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Med Hypotheses. 2020 Jan;134:109419. doi: 10.1016/j.mehy.2019.109419. Epub 2019 Oct 3.

Antioxidant enzymes expression in lymphocytes of patients undergoing carotid endarterectomy.

Author information

1
Vinca Institute of Nuclear Sciences, University of Belgrade, Laboratory of Radiobiology and Molecular Genetics, Mike Petrovica Alasa 12-14, 11000 Belgrade, Serbia. Electronic address: obradovicmilan@hotmail.com.
2
Vinca Institute of Nuclear Sciences, University of Belgrade, Laboratory of Radiobiology and Molecular Genetics, Mike Petrovica Alasa 12-14, 11000 Belgrade, Serbia.
3
King Abdullah University of Science and Technology (KAUST), Computational Bioscience Research Center (CBRC), Computer, Electrical and Mathematical Sciences and Engineering (CEMSE) Division, Thuwal 23955-6900, Saudi Arabia.
4
Faculty of Pharmacy, Department of Physiology, University of Belgrade, Vojvode Stepe 450, 11221 Belgrade, Serbia.
5
Serbian Academy of Sciences and Arts, Belgrade, Serbia.

Abstract

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.

KEYWORDS:

Acute brain ischemia; Catalase; Cerebrovascular hemoglobin oxygen saturation; DNA damage; Superoxide dismutase

PMID:
31622925
DOI:
10.1016/j.mehy.2019.109419
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