title: Effect of ascorbic acid deficiency on catecholamine synthesis in adrenal glands of SMP30/GNL knockout mice.
abstract: OBJECTIVE
  The effect of an AA deficiency on catecholamine biosynthesis in adult mice in vivo is unknown. Therefore, we quantified catecholamine and the expression of catecholamine synthetic enzymes in the adrenal glands of senescence marker protein-30 (SMP30)/gluconolactonase (GNL) knockout (KO) mice placed in an AA-deficient state.
  
  
  METHODS
  At 30 days of age, mice were divided into the following 4 groups: AA (-) SMP30/GNL KO, AA (+) SMP30/GNL KO, AA (-) wild type (WT), and AA (+) WT. The AA (+) groups were given water containing 1.5 g/L AA, whereas the AA (-) groups received water without AA until the experiment ended. In addition, all mice were fed an AA-depleted diet. Catecholamine levels were measured by a liquid chromatographic method. Tyrosine hydroxylase, dopa decarboxylase, dopamine β-hydroxylase, and phenylethanolamine N-methyltransferase mRNA expression levels were measured with the quantitative real-time polymerase chain reaction (qPCR). Tyrosine hydroxylase and dopamine β-hydroxylase protein levels were quantified by Western blot analysis.
  
  
  RESULTS
  In the adrenals of AA (-) SMP30/GNL KO mice, noradrenaline and adrenaline levels decreased significantly compared to other three groups of mice, although there were no significant differences in dopamine β-hydroxylase or phenylethanolamine N-methyltransferase mRNA content. Moreover, there was no significant difference in their dopamine β-hydroxylase protein levels. On the other hand, AA depletion did not affect dopamine levels in adrenal glands of mice.
  
  
  CONCLUSIONS
  An AA deficiency decreases the noradrenaline and adrenaline levels in adrenal glands of mice in vivo.
authors.affiliation: Molecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology (TMIG), 35-2 Sakae-cho, Itabashi-ku, Tokyo, 173-0015, Japan.
authors.forename: Akiko
authors.initials: A
authors.lastname: Amano
authors.forename: Makoto
authors.initials: M
authors.lastname: Tsunoda
authors.forename: Toshiro
authors.initials: T
authors.lastname: Aigaki
authors.forename: Naoki
authors.initials: N
authors.lastname: Maruyama
authors.forename: Akihito
authors.initials: A
authors.lastname: Ishigami
mesh_terms: D000311:Adrenal Glands / Q000378:metabolism*; D000818:Animals; D001206:Ascorbic Acid Deficiency / Q000473:pathology*; D001342:Autonomic Nervous System Diseases / Q000378:metabolism; D001835:Body Weight; D002135:Calcium-Binding Proteins / Q000235:genetics; D002265:Carboxylic Ester Hydrolases / Q000235:genetics; D002395:Catecholamines / Q000096:biosynthesis*; D004299:Dopamine beta-Hydroxylase / Q000172:deficiency / Q000378:metabolism; D005260:Female; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D009638:Norepinephrine / Q000172:deficiency / Q000378:metabolism; D010625:Phenylethanolamine N-Methyltransferase / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D002135:Calcium-Binding Proteins; D002395:Catecholamines; D047908:Intracellular Signaling Peptides and Proteins; D012333:RNA, Messenger; C513324:Rgn protein, mouse; D014446:Tyrosine 3-Monooxygenase; D004299:Dopamine beta-Hydroxylase; D010625:Phenylethanolamine N-Methyltransferase; D002265:Carboxylic Ester Hydrolases; C020579:gluconolactonase; D009638:Norepinephrine