title: Enhancement of iron(II)-dependent reduction of nitrite to nitric oxide by thiocyanate and accumulation of iron(II)/thiocyanate/nitric oxide complex under conditions simulating the mixture of saliva and gastric juice.
abstract: Iron(III) ingested as a food component or supplement for iron deficiencies can react with salivary SCN(-) to produce Fe(SCN)(2+) and can be reduced to iron(II) by ascorbic acid in the stomach. Iron(II) generated in the stomach can react with salivary nitrite and SCN(-) to produce nitric oxide (NO) and FeSCN(+), respectively. The purpose of this investigation is to make clear the reactions among nitrite, SCN(-), iron ions, and ascorbic acid under conditions simulating the mixture of saliva and gastric juice. Iron(II)-dependent reduction of nitrite to NO was enhanced by SCN(-) in acidic buffer solutions, and the oxidation product of iron(II) reacted with SCN(-) to produce Fe(SCN)(2+). Almost all of the NO produced was autoxidized to N(2)O(3) under aerobic conditions. Iron(II)-dependent production of NO was also observed in acidified saliva. Under anaerobic conditions, NO transformed Fe(SCN)(2+) and FeSCN(+) to Fe(SCN)NO(+) in acidic buffer solutions. Fe(SCN)NO(+) was also formed under aerobic conditions when excess ascorbic acid was added to iron(II)/nitrite/SCN(-) systems in acidic buffer solutions and acidified saliva. The Fe(SCN)NO(+) formed was transformed to Fe(SCN)(2+) and iron(III) at pH 2.0 and pH 7.4, respectively, by O(2). Salivary glycoproteins could complex with iron(III) in the stomach preventing the formation of Fe(SCN)(2+). Ascorbic acid reduced iron(III) to iron(II) to react with nitrite and SCN(-) as described above. The above results suggest (i) that iron(II) can have toxic effects on the stomach through the formation of reactive nitrogen oxide species from NO when supplemented without ascorbic acid and through the formation of both reactive nitrogen oxide species and Fe(SCN)NO(+) when supplemented with ascorbic acid, and (ii) that the toxic effects of iron(III) seemed to be smaller than and similar to those of iron(II) when supplemented without and with ascorbic acid, respectively. Possible mechanisms that cause oxidative stress on the stomach through Fe(SCN)NO(+) are discussed.
authors.affiliation: Department of Bioscience, Kyushu Dental College, Kitakyushu 803-8580, Japan. takahama@kyu-dent.ac.jp
authors.forename: Umeo
authors.initials: U
authors.lastname: Takahama
authors.forename: Sachiko
authors.initials: S
authors.lastname: Hirota
mesh_terms: D001205:Ascorbic Acid / Q000378:metabolism; D005296:Ferrous Compounds / Q000378:metabolism; D005750:Gastric Juice / Q000378:metabolism*; D006801:Humans; D007501:Iron / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism*; D009573:Nitrites / Q000378:metabolism; D010084:Oxidation-Reduction; D010101:Oxygen Consumption; D012463:Saliva / Q000378:metabolism*; D013861:Thiocyanates / Q000378:metabolism*
chemical_list: D005296:Ferrous Compounds; D009573:Nitrites; D013861:Thiocyanates; D009569:Nitric Oxide; D007501:Iron; D001205:Ascorbic Acid