Abstract |
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. alpha-Tocopherol (0.1-0.5 mol %), an efficient oxyradical scavenger, inhibits lipid peroxidation and prevents carboxyfluorescein release, 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 Ca(2+)-dependent permeabilization of the inner membrane of rat liver mitochondria promoted by external 0.1-1.0 mM ALA; this mechanism has been implicated in the pathophysiology of acute intermittent porphyria and lead poisoning.
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Authors | P I Oteiza, E J Bechara |
Journal | Archives of biochemistry and biophysics
(Arch Biochem Biophys)
Vol. 305
Issue 2
Pg. 282-7
(Sep 1993)
ISSN: 0003-9861 [Print] United States |
PMID | 8373166
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Cardiolipins
- Fatty Acids
- Lipid Peroxides
- Liposomes
- Phosphatidylcholines
- Vitamin E
- Aminolevulinic Acid
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Topics |
- Aminolevulinic Acid
(chemistry)
- Cardiolipins
(chemistry)
- Fatty Acids
(chemistry)
- In Vitro Techniques
- Lipid Peroxides
(metabolism)
- Liposomes
- Permeability
- Phosphatidylcholines
(chemistry)
- Vitamin E
(pharmacology)
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