5-Aminolevulinic Acid Induces Lipid Peroxidation in Cardiolipin-Rich Liposomes

P. I. Oteiza, E. J H Bechara

Research output: Contribution to journalArticlepeer-review

57 Scopus citations


5-Aminolevulinic acid (ALA), a heme precursor accumulated in lead poisoning and acute intermittent porphyria, is known to undergo metal-catalyzed aerobic oxidation to yield reactive oxygen species. In phosphatidylcholine:cardiolipin (80:20) liposomes ALA (0.1-3.0 mM) promoted lipid peroxidation as evaluated by the formation of conjugated dienes and 2-thiobarbituric-reactive substances (TBARS). TBARS formation was dependent on ALA concentration and incubation time. ALA-induced lipid peroxidation was associated with an increase in liposome permeability as measured by the release of encapsulated carboxyfluorescein. α-Tocopherol (0.1-0.5 mol %), an efficient oxyradical scavenger, inhibits lipid peroxidation and prevents carboxyfluorescein rejease, suggesting that the permeabilization of liposomes is mainly due to lipid peroxidation. Cardiolipin, a major component of mitochondrial inner membrane, was particularly susceptible to ALA-induced lipid peroxidation. These results may be relevant to the previously observed Ca2+-dependent permeabilization of the inner membrane of rat liver mitochondria promoted by external 0.1-1.0mM ALA; this mechanism has been implicated in the pathophysiology of acute intermittent porphyria and lead poisoning.

Original languageEnglish (US)
Pages (from-to)282-287
Number of pages6
JournalArchives of Biochemistry and Biophysics
Issue number2
StatePublished - Sep 1993
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Biology
  • Biophysics
  • Biochemistry


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