Abstract

It was first reported by RIGGS et al. (1953) that pyridoxal stimulates the accumulation of glycine by EMAT cells during an incubation of one hour. This stimulation is maximal at 5 mM pyridoxal (CHRISTENSEN et al. , 1954) , whereas at higher concentrations pyridoxal inhibits the accumulation of glycine and considerably reduces the cellular level of K-ions. The influx of α-aminoisobutyrate (α-AIB) also increases in the presence of pyridoxal (CHRISTENSEN et al. , 1958) . So far no appreciable effect of pyridoxal on the influx of glycine has been demonstrated. We found instead that pyridoxal, used as its ethylacetal, while strongly stimulating the accumulation of glycine by these cells, distinctly reduces the efflux coefficient of this amino acid (1961). A depression of the α-AIB efflux by the phosphate derivative of pyridoxal has been reported by CHRISTENSEN (1960). Such observations suggest that pyridoxal acts merely by tightening the cellular membrane without necessarily influencing the active transport directly. The present studies, however, did not confirm this hypothesis and furthermore revealed a distinct but very rapid and transient effect of pyridoxal on the influx of glycine, which had not previously been observed.

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