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.