An increased incidence of cancer in patients suffering from acute intermittent porphyria (AIP) is thought to be related to δ-aminolevulinic acid (ALA) accumulation. Chronic treatment with ALA augmented 8-oxo-7,8-dihydro-2'-deoxyguanosine levels, decreased microsomal and mitochondrial membrane fluidity and increased lipid peroxidation in blood serum. Co-treatment with melatonin completely counteracted the effects of ALA. Melatonin effectively protects DNA and microsomal and mitochondrial membranes in rat kidney from oxidative damage due to ALA. Because of its low toxicity and anticarcinogenic properties, melatonin could be tested as an agent to reduce oxidative damage in patients with AIP. Copyright (C) 2000 Elsevier Science Ireland Ltd.
- Microsomal and mitochondrial membranes
- Oxidative damage
- δ-Aminolevulinic acid
ASJC Scopus subject areas
- Cancer Research