To remedy carotid artery stenosis and prevent stroke surgical intervention is commonly used, and the gold standard being carotid endarterectomy (CEA). During CEA cerebrovascular hemoglobin oxygen saturation decreases and when this decrease reaches critical levels it leads to cerebral hypoxia that causes neuronal damage. One of the proposed mechanism that affects changes during CEA and contribute to acute brain ischemia (ABI) is oxidative stress. The increased production of reactive oxygen species and reactive nitrogen species during ABI may cause an unregulated inflammatory response and further lead to structural and functional injury of neurons. Antioxidant activity are involved in the protection against neuronal damage after cerebral ischemia. We hypothesized that neuronal injury and poor outcomes in patients undergoing CEA may be results of oxidative stress that disturbed function of antioxidant enzymes and contributed to the DNA damage in lymphocytes.
Bibliographical noteKAUST Repository Item: Exported on 2020-10-01
Acknowledged KAUST grant number(s): BAS/1/1606-01-01, FCC/1/1976-17-01, OSR#4129
Acknowledgements: This work was supported by Grants funded by the Ministry of Science, Education and Technological development, Republic of Serbia, No. 173033 (to E.R.I.), No. 41002 (to Dj.R.) and No. 173034 (to B.P.). The authors are grateful to the COST Action CA15132, ‘hCOMET’, for support. The research reported in this publication was also supported by the KAUST grant OSR#4129 (to E.R.I. and V.B.B.), which also supported M.O., and S.Z. V.B.B. has been supported by the KAUST Base Research Fund (BAS/1/1606-01-01), while V.B.B. and M.E. have been supported by KAUST Office of Sponsored Research (OSR) grant no. FCC/1/1976-17-01.