Document Detail

Effect of the superoxide anion (O2-) on Na+-dependent amino acid transport.
MedLine Citation:
PMID:  6261969     Owner:  NLM     Status:  MEDLINE    
Superoxide anion (O2-) generated either by the autoxidation of dihydroxyfumaric acid (DHF) or enzymatically by the xanthine-xanthine oxidase system inhibited the uptake of 2-aminoisobutyric acid (AIB) in thymocytes. The transport of this non-metabolizable amino acid in thymocytes is mediated by a Na+-dependent mechanism. Inhibition of this transport system by O2- was similar to that observed when radiosensitive lymphocytes are subjected to ionizing radiation. As in irradiated thymocytes, O2- generation affected primarily the maximal rate of uptake of the amino acid (i.e. Vmax). No change was observed in the apparent affinity of the amino acid for its carrier (i.e. Km) or the efflux rate of the amino acid. The data suggests that the superoxide anion may be one of the major species responsible for the observed radiation damage to radiosensitive lymphoid cells.
L Kwock; P S Lin; L Ciborowski
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Cell biology international reports     Volume:  5     ISSN:  0309-1651     ISO Abbreviation:  Cell Biol. Int. Rep.     Publication Date:  1981 Jan 
Date Detail:
Created Date:  1981-07-20     Completed Date:  1981-07-20     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  7708050     Medline TA:  Cell Biol Int Rep     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  83-91     Citation Subset:  IM    
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MeSH Terms
Aminoisobutyric Acids / metabolism*
Biological Transport, Active / drug effects
Cells, Cultured
Depression, Chemical
Oxygen / pharmacology*
Sodium / metabolism
Superoxides / pharmacology*
T-Lymphocytes / metabolism
Grant Support
CA 12178-06/CA/NCI NIH HHS
Reg. No./Substance:
0/Aminoisobutyric Acids; 11062-77-4/Superoxides; 7440-23-5/Sodium; 7782-44-7/Oxygen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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