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Protective effects of riboflavin and selenium on brain microsomal Ca2+-ATPase and oxidative damage caused by glyceryl trinitrate in a rat headache model.
- Source :
-
Biological trace element research [Biol Trace Elem Res] 2015 Mar; Vol. 164 (1), pp. 72-9. Date of Electronic Publication: 2014 Dec 11. - Publication Year :
- 2015
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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.
- Subjects :
- Animals
Brain drug effects
Disease Models, Animal
Female
Headache chemically induced
Headache metabolism
Migraine Disorders chemically induced
Migraine Disorders drug therapy
Migraine Disorders metabolism
Rats
Rats, Wistar
Brain metabolism
Calcium-Transporting ATPases metabolism
Headache drug therapy
Microsomes drug effects
Microsomes metabolism
Nitroglycerin toxicity
Oxidative Stress drug effects
Riboflavin therapeutic use
Selenium therapeutic use
Subjects
Details
- Language :
- English
- ISSN :
- 1559-0720
- Volume :
- 164
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Biological trace element research
- Publication Type :
- Academic Journal
- Accession number :
- 25492827
- Full Text :
- https://doi.org/10.1007/s12011-014-0199-x