title: Ascorbic acid prevents protein oxidation in livers of senescence marker protein-30/gluconolactonase knockout mice.
abstract: OBJECTIVE
  Senescence marker protein-30 (SMP30)/gluconolactonase (GNL) knockout (KO) mice are incapable of synthesizing L-ascorbic acid (AA) in vivo. As AA is known to be a water-soluble anti-oxidant, we assessed protein oxidation levels in livers from SMP30/GNL KO mice maintained in an AA-insufficient condition.
  
  
  METHODS
  Livers were collected from male SMP30/GNL KO mice at the ages of 3, 6 and 12 months, and wild-type (WT) mice at the ages of 3, 6, 12 and 24 months. To assess protein oxidation, we measured the content of protein carbonyl, which is a major protein oxidation marker. AA levels were measured by 2,4-dinitrophenylhydrazine method using high-performance liquid chromatography.
  
  
  RESULTS
  Livers of SMP30/GNL KO mice had just ∼5% as much AA as those of WT mice from 3 to 12 months-of-age. Protein carbonyl levels in livers from SMP30/GNL KO mice were a significant 1.8- to 2.3-fold higher than those from age-atched WT mice. To establish that the AA-insufficiency caused this difference, we added AA to some drinking water, and examined the effect on AA and protein carbonyl levels in livers from SMP30/GNL KO and WT mice. Livers from SMP30/GNL KO mice given extra AA had a significantly higher content than those from their deprived counterparts. Furthermore, protein carbonyl levels in livers from AA-supplemented SMP30/GNL KO mice were significantly lower than those from the SMP30/GNL KO mice without AA supplementation. However, added AA did not affect the protein carbonyl levels in WT mice.
  
  
  CONCLUSIONS
  These results strongly suggest that AA plays an important role in preventing protein oxidation in vivo, thus enhancing overall health.
authors.affiliation: Molecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Sato
authors.forename: Akiko
authors.initials: A
authors.lastname: Amano
authors.forename: Yuki
authors.initials: Y
authors.lastname: Kishimoto
authors.forename: Keita
authors.initials: K
authors.lastname: Takahashi
authors.forename: Setsuko
authors.initials: S
authors.lastname: Handa
authors.forename: Naoki
authors.initials: N
authors.lastname: Maruyama
authors.forename: Akihito
authors.initials: A
authors.lastname: Ishigami
mesh_terms: D000375:Aging / Q000187:drug effects*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001205:Ascorbic Acid / Q000494:pharmacology*; D002135:Calcium-Binding Proteins / Q000378:metabolism*; D002265:Carboxylic Ester Hydrolases / Q000378:metabolism*; D002851:Chromatography, High Pressure Liquid; D004195:Disease Models, Animal; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism*; D050356:Lipid Metabolism / Q000187:drug effects / Q000502:physiology*; D008099:Liver / Q000378:metabolism*; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D010084:Oxidation-Reduction / Q000187:drug effects; D050050:Protein Carbonylation / Q000187:drug effects; D012614:Scurvy / Q000378:metabolism / Q000517:prevention & control*
chemical_list: D000975:Antioxidants; D002135:Calcium-Binding Proteins; D047908:Intracellular Signaling Peptides and Proteins; C513324:Rgn protein, mouse; D002265:Carboxylic Ester Hydrolases; C020579:gluconolactonase; D001205:Ascorbic Acid
keywords: aging; ascorbic acid; gluconolactonase; protein carbonyl; senescence marker protein-30