Oxidative stress in ischaemic stroke
Article first published online: 30 MAY 2011
© 2011 The Authors. European Journal of Clinical Investigation © 2011 Stichting European Society for Clinical Investigation Journal Foundation
European Journal of Clinical Investigation
Volume 41, Issue 12, pages 1318–1322, December 2011
How to Cite
Nanetti, L., Raffaelli, F., Vignini, A., Perozzi, C., Silvestrini, M., Bartolini, M., Provinciali, L. and Mazzanti, L. (2011), Oxidative stress in ischaemic stroke. European Journal of Clinical Investigation, 41: 1318–1322. doi: 10.1111/j.1365-2362.2011.02546.x
- Issue published online: 16 NOV 2011
- Article first published online: 30 MAY 2011
- Received 8 November 2010; accepted 19 April 2011
- Hydroperoxide and conjugated diene;
- oxidative stress;
- total antioxidant capacity
Eur J Clin Invest 2011; 41 (12): 1318–1322
Background Production of reactive oxygen species after ischaemic stroke may enhance tissue damage through multiple molecular pathways.
Materials and methods In this study, we examined the serum levels of lipoperoxide and hydroperoxide, conjugated dienes and total antioxidant capacity levels in 50 patients with acute ischaemic stroke (T0) to evaluate the possibility to use them as specific biochemical markers for cerebral ischaemia. Determinations were repeated after a month (T1) to correlate their relative changes with clinical evolution.
Results Lipoperoxide, hydroperoxide and conjugated diene levels in platelets were significantly higher in the early stages with respect to their late evaluation. On the contrary, total antioxidant capacity showed a significant increase at T1 with respect to T0. A significant negative correlation between total antioxidant capacity and NIHSS score at T0 and T1 was found. There was a significant positive correlation between lipoperoxide, hydroperoxide and conjugated dienes levels and NIHSS score at T0 and at T1.
Conclusions These findings suggest that changes in free radical generation and consequent oxidative stress may have a role in the pathogenesis of acute ischaemic lesions. The activation of defence mechanisms like total antioxidant capacity could be involved in the limitation of ischaemic damage progression.