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Summary: Elevated amounts of glycine in serum and urine were demonstrated in patients and rats receiving the antiepileptic drug valproic acid. The hyperglycinuria in the patients was correlated to the dose of the anticonvulsant. The activity of the glycine cleavage system, the major catabolic pathway of glycine, in liver homogenates from rats treated with valproic acid was clearly reduced. Further in vitro studies on intact rat liver mitochondria and the sol‐ubilized glycine cleavage system showed that valproic acid and valproyl‐CoA significantly inhibited the glycine cleavage enzyme complex. It was concluded that the hyperglycinemia and hyperglycinuria seen in patients and rats during the administration of valproic acid are due to the inhibition of the glycine cleavage system, most probably by valproic acid and/or valproyl‐CoA. RÉSUMÉ Des taux élevés de glycine sérique et urinaire ont été décrits chez des patients et des rats traités par un an‐tiépileptique, le valproate de Na, 1'hyperglycinurie étant corrélée à la dose de 1'anticonvulsivant. L'acti‐vité du systeme de dégradation de la glycine par rupture de la molécule (clivage) est nettement réduite au niveau d'homogénats de foie de rats traités par le valproate de Na. D'autre part des études in vitro sur des mitochondries hépatiques de rat et au niveau du système de clivage de la glycine solubilisée ont montré que le valproate de Na et le valproyl‐CoA inhibent de façon significative le complexe enzymatique de clivage. Les auteurs concluent que l'hyperglycinémie et l'hyperglycinurie observées chez les patients et les rats sont dûes à une inhibition du système de clivage de la glycine, plus vraisemblablement par le valproate de Na et/ou le valproyl‐CoA. RESUMEN Se demostró la presencia de cantidades elevadas de glicina en el suero y en la orina de pacientes y de ratas que habian recibido el fármaco anticomicial ácido valproico. Al mismo tiempo, se correlacionó la hiperglicinuria con la dosis del anticomicial. La ac‐tividad del sistema de desdoblamiento de la glicina (la vía catabólica mayor) estaba reducido claramente en homogeneizados hepáticos de ratas tratadas con ácido valproico. Más aiin: en estudios “in vitro” usando mitocondrias hepáticas y sistemas de desdoblamiento de la glicina solubilizados en ratas intactas, se vió que tanto el ácido valproico como el valproil‐CoA disminuian de manera significativa el complejo en‐zimático esencial en el desdoblamiento de la glicina. La conclusión fue que la hiperglicinemia y la hiperglicinuria observadas, tanto en pacientes como en ratas, durante la administración de ácido valproico eran debidas a una inhibición del sistema de desdoblamiento de la glicina, probablemente por la acción del ácido valproico y/o del valproil Co A. ZUSAMMENFASSUNG Bei Patienten und Ratten, die Valproinsäure (VA) erhielten, wurden erhöhte Mengen von Glycin im Serum und Urin beobachtet. Die Hyperglycinurie der Patienten war mit der Dosis des Antikonvulsivums korreliert. Die Aktivität des Glycin‐Spaltungssystems, des Hauptweges der Katabolisierung des Glycins war in Leberhomogenaten von Ratten, die mit VA behan‐delt wurden, eindeutig reduziert. Weitere in Vitro‐Studien der intakten Rattenleber Mitochondrien und des gelosten Glycin‐Spaltungssystems zeigten, da(J VA und V‐CoA den Glycinspaltungsenzymkomplex signifikant hemmten. Es wurde geschlossen, dali Hyperglycinamie und Hyperglycinurie bei Patienten und Ratten während der Anwendung von VA Folge einer Hemmung des Glycin‐Spaltungssystems hochst wahrscheinlich durch VA und/oder V‐CoA sind.
Epilepsia – Wiley
Published: Dec 1, 1980
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