Ascorbate recycling in human neutrophils: Induction by bacteria

被引:88
作者
Wang, YH
Russo, TA
Kwon, O
Chanock, S
Rumsey, SC
Levine, M
机构
[1] NIDDKD, MOL & CLIN NUTR SECT, NIH, BETHESDA, MD 20892 USA
[2] SUNY BUFFALO, DEPT MED, BUFFALO, NY 14215 USA
[3] SUNY BUFFALO, DEPT MICROBIOL, BUFFALO, NY 14215 USA
[4] SUNY BUFFALO, CTR MICROBIAL PATHOGENESIS, BUFFALO, NY 14215 USA
[5] NCI, PEDIAT ONCOL BRANCH, NIH, BETHESDA, MD 20892 USA
关键词
D O I
10.1073/pnas.94.25.13816
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 recycling reduced dehydroascorbic acid to ascorbate, ascorbate recycling was absent because or negligible entry of the substrate dehydroascorbic acid. Because ascorbate recycling occurs in human neutrophils but: not in microorganisms, it mag represent a eukaryotic defense mechanism against oxidants with possible clinical implications.
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收藏
页码:13816 / 13819
页数:4
相关论文
共 35 条
[1]  
[Anonymous], PRESENT KNOWLEDGE NU
[2]  
CLEMETSON CA, 1989, VITAMIN C, V1, P65
[3]   CHRONIC GRANULOMATOUS-DISEASE - THE SOLVING OF A CLINICAL RIDDLE AT THE MOLECULAR-LEVEL [J].
CURNUTTE, JT .
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 1993, 67 (03) :S2-S15
[4]   ASCORBIC-ACID AND DEHYDROASCORBIC ACID MEASUREMENTS IN HUMAN PLASMA AND SERUM [J].
DHARIWAL, KR ;
HARTZELL, WO ;
LEVINE, M .
AMERICAN JOURNAL OF CLINICAL NUTRITION, 1991, 54 (04) :712-716
[5]   EXPRESSION OF A RABBIT RENAL ASCORBIC-ACID TRANSPORTER IN XENOPUS-LAEVIS OOCYTES [J].
DYER, DL ;
KANAI, Y ;
HEDIGER, MA ;
RUBIN, SA ;
SAID, HM .
AMERICAN JOURNAL OF PHYSIOLOGY, 1994, 267 (01) :C301-C306
[6]   Drug therapy - Antimicrobial-drug resistance [J].
Gold, HS ;
Moellering, RC .
NEW ENGLAND JOURNAL OF MEDICINE, 1996, 335 (19) :1445-1453
[7]   BIOLOGICALLY SIGNIFICANT SCAVENGING OF THE MYELOPEROXIDASE-DERIVED OXIDANT HYPOCHLOROUS ACID BY ASCORBIC-ACID - IMPLICATIONS FOR ANTIOXIDANT PROTECTION IN THE INFLAMED RHEUMATOID JOINT [J].
HALLIWELL, B ;
WASIL, M ;
GROOTVELD, M .
FEBS LETTERS, 1987, 213 (01) :15-17
[8]   ACTIVATED POLYMORPHONUCLEAR LEUKOCYTES CONSUME VITAMIN-C [J].
HEMILA, H ;
ROBERTS, P ;
WIKSTROM, M .
FEBS LETTERS, 1984, 178 (01) :25-30
[9]   DISSECTION OF DISCRETE KINETIC EVENTS IN THE BINDING OF ANTIBIOTICS AND SUBSTRATES TO THE GALACTOSE-H+ SYMPORT PROTEIN, GALP, OF ESCHERICHIA-COLI [J].
HENDERSON, PJF ;
MARTIN, GEM ;
MCDONALD, TP ;
STEEL, A ;
WALMSLEY, AR .
ANTONIE VAN LEEUWENHOEK INTERNATIONAL JOURNAL OF GENERAL AND MOLECULAR MICROBIOLOGY, 1994, 65 (04) :349-358
[10]   TRANSPORT OF GALACTOSE, GLUCOSE AND THEIR MOLECULAR ANALOGS BY ESCHERICHIA-COLI-K12 [J].
HENDERSON, PJF ;
GIDDENS, RA ;
JONESMORTIMER, MC .
BIOCHEMICAL JOURNAL, 1977, 162 (02) :309-320