title: Riboflavin and vitamin E increase brain calcium and antioxidants, and microsomal calcium-ATP-ase values in rat headache models induced by glyceryl trinitrate.
abstract: The essential use of riboflavin is the prevention of migraine headaches, although its effect on migraines is considered to be associated with the increased mitochondrial energy metabolism. Oxidative stress is also important in migraine pathophysiology. Vitamin E is a strong antioxidant in nature and its analgesic effect is not completely clear in migraines. The current study aimed to investigate the effects of glyceryl trinitrate (GTN)-sourced exogen nitric oxide (NO), in particular, and also riboflavin and/or vitamin E on involved in the headache model induced via GTN-sourced exogen NO on oxidative stress, total brain calcium levels, and microsomal membrane Ca(2+)-ATPase levels. GTN infusion is a reliable method to provoke migraine-like headaches in experimental animals and humans. GTN resulted in a significant increase in brain cortex and microsomal lipid peroxidation levels although brain calcium, vitamin A, vitamin C, and vitamin E, and brain microsomal-reduced glutathione (GSH), glutathione peroxidase (GSH-Px), and plasma-membrane Ca(2+)-ATPase values decreased through GTN. The lipid peroxidation, GSH, vitamin A, β-carotene, vitamin C, and vitamin E, and calcium concentrations, GSH-Px, and the Ca(2+)-ATPase activities were increased both by riboflavin and vitamin E treatments. Brain calcium and vitamin A concentrations increased through riboflavin only. In conclusion, riboflavin 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. However, the effects of vitamin E on the values seem more important than in riboflavin.
authors.affiliation: Department of Neurology, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey.
authors.forename: Ayşe
authors.initials: A
authors.lastname: Bütün
authors.forename: Mustafa
authors.initials: M
authors.lastname: Nazıroğlu
authors.forename: Serpil
authors.initials: S
authors.lastname: Demirci
authors.forename: Ömer
authors.initials: Ö
authors.lastname: Çelik
authors.forename: Abdulhadi Cihangir
authors.initials: AC
authors.lastname: Uğuz
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001205:Ascorbic Acid / Q000378:metabolism; D001921:Brain / Q000187:drug effects* / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism*; D000252:Calcium-Transporting ATPases / Q000378:metabolism*; D004195:Disease Models, Animal; D004789:Enzyme Activation; D005260:Female; D005978:Glutathione; D005979:Glutathione Peroxidase; D006261:Headache / Q000139:chemically induced / Q000378:metabolism; D015227:Lipid Peroxidation; D008861:Microsomes / Q000378:metabolism*; D005996:Nitroglycerin / Q000009:adverse effects; D018384:Oxidative Stress; D051381:Rats; D012256:Riboflavin / Q000494:pharmacology*; D014801:Vitamin A / Q000378:metabolism; D014810:Vitamin E / Q000494:pharmacology*; D019207:beta Carotene / Q000378:metabolism
chemical_list: D000975:Antioxidants; D019207:beta Carotene; D014801:Vitamin A; D014810:Vitamin E; D005979:Glutathione Peroxidase; D000252:Calcium-Transporting ATPases; D005996:Nitroglycerin; D005978:Glutathione; D001205:Ascorbic Acid; D002118:Calcium; D012256:Riboflavin