How Does Early and Late Reoxygenation Following Hypoxia Affect Human Umbilical Vascular Endothelial Cells in Respect to Oxidative Stress?

Objectives: Vascular damage induced by hypoxia or hypoxia-reoxygenation has a crucial role in various clinicopathological conditions such as myocardial infarction, renal and cerebral ischemia. Endothelial cells might have a barrier function to vascular damage triggered by diverse stimuli or might be involved in this process. The aim of this study was to evaluate the roles of nitric oxide (NO), nitrotyrosine, endothelial nitric oxide synthase (eNOS), superoxide dismutase (SOD) and malondialdehyde (MDA) in hypoxia and hypoxia-reoxygenation in human vascular endothelial cells in-vitro. Methods: Human umbilical vein endothelial cells were subjected to normoxia (4 hours), hypoxia (4 hours), early (4 hours hypoxia-4 hours reoxygenation) or late hypoxia-reoxygenation (4 hours hypoxia-24 hours reoxygenation) conditions. SOD and eNOS activity, MDA. NO and nitrotyrosine levels were measured. Results: SOD activities were decreased with hypoxia with respect to normoxia. In early reoxygenation however, SOD levels showed statistically significant increase when compared to hypoxia. As compared to hypoxia, MDA levels were decreased in early reoxygenation and late reoxygenation, although insignificant, raised MDA levels were observed in hypoxia compared to normoxia. NO, nitrotyrosine and eNOS levels were unchanged in all groups. Conclusion: Reoxygenation, starting from early phases leads oxidative stress in human umbilical vascular endothelial cells, however, early reoxygenation conditions following hypoxia causes a transient enhancement in antioxidant SOD enzyme activity which probably protects from lipid peroxidation.