Human umbilical vein endothelial cells submitted to hypoxia-reoxygenation in vitro: Implication of free radicals, xanthine oxidase, and energy deficiency
✍ Scribed by Carine Michiels; Thierry Arnould; Andrée Houbion; José Remacle
- Publisher
- John Wiley and Sons
- Year
- 1992
- Tongue
- English
- Weight
- 988 KB
- Volume
- 153
- Category
- Article
- ISSN
- 0021-9541
No coin nor oath required. For personal study only.
✦ Synopsis
Ischemia-reperfusion is observed in various diseases such as myocardium infarct. Different theories have been proposed to explain the reperfusion injury, among them that the free radical generation plays a crucial role. To study the mechanisms of the reperfusion injury, a hypoxia (H)-reoxygenation (R) model upon human umbilical vein endothelial cells in culture was developed in order to mimic the in vivo situation. Different parameters were quantified and compared under H or H/R, and we found that oxygen readmission led to damage amplification after a short hypoxia period. To estimate the importance of various causes of toxicity, the effects of various protective molecules were compared. Different antioxidant molecules, iron-chelating agent, xanthine oxidase inhibitors, and energy-supplying molecules were very efficient protectors. Synergy could also be observed between the antioxidants and the energy-supplying molecules or the xanthine oxidase inhibitors. The toxic effect of 0, . (-) could be lowered by the presence of SOD or glutathione peroxidase in the culture medium, whereas glutathione peroxidase was the most efficient cnzyme when injected into the cells. The production of 0,. (-) and of H, O, by endothelial cell3 was directly estimated to be, respectively, of 0.1 7 and 0.(135 pmol/minlmg prot during the R period. 0, . (-) production was completely inhibited whcn allopurinol was added during H and R. In addition, a xanthine oxidase activity of 21.5 10 U/mg prot could he observed by a direct assay in cells after H but not in control cells, thus confirming