Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-10-16
pubmed:abstractText
Sulindac is a non-steroidal antiinflammatory drug (NSAID) known to inhibit cyclooxygenases (COX) 1 and 2, and at present of interest for cancer prevention. However, its therapeutic use has been limited by its toxicity to the gastrointestinal tract and liver. We address the effects of sulindac, of the pharmacologically inactive metabolite, sulindac sulfone, and of the pharmacologically active metabolite, sudindac sulfide, on isolated rat liver mitochondria and HepG2 cells. Sulindac sulfide, but not sulindac sulfone or sulindac itself, caused mitochondrial uncoupling, released preaccumulated Ca2+ from the organelle, and decreased Hep-G2 cell viability in apparent association with cell ATP depletion resulting from mitochondrial uncoupling-associated membrane potential dissipation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1742-7835
pubmed:author
pubmed:issnType
Print
pubmed:volume
99
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
294-9
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Mitochondrial uncoupling by the sulindac metabolite, sulindac sulfide.
pubmed:affiliation
Department of Clinical Analysis, Toxicology, Bromatology, Faculty of Pharmaceutical Sciences, Ribeirao Preto-USP, Sao Paulo, Brazil.
pubmed:publicationType
Journal Article