title: The in vivo cytoprotection of ascorbic acid against ischemia/reoxygenation injury of rat liver.
abstract: The in vivo effects of ascorbic acid on the reoxygenated liver tissue were examined, with regard to the following effects: (i) the effects of scavenging radicals and/or reducing peroxidative reactions, and (ii) the effects of the chelation with low-molecular-weight iron and increasing its reactivity (radical production). Ascorbic acid is one of the water-soluble vitamins known to have various physiological effects involving both chelating and reducing properties at once. Lipid peroxidation of the reoxygenated liver tissue estimated by the production of TBARS (thiobarbituric acid-reactive substance) and LPO (lipid hydroperoxides) was suppressed effectively by the preischemic intraperitoneal administration of ascorbic acid. Ascorbic acid also showed this anti-oxidant effect in a dose-dependent manner. The analysis of the levels of ascorbic acid and glutathione of the liver tissue revealed that ascorbic acid works as an anti-oxidant probably by being oxydized finally to dehydroascorbic acid just after the reoxygenation. The latter was reduced to ascorbic acid again, coupled with the conversion of GSH to GSSG in the postischemic time course. The predominant effect of ascorbic acid on the reoxygenated liver tissue seems to be caused by the scavenging radicals and/or reducing peroxidative reactions, rather than by chelating iron and increasing its reactivity (radical production). Cellular integrity (estimated by the release of GOT, GPT, and LDH) and the energy state of the postischemic liver tissue (estimated by the tissue ATP level) were also well preserved by the administration of ascorbic acid.
authors.affiliation: Department of Surgery III, Tokyo Women's Medical College, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Ozaki
authors.forename: S
authors.initials: S
authors.lastname: Fuchinoue
authors.forename: S
authors.initials: S
authors.lastname: Teraoka
authors.forename: K
authors.initials: K
authors.lastname: Ota
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism* / Q000494:pharmacology*; D001219:Aspartate Aminotransferases / Q000378:metabolism; D003676:Deferoxamine / Q000494:pharmacology; D003683:Dehydroascorbic Acid / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005978:Glutathione / Q000378:metabolism*; D007501:Iron / Q000032:analysis / Q000378:metabolism; D007511:Ischemia / Q000378:metabolism*; D007700:Kinetics; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects*; D008099:Liver / Q000098:blood supply* / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000517:prevention & control*; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D013997:Time Factors
chemical_list: D017392:Thiobarbituric Acid Reactive Substances; D000255:Adenosine Triphosphate; D007501:Iron; D007770:L-Lactate Dehydrogenase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D005978:Glutathione; D003676:Deferoxamine; D001205:Ascorbic Acid; D003683:Dehydroascorbic Acid