ビタミンB6酵素と痙攣

V.t. B6-Enzymes and Convulsion

　さきに牧野らはビタミンB₁のピリミジン部分つまりToxopyrimidine（TXP）を動物に注射するときおこる特有なけいれんがB₆群pyridoxine（PIN），pyridoxal（PAL），pyridoxamine（PAM）によつて防止されることを認め，B₆とけいれんの間に密接な関係があることをみとめた。われわれはさらにINAH，desoxypyridoxine，penicillamineなどもTXPに酷似するけいれん，すなわち，注射後1時間ないし2時間して，興奮状態となり，にわかに疾走を始め，これの終ると同時に間代性けいれんを始め，間もなく強直性けいれんに移行し，多くの場合またもとの状態に復す。これらB₆阻害剤の種類により多少異なるが多くの場合，このような形のけいれんを10〜15分のintervalをおいて数回くりかえし死亡するのを常とする。今回はこれらB₆の拮抗ないし阻害剤の脳B₆酵素系におよぼす影響ならびにその機作について検討し，また特にpenicillamineについては，その光学異性体（つまりD,L-peniciblamine）はおのおのけいれん誘発作用について異なる（D型は全くけいれんをおこさない）のでその機序についても検討を試みた。

　Effect of vitamin B₆ on the nervous system inexperimental animals have been interesting in relation to study of epilepsy, involving in pig ataxiaand "spontaneous" convulsion. The convulsionin mouse has been further investigated by inducing the convulsion by injecting vitamin B₆-antagonists or inhibitors, such as toxopyrimidine, desoxypyridoxine, INAH, penicillamine, etc. Andthe convulsion was found to protect by injectingvitamine B₆.

　One of the glutamic acid metabolism requiringfor vitamin B₆ is the decarboxylation of the acid, which in brain was depressed some 40~50% inconvulsion by injection of B₆-antagonists but recovered with administered vitamin B₆. The otherreaction, the transamination with oxaloacetateyielding aspartate and α-ketoglutalate in brainwas depressed only 5-10%.

　γ-Aminobutyric acid is the product of decarboxylation of glutamic acid, and γ-amino-β-oxybutyric acid is the product of oxidation ofγ-aminobutyric acid. Accordingly the convulsionby B₆-antagonists may be due to the decrease of γ-aminobutyric acid or γ-amino-β-oxybutyric acid. In this view it is understandable that attemptsshould have been made to influence experimentalconvulsion by administering these two acids. However these acids do not antagonize to theconvulsion by B₆-antagonists in mouse or dogs, and this may he clue either to a difference inthe species of decarboxylation reaction, for example decarboxylation of other amino acid, or todifference in the behaviour of the γ-aminobutyricacid and γ-amino-β-oxybutyric acid injected fromthat in brain.