The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Damage to rat liver mitochondria promoted by delta-aminolevulinic acid-generated reactive oxygen species: connections with acute intermittent porphyria and lead-poisoning.

delta-Aminolevulinic acid is a heme precursor accumulated in acute intermittent porphyria and lead-poisoning, which supposedly triggers the typical clinical expression associated with these diseases. Considering that: (i) erythrocyte anti-oxidant enzymes are abnormally high in patients with both disorders and (ii) delta-aminolevulinic acid autoxidation generates reactive oxygen species, a possible contribution of reactive oxygen species in the pathophysiology of these disorders is explored here. Evidence is provided that delta-aminolevulinic acid (2-15 mM) induces damage to isolated rat liver mitochondria. Addition of delta-aminolevulinic acid disrupts the mitochondrial membrane potential, promotes Ca2+ release from the intramitochondrial matrix and releases the state-4 respiration, thus enhancing the permeability of the membrane to H+. The lesion was abolished by catalase, superoxide dismutase (both enzymes inhibit delta-aminolevulinic acid autoxidation) and ortho-phenanthroline, but not by mannitol; added H2O2 induces damage poorly. These results suggest the involvement of deleterious reactive oxygen species formed at particular mitochondrial sites from transition metal ions and delta-aminolevulinic acid-generated peroxide and/or superoxide species. These observations might be compatible with previous work showing hepatic mitochondrial damage in liver biopsy samples of acute intermittent porphyria patients.[1]


WikiGenes - Universities