Linked Life Data

10616192

Source:http://linkedlifedata.com/resource/pubmed/id/10616192

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2000-1-11
pubmed:abstractText
Particles can cause cytotoxicity in pulmonary alveolar macrophages (AM). Several mechanisms to explain this cytotoxicity have been suggested. However, the exact mechanism of particle-induced cytotoxicity in AM remains to be established. Silica and TiO2 produced a concentration-dependent cytotoxicity as evidenced by loss of cell viability and fall in ATP levels. While silica induced a greater cytotoxicity, TiO2 produced a higher reduction in ATP levels. Silica increased the release of LDH, but TiO2 did not affect enzymatic release. TiO2 suppressed succinate-triggered oxygen consumption, whereas silica did not markedly change the effect of succinate on oxygen consumption. Polyinosinic acid (PI), a ligand of the scavenger receptor, inhibited the TiO2-induced fall in ATP content, but could not prevent the effect of silica on cellular ATP content. Data suggest that silica and TiO2 can induce cytotoxicity in AM, probably through different mechanisms.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1528-7394
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
58
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
437-50
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Mechanism of silica- and titanium dioxide-induced cytotoxicity in alveolar macrophages.
pubmed:affiliation
Department of Pharmacology, College of Medicine, The Catholic University of Korea, Seoul.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't