title: [Mechanisms of nitroxide-ergic dysregulation in tissues of parodontium in rats under combined excessive sodium nitrate and fluoride intake].
abstract: BACKGROUND
  intake of inorganic nitrates is typically accompanied by production of excessive amount of nitric oxide (NO), which level is maintained by the mechanism of autoregulation known as the NO cycle. Hypothetically, this process may be disrupted with fluorides that are able to suppress arginase pathway of L-arginine metabolism, which competes with NO-synthase pathway.
  
  
  OBJECTIVE
  to study mechanisms of disregulation of oxidative (NO-synthase) and non-oxidative (arginase) metabolic pathways of L-arginine in the tissues of periodontium under combined excessive sodium nitrate and fluoride intake.
  
  
  METHODS
  these investigations were carried out on 90 white Wistar rats. Homogenates of parodontium soft tissues were used to assess spectrophotometrically the total activities of NO-synthase (NOS), arginase, ornithine decarboxylase as well as the peroxynitrite concentration.
  
  
  RESULTS
  typical for the isolated sodium nitrate administration inhibition of total NOS activity varies under combined administration of nitrate and sodium fluoride and is usually manifested by its hyperactivation that is accompanied by an increase in peroxynitrite concentration. At this time arginase and ornithine decarboxylase activity is observed to be substantially reduced. The administration of aminoguanidine, an iNOS inhibitor, (20 mg/kg, twice a week during the experiment) increases arginase and ornithine decarboxylase activities, and the administration of L-arginine (500 mg/kg, twice a week) results in the increase of arginase activity. The administration of L-selenomethionine, a peroxynitrite scavenger (3 mg/kg, twice a week), and JSH-23 (4-methyl-N-(3-phenylpropyl) benzene-1,2-diamine, an inhibitor of NF-κB activation (1 mg/kg, twice a week) for modeling binary nitrate and fluoride intoxication reduces the total concentration of NOS activity and peroxynitrite concentration, and increases ornithine decarboxylase activity.
  
  
  CONCLUSIONS
  the combined effect of nitrate and sodium fluoride for 30 days leads to disregulatory increased activity of NO-synthase enzymes and reduction of arginase pathway of L-arginine in the soft tissues of parodontium that is promoted by hyperactivation of iNOS and NF-κB, and increased peroxynitrite production.
authors.affiliation: Высшее государственное учебное заведение Украины ≪Украинская медицинская стоматологическая академия≫, Полтава, Украина.
authors.forename: Алексей В
authors.initials: АВ
authors.lastname: Богданов
authors.affiliation: Высшее государственное учебное заведение Украины ≪Украинская медицинская стоматологическая академия≫, Полтава, Украина.
authors.forename: Юлия М
authors.initials: ЮМ
authors.lastname: Гришко
authors.affiliation: Высшее государственное учебное заведение Украины ≪Украинская медицинская стоматологическая академия≫, Полтава, Украина, e-mail: kostenko11111@rambler.ru.
authors.forename: Виталий А
authors.initials: ВА
authors.lastname: Костенко
mesh_terms: D000284:Administration, Oral; D000818:Animals; D001119:Arginase / Q000032:analysis / Q000187:drug effects; D005459:Fluorides / Q000008:administration & dosage / Q000494:pharmacology* / Q000633:toxicity; D009566:Nitrates / Q000008:administration & dosage / Q000494:pharmacology* / Q000633:toxicity; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D009955:Ornithine Decarboxylase / Q000378:metabolism*; D010519:Periodontium / Q000187:drug effects* / Q000201:enzymology; D030421:Peroxynitrous Acid / Q000032:analysis / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
chemical_list: D009566:Nitrates; D030421:Peroxynitrous Acid; C031618:sodium nitrate; D019001:Nitric Oxide Synthase; D001119:Arginase; D009955:Ornithine Decarboxylase; D005459:Fluorides
keywords: NO-synthase; arginase; nitrate and fluoride poisoning; parodontium