Antioxidant enzymes expression in lymphocytes of patients undergoing carotid endarterectomy
Bajic, Vladimir B.
Isenovic, Esma R.
KAUST DepartmentComputational Bioscience Research Center (CBRC)
Applied Mathematics and Computational Science Program
Computer, Electrical and Mathematical Sciences and Engineering (CEMSE) Division
Online Publication Date2019-10-03
Print Publication Date2020-01
Permanent link to this recordhttp://hdl.handle.net/10754/658647
MetadataShow full item record
AbstractTo 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.
CitationObradovic, M., Zafirovic, S., Essack, M., Dimitrov, J., Zivkovic, L., Spremo-Potparevic, B., … Isenovic, E. R. (2020). Antioxidant enzymes expression in lymphocytes of patients undergoing carotid endarterectomy. Medical Hypotheses, 134, 109419. doi:10.1016/j.mehy.2019.109419
SponsorsThis 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.