Abstract
5-Aminolevulinic acid (ALA), a heme precursor accumulated in chemical and inborn porphyrias, has been demonstrated to produce reactive oxygen species upon metal-catalyzed aerobic oxidation and to cause oxidative damage to proteins, liposomes and subcellular structures. Exposure of plasmid pBR322 DNA to ALA (0.01–3 mM) in the presence of 10 μM Fe 2+ ions causes DNA single-strand breaks (ssb), revealed by agarose gel electrophoresis as an increase in the proportion of the open circular from (75 ± 7.5 at 3 mM ALA) at the expense of the supercoiled form. Addition of either anti-oxidant enzymes such as superoxide dismutase (10 μg/ml) and catalase (20 μg/ml), or a metal chelator (DTPA, 2.5 mM), or a HO . scavenger (mannitol, 100 mM) inhibited the damage (by 30, 45, 55, and 81%, respectively), evidencing the involvement of O 2 −·, H 2O 2 and HO . (by the Haber-Weiss reaction) in this process. Hydrogen peroxide (100 μM) or Fe 2+ (10 μM) alone were of little effect on the extent of DNA ssb. The present data may shed light on the correlation reported between primary liver-cell carcinoma and intermittent acute porphyria.
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