Effect of ascorbic acid deficiency on catecholamine synthesis in adrenal glands of SMP30/GNL knockout mice

Eur J Nutr. 2014 Feb;53(1):177-85. doi: 10.1007/s00394-013-0515-9. Epub 2013 Mar 19.


Purpose: 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.

Conclusion: An AA deficiency decreases the noradrenaline and adrenaline levels in adrenal glands of mice in vivo.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenal Glands / metabolism*
  • Animals
  • Ascorbic Acid Deficiency / pathology*
  • Autonomic Nervous System Diseases / metabolism
  • Body Weight
  • Calcium-Binding Proteins / genetics
  • Carboxylic Ester Hydrolases / genetics
  • Catecholamines / biosynthesis*
  • Dopamine beta-Hydroxylase / deficiency
  • Dopamine beta-Hydroxylase / metabolism
  • Female
  • Intracellular Signaling Peptides and Proteins / genetics
  • Male
  • Mice
  • Mice, Knockout
  • Norepinephrine / deficiency
  • Norepinephrine / metabolism
  • Phenylethanolamine N-Methyltransferase / metabolism
  • RNA, Messenger / metabolism
  • Tyrosine 3-Monooxygenase / metabolism


  • Calcium-Binding Proteins
  • Catecholamines
  • Intracellular Signaling Peptides and Proteins
  • RNA, Messenger
  • Rgn protein, mouse
  • Tyrosine 3-Monooxygenase
  • Dopamine beta-Hydroxylase
  • Phenylethanolamine N-Methyltransferase
  • Carboxylic Ester Hydrolases
  • gluconolactonase
  • Norepinephrine

Supplementary concepts

  • dopamine beta hydroxylase deficiency