Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
19
pubmed:dateCreated
2005-1-24
pubmed:abstractText
Recent evidence suggests that following visible-light (VL) irradiation, CQ and the CQ-related photosensitizers benzil (BZ), benzophenone (BP), and 9-fluorenone (9-F) generate initiating radicals that may indiscriminately react with molecular oxygen forming reactive oxygen species (ROS). The purpose of this investigation was to determine whether VL-irradiated CQ, BZ, BP, and 9-F cause DNA damage due to the generation of ROS in vitro. ROS formation by CQ and CQ-related photosensitizers+/-dimethyl-p-toluidine (DMT) was investigated in a cell-free system with VL irradiation. DNA damage was determined using PhiX-174 RF I supercoiled double-stranded plasmid DNA and ROS quantified with 4-((9-acridinecarbonyl)amino)-2,2,6,6-tetramethylpiperidin-1-oxyl (TEMPO-9-AC), a fluorogenic ROS-sensitive probe. VL-irradiated CQ, BZ, BP, and 9-F (+/-DMT) produced significant DNA damage at 0.1, 0.5, and 1.0 mM and in a concentration-dependent manner (p<0.05). TEMPO-9-AC revealed that all investigated VL-irradiated photosensitizers produced significant amounts of ROS with BZ in the presence of DMT generating the most ROS after 30, 60, and 90 min. VL-irradiated CQ, BZ, BP, and 9-F +/-DMT continued to generate significant amounts of ROS 90 min after VL irradiation. As a result, future investigations should evaluate the effect of VL-irradiated photosensitizers in cells and possible protective effects provided by antioxidants.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0142-9612
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4091-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
The effect of camphorquinone (CQ) and CQ-related photosensitizers on the generation of reactive oxygen species and the production of oxidative DNA damage.
pubmed:affiliation
Department of Restorative Dentistry, University of Washington, D-770, Health Science Building, Box 357456, Seattle, WA 98195-7456, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't, Evaluation Studies