δ‐Aminolaevulinic Acid Uptake, Toxicity, and Effect on [14C]γ‐Aminobutyric Acid Uptake into Neurons and Glia in Culture

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Abstract
.delta.-Aminolevulinic acid (ALA) uptake into chick neurons and glia in primary culture and ALA toxicity and its effects on .gamma.-aminobutyric acid (GABA) uptake were examined. [4-14C]ALA uptake into neurons and glia was nonsaturable, partially Na+- and temperature-dependent and appeared to comprise mainly diffusion into the cell. 2,4-Dinitrophenol caused some inhibition of [4-14C]ALA uptake, ouabain, KCN or amino acids at 1 mM were without effect. ALA (1 mM) caused a slight inhibition of [U-14C]GABA uptake into neurons (14%) and glia (9%) but was without effect at lower concentrations. In acute porphyria ALA probably does not reach a sufficiently high level in nervous tissue to interfere with the reuptake of GABA into neurons or glia. ALA was toxic, judged by the loss of cells, to neurons and glia at concentrations as low as 10 .mu.M. A similar concentration of ALA may be expected to occur in the CSF of porphyric patients in the acute attack. The dispersed cells in culture may not necessarily reflect the situation in vivo where the cell may have a far greater resistance to the effects of toxic agents.