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Oxidative stress in ischaemic stroke
Author(s) -
Nanetti Laura,
Raffaelli Francesca,
Vignini Arianna,
Perozzi Cecilia,
Silvestrini Mauro,
Bartolini Marco,
Provinciali Leandro,
Mazzanti Laura
Publication year - 2011
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.2011.02546.x
Subject(s) - oxidative stress , antioxidant capacity , antioxidant , stroke (engine) , ischaemic stroke , conjugated diene , medicine , ischemia , reactive oxygen species , positive correlation , pathogenesis , brain ischemia , conjugated system , oxidative phosphorylation , chemistry , biochemistry , mechanical engineering , monomer , organic chemistry , engineering , polymer
Eur J Clin Invest 2011; 41 (12): 1318–1322 Abstract 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.