Superoxide Dismutase and Catalase Genotypes in Pediatric Migraine Patients

Saygı, Semra; Erol, İlknur; Alehan, Füsun; Yalçın, Yaprak Yılmaz; Kubat, Gözde; Ataç, Fatma Belgin

doi:10.1177/0883073815575366

Cited by 17 publications

(8 citation statements)

References 21 publications

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“… 22 , 26 By contrast, children with migraine were found to have higher CAT levels than healthy controls. 27 Several studies have demonstrated that inadequate antioxidant defense systems are associated with different types of headache. 22 , 28 – 30 Eren et al 6 reported that the TAS values of migraine patients and controls were similar, and another recent study of patients with migraine also showed similar TAS in migraineurs and controls.…”

Section: Discussionmentioning

confidence: 99%

Oxidative/antioxidative status, lymphocyte DNA damage, and urotensin-2 receptor level in patients with migraine attacks

Yigit¹,

Söğüt²,

Tataroglu³

et al. 2018

NDT

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Background: The present study investigated the potential roles of plasma lymphocyte DNA damage, the urotensin-2 receptor (UTS2R), and oxidative changes in patients with varying degrees of migraine-related disability who were in the ictal phase and presented to our emergency department. Methods: This study enrolled 40 consecutive adult patients with migraine attack and 40 age-and sex-matched healthy controls. The same health care professional determined the headache-related disability of each patient's migraine attack using the Migraine Disability Assessment Scale (MIDAS); patients were divided into three groups based on MIDAS score. Plasma lymphocyte DNA damage; UTS2R, malondialdehyde (MDA), and catalase (CAT) levels; total oxidant status (TOS); total antioxidant status (TAS); and the oxidative stress index (OSI) were used as predictors of early oxidative changes. Results: Plasma lymphocyte DNA damage, TOS, MDA levels, and OSI values were significantly higher in patients with migraine compared to controls. Conversely, TAS and CAT and UTS2R levels were markedly lower in patients with migraine compared to controls. Comparisons of the patient groups by MIDAS score revealed significant differences in plasma lymphocyte DNA damage and CAT levels but no differences in TOS, MDA levels, OSI, TAS, or UTS2R levels. MIDAS scores were positively correlated with the degree of lymphocyte DNA damage, but neither of these factors was significantly related to CAT levels. Conclusion: The present data suggest that lymphocyte DNA damage and changes in oxidative/ antioxidative status may reflect an enhanced oxidative damage and an ineffective antioxidant defense system in migraineurs during headache attacks. In addition, lymphocyte DNA damage levels may be an indicator of the degree of migraine-related disability as assessed by MIDAS score.

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Section: Discussionmentioning

confidence: 99%

Oxidative/antioxidative status, lymphocyte DNA damage, and urotensin-2 receptor level in patients with migraine attacks

Yigit¹,

Söğüt²,

Tataroglu³

et al. 2018

NDT

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“…For example, a polymorphism (the rs4880 TT (Val/Val) genotype) in the gene that enco des superoxide dismutase 2 (SOD2), a crucial enzyme in the clearance of mitochondrial ROS, has been associated with unilateral cranial autonomic symptoms in patients with migraine with aura 133 . In paediatric patients with migraine, the C-T genotype and C allele at position 16 of SOD2 and the A-A genotype and A allele at position 21 of CAT (which encodes catalase) were more frequent among patients with migraine with or without aura than among healthy controls 134 . Both enzymes act in concert to reduce ROS accumu lation, and the polymorphisms reported in this study are thought be associated with reduced transcriptional and/or enzyme activity, meaning people with migraine are more vulnerable to oxidative stress.…”

Section: Non-mitochondrial Genesmentioning

confidence: 96%

The metabolic face of migraine — from pathophysiology to treatment

et al. 2019

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Migraine can be regarded as a conserved, adaptive response that occurs in genetically predisposed individuals with a mismatch between the brain's energy reserve and workload. Given the high prevalence of migraine, genotypes associated with the condition seem likely to have conferred an evolutionary advantage. Technological advances have enabled the examination of different aspects of cerebral metabolism in patients with migraine, and complementary animal research has highlighted possible metabolic mechanisms in migraine pathophysiology. An increasing amount of evidence-much of it clinical-suggests that migraine is a response to cerebral energy deficiency or oxidative stress levels that exceed antioxidant capacity and that the attack itself helps to restore brain energy homeostasis and reduces harmful oxidative stress levels. Greater understanding of metabolism in migraine offers novel therapeutic opportunities. In this Review , we describe the evidence for abnormalities in energy metabolism and mitochondrial function in migraine, with a focus on clinical data (including neuroimaging, biochemical, genetic and therapeutic studies), and consider the relationship of these abnormalities with the abnormal sensory processing and cerebral hyper-responsivity observed in migraine. We discuss experimental data to consider potential mechanisms by which metabolic abnormalities could generate attacks. Finally , we highlight potential treatments that target cerebral metabolism, such as nutraceuticals, ketone bodies and dietary interventions.

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“…Three genetic polymorphisms have been reported in the promoter region of the CAT named A-21T (rs7943316), C-262T (rs1001179) and C-844T (rs769214) [2][3][4]. Previous studies have shown that CAT polymorphisms were associated with the risks of several multifactorial diseases [4][5][6][7][8][9][10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%