Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
21
pubmed:dateCreated
1987-12-14
pubmed:abstractText
The 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0006-2952
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
36
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3629-33
pubmed:dateRevised
2000-12-18
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Oxygen radical damage to DNA by rifamycin SV and copper ions.
pubmed:affiliation
Division of Chemistry, National Institute for Biological Standards and Control, Hertfordshire, U.K.
pubmed:publicationType
Journal Article