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Updated: Jan 15, 2026
Comet Assay as an Indirect Measure of Systemic Oxidative Stress
Published on: May 22, 2015
Cardiovascular comorbidities are risk factors for increased oxidative stress and DNA damage in migraine patients: a
Mustafa Gokce1, Muhammed Yunus Bektay2, Mustafa Uzun3
1Department of Pharmacology, Faculty of Pharmacy, Bezmialem Vakif University, Istanbul, Turkey. mustafagokce@outlook.com.
Insights
Migraine patients show higher oxidative stress and DNA damage, especially those with cardiovascular comorbidities. Treatment reduced these markers, but they remained elevated, indicating potential long-term cardiovascular risks.
Area of Science:
- Neuroscience
- Cardiology
- Biochemistry
Background:
- Migraine is a common neurovascular disorder.
- It is associated with oxidative stress and increased cardiovascular disease (CVD) risk, particularly in patients with comorbidities.
- This study investigates the link between oxidative stress, DNA damage, CVD, and migraine treatment outcomes.
Purpose of the Study:
- To examine the relationship between oxidative stress and DNA damage biomarkers in migraine patients.
- To assess the impact of cardiovascular comorbidities on these biomarkers.
- To evaluate the effect of six months of migraine prophylaxis on oxidative stress and DNA damage.
Main Methods:
- A prospective cohort study included 75 women: migraine with CVD (MC), migraine without CVD (M), and controls (C).
- Blood samples were analyzed for total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), DNA damage (comet assay), ischemia-modified albumin (IMA), and hypoxia-inducible factor-1α (HIF-1α).
- Measurements were taken at baseline and after six months of treatment.
Main Results:
- Migraine patients, especially the MC group, had significantly higher oxidative stress and DNA damage compared to controls.
- Biomarker levels decreased after treatment but remained elevated versus controls.
- Ischemic markers (IMA, HIF-1α) were higher in migraineurs and reduced post-treatment but did not normalize.
Conclusions:
- Cardiovascular comorbidities exacerbate oxidative stress and DNA damage in migraine patients.
- These factors may increase long-term cardiovascular risks.
- Monitoring biomarkers could aid personalized risk stratification and management for migraine patients.
Background:
Migraine is a prevalent neurovascular disorder frequently linked with oxidative stress and an elevated risk of cardiovascular diseases (CVDs), particularly in patient with comorbidities. This study aimed to investigate the relationships between oxidative stress and DNA damage biomarkers, cardiovascular comorbidities, and the effects of six months of migraine prophylaxis.
Methods:
A prospective cohort study was conducted between January and September 2024 at a tertiary neurology clinic, enrolling 75 women who were divided into three groups: migraine with cardiovascular comorbidities (MC, n = 25), migraine without comorbidities (M, n = 25), and age-matched healthy controls (C, n = 25). Migraine diagnosis was confirmed according to the International Classification of Headache Disorders, 3rd edition (ICHD-3), and patients with renal/hepatic dysfunction, active infections, migraine with aura, pregnancy, or other neurological/psychiatric disorders were excluded. Venous blood samples were obtained during the interictal period (≥ 72 h migraine-free) at baseline and after 6 months of standard acute migraine treatment. Biochemical analyses included total oxidant status (TOS), total antioxidant status (TAS), and calculation of oxidative stress index (OSI) using automated colorimetric assays. DNA damage was quantified by comet assay (single-cell gel electrophoresis), whereas ischemia-modified albumin (IMA) and hypoxia-inducible factor-1α (HIF-1α) were measured via ELISA. Statistical analyses were performed using ANOVA, paired and independent t tests, and Pearson correlation, with p < 0.05 considered significant.
Results:
Migraine patients exhibited significantly higher oxidative stress and DNA damage levels compared to controls, with the highest levels in those with cardiovascular comorbidities. After six months of treatment, biomarker levels decreased but remained elevated relative to controls. Ischemic markers (IMA and HIF-1α) were consistently higher in migraine patients, especially in the MC group, and although reduced post-treatment, did not normalise to control values.
Conclusions:
Cardiovascular comorbidities substantially increase oxidative stress and DNA damage in migraine patients, potentially heightening long-term cardiovascular risks. Monitoring these biomarkers may facilitate personalised risk stratification and management in clinical practice.
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