Methyl 5-diazolevulinate intervention in chemically induced porphyria of rats

Nechama S. Kosower*, Edward M. Kosower, Arthur B. Zinn, Robert Carraway

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


We have found that methyl 5-diazolevulinate (diazoester) abolishes the excretion of porphobilinogen from rats made porphyric with allylisopropylacetamide. At the same time, the high levels of δ-aminolevulinic acid found in the urine of porphyric rats are not significantly altered by diazoester. Induction of convulsions in porphyric rats by 4-methoxymethylpyridoxine is unaffected by diazoester, indicating that porphobilinogen is not a factor in the neurological consequences of porphyria, and that a precursor of porphobilinogen must be responsible. Only one precursor, δ-aminolevulinic acid, in a reasonable choice as the agent involved in the neurological changes. It was postulated that pyridoxal derivatives of δ-aminolevulinic acid strongly inhibit enzymes controlling the metabolism of γ-aminobutyric acid, a neurotransmitter, and that the neurological effects observed arise from an imbalance in γ-aminobutyric acid concentrations. It was suggested that a strong inhibitor for δ-aminolevulinic acid synthetase might be useful in the treatment of acute intermittent porphyria. The diazoester represents an example of a potentially useful class of compounds, the diazoketones, and its use in rats at relatively high dosages demonstrates that such compounds, given the appropriate specificities, are not very toxic on a short-term basis.

Original languageEnglish
Pages (from-to)389-406
Number of pages18
JournalBiochemical Medicine
Issue number5
StatePublished - Apr 1969
Externally publishedYes


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