/inward/record.url?scp=0031458008&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031458008&partnerID=8YFLogxK

U2 - 10.1073/pnas.94.25.13816

DO - 10.1073/pnas.94.25.13816

M3 - Article

C2 - 9391110

AN - SCOPUS:0031458008

VL - 94

SP - 13816

EP - 13819

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 25

ER -