Premium
δ‐Aminolaevulinic Acid Uptake, Toxicity, and Effect on [ 14 C]γ‐Aminobutyric Acid Uptake into Neurons and Glia in Culture
Author(s) -
Percy V. A.,
Lamm M. C. L.,
Taljaard J. J. F.
Publication year - 1981
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1981.tb02378.x
Subject(s) - toxicity , aminooxyacetic acid , ouabain , dinitrophenol , in vivo , neuroglia , biochemistry , reuptake , metabolism , biology , chemistry , in vitro , central nervous system , pharmacology , endocrinology , serotonin , sodium , enzyme , receptor , microbiology and biotechnology , organic chemistry
δ‐Aminolaevulinic acid (ALA) uptake into neurons and glia in primary culture as well as ALA toxicity and its effects on γ‐aminobutyric acid (GABA) uptake were examined. [4‐ 14 C]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‐ 14 C]ALA uptake whereas ouabain, KCN, or amino acids at 1 mM concentration were without effect. ALA (1 mM) caused a slight inhibition of [U‐ 14 C]GABA uptake into neurons (14%) and glia (9%), but was without effect at lower concentrations. It is unlikely that, in acute porphyria, ALA reaches sufficiently high levels in nervous tissue to interfere with the reuptake of GABA into neurons or glia. ALA was shown to be toxic, judged by the loss of cells, to both neurons and glia at concentrations as low as 10 μM. Such a concentration of ALA may be expected to occur in the CSF of porphyric patients in the acute attack. However, results obtained with 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.