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Antioxidant enzymes expression in lymphocytes of patients undergoing carotid endarterectomy
Milan Obradovic1, Sonja Zafirovic1, Magbubah Essack2
1Vinca Institute of Nuclear Sciences, University of Belgrade, Laboratory of Radiobiology and Molecular Genetics, Mike Petrovica Alasa 12-14, 11000 Belgrade, Serbia.
Insights
Carotid endarterectomy (CEA) can cause brain injury due to oxidative stress. This study suggests that oxidative stress during CEA may damage DNA and impair antioxidant enzymes, leading to poor patient outcomes.
Area of Science:
- Neuroscience
- Vascular Surgery
- Biochemistry
Background:
- Carotid endarterectomy (CEA) is a standard surgical procedure to prevent stroke in patients with carotid artery stenosis.
- Cerebral hypoxia and acute brain ischemia (ABI) can occur during CEA due to decreased cerebrovascular hemoglobin oxygen saturation.
- Oxidative stress, characterized by increased reactive oxygen and nitrogen species, is implicated in neuronal damage during ABI.
Purpose of the Study:
- To investigate the role of oxidative stress in neuronal injury and poor outcomes following CEA.
- To explore the hypothesis that impaired antioxidant enzyme function and DNA damage in lymphocytes are consequences of oxidative stress during CEA.
Main Methods:
- The study focuses on analyzing the biochemical changes, specifically oxidative stress markers and antioxidant enzyme activity, in patients undergoing CEA.
- Assessment of DNA damage in lymphocytes will be conducted to correlate with oxidative stress levels and clinical outcomes.
Main Results:
- Preliminary findings suggest a correlation between increased oxidative stress during CEA and compromised antioxidant enzyme function.
- Evidence indicates that oxidative stress contributes to DNA damage in lymphocytes, potentially impacting neuronal health.
- A link is observed between these biochemical changes and poorer patient outcomes post-CEA.
Conclusions:
- Oxidative stress is a significant factor contributing to neuronal injury and adverse outcomes in patients undergoing CEA.
- Impaired antioxidant defenses and DNA damage are key mechanisms through which oxidative stress affects brain health during this procedure.
- Further research into antioxidant therapies could mitigate CEA-related brain injury and improve patient prognosis.
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.
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