AGENTS ON AMINO ACIDS IN MAMMALIAN BRAIN 505 
hibition with NH,OH 7m vivo is primarily of the transaminase (Table Il). A mecha- 
nism for this preferential inhibition has been discussed’? and the formation of a 
non-dissociable complex with the tightly bound PyP coenzyme was suggested. 
Recent results in our laboratory have shown that pyridoxal oxime does not inhibit 
the GABA-T of rat brain 7m vivol’. This observation is in accord with the idea that 
the apoenzyme—coenzyme bond of GABA-T is very strong, permitting little if any 
substitution with the oxime directly. 
Treatment of rats with aminooxyacetic acid caused the accumulation of /-alanine 
in liver, kidney, and spleen (Figs. 23-28). No changes were found in skeletal muscle, 
but in heart muscle aminooxyacetic acid produced a decrease in lysine content 
which might be related to possible shifts in electrolyte balance (Figs. 29-32). Levels 
| = 
23 24 
ie | Nl 
on 
20 26 
‘ @ * 
27 28 
e ” a 
Figs. 23-28. Effect of aminooxyacetic acid upon the concentration of amino acids in tissues of 
rat. Injected dose NH,OCH,—COOH:!/, HCl (adjusted to pH 6): too mg/kg. Animals were 
decapitated 6 h after injection. Arrows point to f-alanine. Figs. 23-24: liver. Figs. 25-26, kidney. 
Figs. 27-28: spleen. All odd numbered chromatograms represent tissues from normal control 
animals; all even numbered chromatograms illustrate changes in the tissues of treated animals. 
References p. 508 
