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pubmed-article:21512303pubmed:abstractTextGuttiferone-A (GA) is a natural occurring polyisoprenylated benzophenone with several reported pharmacological actions. We have assessed the protective action of GA on iron-induced neuronal cell damage by employing the PC12 cell line and primary culture of rat cortical neurons (PCRCN). A strong protection by GA, assessed by the 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carbox-anilide (XTT) assay, was revealed, with IC(50) values <1 µM. GA also inhibited Fe(3+)-ascorbate reduction, iron-induced oxidative degradation of 2-deoxiribose, and iron-induced lipid peroxidation in rat brain homogenate, as well as stimulated oxygen consumption by Fe(2+) autoxidation. Absorption spectra and cyclic voltammograms of GA-Fe(2+)/Fe(3+) complexes suggest the formation of a transient charge transfer complex between Fe(2+) and GA, accelerating Fe(2+) oxidation. The more stable Fe(3+) complex with GA would be unable to participate in Fenton-Haber Weiss-type reactions and the propagation phase of lipid peroxidation. The results show a potential of GA against neuronal diseases associated with iron-induced oxidative stress.lld:pubmed
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pubmed-article:21512303pubmed:articleTitleA strong protective action of guttiferone-A, a naturally occurring prenylated benzophenone, against iron-induced neuronal cell damage.lld:pubmed
pubmed-article:21512303pubmed:affiliationLaboratorio de Farmacología Molecular, Centro de Investigación y Desarrollo de Medicamentos, Ciudad Habana, Cuba.lld:pubmed
pubmed-article:21512303pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21512303pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed