Relationship of endothelial cell selective adhesion molecule to markers of oxidative stress in type 2 diabetes

Abstract

Background. Endothelial dysfunction is an important contributor to micro and macrovascular complications of type 2 diabetes (T2D) and is reflected by increased systemic oxidative stress. Endothelial cell selective adhesion molecule (ESAM) influences endothelial function. We aimed to assess, for the first time to our knowledge, the relationship of soluble ESAM to markers of systemic oxidative stress. Materials and methods. ESAM, malondialdehyde (MDA) level and catalase activity were determined in 54 T2D patients and 43 controls. Results. T2D patients had significantly higher ESAM when compared to controls (16.07 ± 5.77 μg/L versus 8.57 ± 5.28 μg/L, p < 0.0001), they also had higher MDA level (3.88 ± 1.50 μmol/L vs. 1.58 ± 0.72 μmol/L, p < 0.0001) and lower catalase activity (3.07 (2.63–3.44) U/mg vs. 8.72 (4.55–10.46) U/mg, p < 0.0001). In T2D patients ESAM was inversely related to catalase activity (r = −0.27, p = 0.04), relationship to MDA level was direct but not significant (r = 0.16, p = 0.24). MDA concentration correlated inversely to catalase activity (r = −0.28, p = 0.04). In multiple regression catalase activity remained significantly correlated to ESAM (p = 0.02) and MDA level was significantly related to glycated hemoglobin (p = 0.01); there was trend towards a positive correlation of MDA level to ESAM (p = 0.08). When patients were divided according to oxidative stress, those with increased oxidative stress (defined as MDA concentration > 2.98 μmol/L and catalase activity < 3.38 U/mg) had higher ESAM than the rest of the patients (17.99 ± 5.02 μg/L vs. 14.29 ± 5.94 μg/L p = 0.01). Conclusion. ESAM is higher in T2D than in controls and parallels oxidative stress: ESAM is inversely related to catalase activity and higher ESAM is found in T2D patients with increased oxidative stress.

Key Words::

• Atherosclerosis
• diabetes mellitus
• catalase
• malondialdehyde
• inflammation
• oxidative stress

Acknowledgements

We hereby thank the Laboratory of Oxidative Stress/Department of Physiology, University of Medicine and Pharmacy “Iuliu Hatieganu Cluj” for their support in determining markers of oxidative stress.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

This work was partly funded by grant CNCSIS Idei 1167/ and partly 2008 and partly by the European Social Fund within the Sectorial Operational Program Human Resources Development 2007-2013-POSDRU /89/1.5/S/58965.