Protective Effects of Riboflavin and Selenium on Brain Microsomal Ca2+-ATPase and Oxidative Damage Caused by Glyceryl Trinitrate in a Rat Headache Model

Abstract

Migraine headaches are considered to be associated with increased mitochondrial energy metabolism. Mitochondrial oxidative stress is also important in migraine headache pathophysiology although riboflavin and selenium (Se) induced a modulator role on mitochondrial oxidative stress in the brain. The current study aimed to determine the effects of Se with/without riboflavin on the microsomal membrane Ca(2+)-ATPase (MMCA), lipid peroxidation, antioxidant, and electroencephalography (EEG) values in glyceryl trinitrate (GTN)-induced brain injury rats. Thirty-two rats were randomly divided into four groups. The first group was used as the control, and the second group was the GTN group. Se and Se plus oral riboflavin were administered to rats constituting the third and fourth groups for 10 days prior to GTN administration. The second, third, and fourth groups received GTN to induce headache. Ten hours after the administration of GTN, the EEG records and brain cortex samples were obtained for all groups. Brain cortex microsomes were obtained from the brain samples. The brain and microsomal lipid peroxidation levels were higher in the GTN group compared to the control group, whereas they were decreased by selenium and selenium + riboflavin treatments. Vitamin A, vitamin C, vitamin E, and reduced glutathione (GSH) concentrations of the brain and MMCA, GSH and glutathione peroxidase values of microsomes were decreased by the GTN administration, although the values and β-carotene concentrations were increased by Se and Se + riboflavin treatments. There was no significant change in EEG records of the four groups. In conclusion, Se with/without riboflavin administration protected against GTN-induced brain oxidative toxicity by inhibiting free radicals and the modulation of MMCA activity and supporting the antioxidant redox system.

Riboflavin: The Health Benefits of a Forgotten Natural Vitamin

“…RF and selenium (SE) can decrease lipid peroxidation (LP) levels and increase glutathione and reduced glutathione levels in microsomal brains. The co-administration of RF and vitamin E induced a decrease in calcium and a decrease in brain and microsomal lipid peroxidation levels [19,20]. The brain and microsomal lipid peroxidation levels (LP) have been found to be higher in the GTN-induced rats with migraine headaches compared to healthy rats [19]; whereas SE orally pre-treated rats with or without RF were protected against GTN-induced brain oxidative toxicity, by inhibiting free radicals and MMCA activity and supporting the antioxidant effect of RF [19].…”

“…The co-administration of RF and vitamin E induced a decrease in calcium and a decrease in brain and microsomal lipid peroxidation levels [19,20]. The brain and microsomal lipid peroxidation levels (LP) have been found to be higher in the GTN-induced rats with migraine headaches compared to healthy rats [19]; whereas SE orally pre-treated rats with or without RF were protected against GTN-induced brain oxidative toxicity, by inhibiting free radicals and MMCA activity and supporting the antioxidant effect of RF [19]. It has been demonstrated that RF plays a protective role in a time-and dose-dependent manner against excitotoxicity of cerebellar granule neurons induced by glutamate/NMDA in C57/B strain mice [21].…”

“…Anti-aging in Drosophila melanogaster (fruit fly) RF at 120 µg/mL SOD1 ↑; CAT ↑; lipofuscin (LF) ↓ RF prolonged the life span and increased reproductive capacity through anti-oxidative stress pathway involving enhancing the activity of SOD1 and CAT and inhibiting lipofuscin accumulation [11] Keratoconus corneal stroma cells RF with selenium administration protected against GTN-induced brain oxidative toxicity by protecting brain MMCA activity, inhibiting free radicals and supporting the antioxidant redox system. [19] Migraine model RF 100 mg/kg was treated before GTN-induced migraine Lipid peroxidation↓, GSH↑ RF and vitamin E had a protective effect on the GTN-induced brain injury by inhibiting free radical production, regulation of calcium-dependent processes, and supporting the antioxidant redox system.…”

Selenium, selenoproteins and neurodegenerative diseases

“…53 Selenium treatment as organic selenomethionine and inorganic SeO 3 2À resulted in a similar increased activity of antioxidant enzymes, scavenging of reactive oxygen species (ROS) and reduced protein carbonyl content of patulin-induced brain damaged rats, 54 and reduced the pro-oxidant effects of glyceryl trinitrate in a rat model of migraine headaches. 55 Administration of SeO 3 2À to suckling pups whose dams had methimazole-induced hypothyroidism decreased total oxidant status and reduced degenerative changes in the granular cell layer of the dental gyrus, 56 and increased levels of brain-derived neurothophic factor (BDNF) in the hippocampus and cerebellum of both hypothyroid and control groups. 57 In a rat model of postnatal protein malnutrition oral Se and zinc (Zn) supplementation increased not only antioxidant enzyme activity, but also corrected the neurobehavioral deficits caused by a protein-deficient diet.…”

The efficiency of Poly(ADP‐Ribose) Polymerase (PARP) cleavage on detection of apoptosis in an experimental model of testicular torsion

“…The dosage was determined according to Ethical Committee of Suleyman Demirel University and literature (Nazıroğlu et al . ). Ketamine was purchased from Pfizer, Istanbul, Turkey, and xylazine was purchased from Egevet, Izmir, Turkey.…”