Linked Life Data

16004928

Source:http://linkedlifedata.com/resource/pubmed/id/16004928

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-7-11
pubmed:abstractText
Unphysiologically high levels of nitric oxide (NO*) are mutagenic and may contribute to carcinogenesis. Proapoptotic and anitiapoptotic functions of NO* have been reported in various in vivo and in vitro experimental models. The complexity of biological responses induced is a consequence of the multiple chemical pathways through which NO* causes damage to critical cellular macromolecules. The extent and kinetics of apoptotic and other responses are highly dependent on steady-state NO* levels, cumulative total dose and cell type. Steady-state and total dose thresholds have been defined, both of which must be exceeded for the induction of apoptosis and other responses in human lymphoblastoid cells. DNA damage, protein modifications, p53 activation and mitochondrial respiratory inhibition contribute to NO*-mediated apoptosis via mitochondrial and Fas receptor pathways. Multifaceted cellular defense systems including glutathione, antioxidant enzymes and Nrf2-Keap1 signaling participate in protective responses to mitigate damage by toxic levels of NO*.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0304-3835
pubmed:author
pubmed:issnType
Print
pubmed:day
8
pubmed:volume
226
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-15
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Nitric oxide as a modulator of apoptosis.
pubmed:affiliation
Biological Engineering Division and Department of Chemistry, Massachusetts Institute of Technology, 77 Massachusetts Ave., Room 26-009, Cambridge, MA 02139, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, N.I.H., Extramural