Guest guest Posted May 3, 2001 Report Share Posted May 3, 2001 1: Mol Cell Biochem 2001 Feb;218(1-2):87-92 <A HREF= " http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Link & db=PubMed & dbFrom=Pu\ bMed & from_uid=11330842 " >Related Articles, </A><A HREF= " http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_\ uids=11330842 & dopt=Books " >Books</A> Melatonin prevents delta-aminolevulinic acid-induced oxidative DNA damage in the presence of Fe2+. Qi W, Reiter RJ, Tan DX, Manchester LC, Calvo JR. Department of Cellular and Structural Biology, The University of Texas Health Science Center San , 78229-3900, USA. Delta-aminolevulinic acid (ALA), a heme precursor which accumulates during lead poisoning and acute intermittent porphyria, is reported to cause liver cancer. The carcinogenic mechanisms of ALA may relate to its ability to generate free radicals through metal-catalyzed oxidation which cause oxidative DNA damage. The aim of this study was to compare the efficacy of melatonin, trolox (vitamin E) and mannitol in altering DNA damage induced by ALA. Herein, we found, in the presence of Fe2+, that ALA-induced formation of 8-hydroxydeoxyguanosine in calf thymus DNA was dose and time-dependent. Melatonin, mannitol and trolox, all of which are free radical scavengers, inhibited the formation of 8-hydroxydeoxyguanosine in a concentration-dependent manner. The concentration of each (melatonin, mannitol and trolox) required to reduce DNA damage by 50%, i.e., the IC50, was 0.52, 0.84 and 0.90 mM, respectively. PMID: 11330842 [PubMed - in process] Quote Link to comment Share on other sites More sharing options...
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