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pubmed-article:2823829pubmed:dateCreated1987-12-14lld:pubmed
pubmed-article:2823829pubmed:abstractTextThe hydroquinone moiety of the antibiotic rifamycin SV reacts with molecular oxygen to form reduced oxygen intermediates such as superoxide (O2-.) and hydrogen peroxide (H2O2). The antibiotic semiquinone is also formed. Rifamycin SV in the presence of iron and copper salts can lead to the formation of the highly reactive hydroxyl radical (OH) which degrades the sugar deoxyribose. This damage is substantially inhibited by the enzyme catalase and scavengers of the hydroxyl radical such as formate, mannitol and thiourea. When linear duplex DNA is substituted for deoxyribose only rifamycin SV and copper ions substantially degrade DNA with release from the DNA molecule of thiobarbituric acid-reactive products. Damage to DNA by rifamycin and copper ions is significantly inhibited by catalase but poorly inhibited by scavengers of the hydroxyl radical consistent with a site-specific radical reaction of the DNA molecule. Several biological properties of rifamycin SV are known to resemble those of the metal chelating agent 1,10-phenanthroline. Here, we show that similarities extend to an unusual chemical property whereby thiobarbituric acid-reactive material is released from DNA in the presence of a copper salt.lld:pubmed
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pubmed-article:2823829pubmed:dateRevised2000-12-18lld:pubmed
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pubmed-article:2823829pubmed:year1987lld:pubmed
pubmed-article:2823829pubmed:articleTitleOxygen radical damage to DNA by rifamycin SV and copper ions.lld:pubmed
pubmed-article:2823829pubmed:affiliationDivision of Chemistry, National Institute for Biological Standards and Control, Hertfordshire, U.K.lld:pubmed
pubmed-article:2823829pubmed:publicationTypeJournal Articlelld:pubmed
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