Oxidative stress decreases extracellular homocysteine concentration in human hepatoma (HepG2) cell cultures
Author
Summary, in English
Background: Mild hyperhomocysteinemia is associated with premature vascular disease. The mechanism behind the vascular injuries is, however, still unknown. Homocysteine may be catabolized in the trans sulfuration pathway to cysteine. Cystathionine beta-synthase, which catalyses the first step in the transsulfuration pathway is redox-sensitive. We have therefore investigated total extracellular homocysteine turnover in the presence of oxidative stress in human cell lines. Methods: The turnover of total extracellular homocysteine in HeLa and hepatoma cell cultures has been investigated in the presence of hydrogen peroxide. Furthermore, the effect of hydrogen peroxide on the removal of high amounts of exogenously added homocysteine was also studied. Results: Total extracellular homocysteine concentration in hepatoma cell cultures decreased in the presence of hydrogen peroxide, whereas the extracellular homocysteine concentration in HeLa cell cultures was not influenced. There was no significant change of intracellular homocysteine in any type of cell cultures. Furthermore, the presence of hydrogen peroxide did not increase the removal of exogenously added homocysteine. Conclusion: The presence of hydrogen peroxide probably increases the activity of the transsulfuration pathway in hepatoma cell cultures, which increases the intracellular use of homocysteine and lowers its extracellular release. Consequently this mechanism might tend to lower total plasma homocysteine concentration in oxidative stress. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
Department/s
Publishing year
2007
Language
English
Pages
54-58
Publication/Series
Chemico-Biological Interactions
Volume
165
Issue
1
Document type
Journal article
Publisher
Elsevier
Topic
- Biochemistry and Molecular Biology
Keywords
- transsulfuration
- hydrogen peroxide
- hepatoma cell lines
- homocysteine
- HeLa cell lines
Status
Published
ISBN/ISSN/Other
- ISSN: 1872-7786