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Forskningsartikel2007Vetenskapligt granskad

Oxidative stress decreases extracellular homocysteine concentration in human hepatoma (HepG2) cell cultures

Hultberg M, Hultberg B

Sammanfattning

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

Nyckelord

Homocysteine; HeLa cell lines; Hepatoma cell lines; Hydrogen peroxide; Transsulfuration

Publicerad i

Chemico-Biological Interactions
2007, Volym: 165, nummer: 1, sidor: 54-58
Utgivare: ELSEVIER IRELAND LTD

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    Livsmedelsvetenskap

    Publikationens identifierare

    DOI: https://doi.org/10.1016/j.cbi.2006.10.009

    Permanent länk till denna sida (URI)

    https://res.slu.se/id/publ/14912