Founded in 1993
  Year: 1999 | Volume: 7 | Issue: 4 | Pages: 141-144
  Original Article
  SENSITIVITY OF THE POOL OF ADENINE NUCLEOTIDES TO OXIDATIVE STRESS AND PROTECTIVE EFFECT OF GLUTAMINE
Karmen STANKOV, Zoran KOVACEVIC
  DOI:
  Abstract:
  Background: Glutamine plays a central role in multiple metabolic pathways. Our previous investigations of energy metabolism of ascites tumor cells and solid carcinomas revealed that glutamine is very important energy fuel for malignant cells and it can markedly change energy state of the cells. The aim of our investigation was to elucidate its effect on the pool of adenine nucleotides and redox state of glutathione in the presence of oxidizing agent, and how glutamine can protect ascites cells from oxidative stress.
Methods: Concentration of total glutathione content and oxidized glutathione was determined by an enzymatic method. Concentrations of nucleotides (ATP, ADP, AMP, IMP and GTP) were measured by HPLC instrument using anion exchange column.
Results: Experiments carried out with the cells of ascites carcinoma showed that t-butyl hydroperoxyde causes not only oxidation and degradation of glutathione but also depletion of the pool of adenine nucleotides. This is manifested by a large decrease of the concentrations of GSH, ATP, GTP and the ATP/ADP ratio and by an increase of concentrations of GSSG, AMP and IMP. Addition of glutamine abolished the effect of hydroperoxyde on the pool of adenylates, whereas its protective action on GSH was significant but partial.
Conclusion: These and previous data suggest that glutamine probably acts as the source of aspartate which is an important substrate for regeneration of adenylates and that adenylates protect the cells from oxidative stress.
  Key words: Glutamine; Adenylates and oxidative stress
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Founder and owner: Oncology Institute of Vojvodina, Serbia
Publisher: Oncology Institute of Vojvodina
Co-publisher: Faculty of Medicine, University of Novi Sad
Online since 1997 (Abstracts only); 2000 (Abstracts and Full text)
ISSN: 0354-7310 eISSN: 1450-9520