Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1988-11-15
pubmed:abstractText
An elevation in cytosolic free calcium (Cai) produced by cellular ATP depletion may contribute to the initiation of cytotoxic events in renal ischemia. To evaluate whether ATP depletion results in a rise in Cai we examined the effect of cyanide and 2-deoxy-D-glucose on the Cai of Madin-Darby canine kidney cells. Exposure to the metabolic inhibitors resulted in a rise in Cai from 112 +/- 11 to 649 +/- 99 nM in 15 min. This combination of metabolic inhibitors also resulted in a decrement of cell ATP to 11 +/- 2% of control by 15 min. Experiments that were performed with other metabolic inhibitors confirm that the increment in Cai is due to inhibition of ATP synthesis. With the removal of cyanide and 2-deoxy-D-glucose, Cai recovered to 101 +/- 16 nM. In the absence of extracellular calcium activity (Ca0), Cai declined from 127 +/- 7 to 38 +/- 6 nM, whereas with cyanide plus 2-deoxy-D-glucose in the absence of Ca0 the Cai rose from 108 +/- 21 to 151 +/- 28 nM. Because the rise in Cai produced by ATP depletion in the absence of Ca0 is significantly less than that which occurs in the presence of Ca0, influx of Ca0 is necessary for the maximal rise of Cai. The rise in Cai that occurred in the absence of Ca0 suggests that the release of calcium from intracellular stores contributes to the increment in Cai seen with ATP depletion. TMB-8, an inhibitor of calcium release from intracellular stores, blunted the rise in Cai by nearly 50%. Neither verapamil nor nifedipine inhibited the rise in Cai. This study demonstrates that ATP depletion induced by the metabolic inhibitors cyanide and 2-deoxy-D-glucose is associated with a rapid and reversible increase in Cai. Both Ca0 influx and Cai redistribution contribute to this rise.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-2029, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-2408488, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-2417494, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-3001141, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-3010736, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-3014901, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-3020990, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-3091082, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-3099216, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-3515968, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-3520320, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-3578502, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-3723395, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-3755550, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-3837823, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-3838314, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-3930481, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-4003558, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-4044830, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-6192238, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-6220639, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-6303206, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-6501573, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-6605093, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-6660294, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-6703046, http://linkedlifedata.com/resource/pubmed/commentcorrection/2844853-6737843
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0021-9738
pubmed:author
pubmed:issnType
Print
pubmed:volume
82
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1326-32
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Adenosine triphosphate depletion induces a rise in cytosolic free calcium in canine renal epithelial cells.
pubmed:affiliation
Thorndike Memorial Laboratory, Boston City Hospital, MA 02118.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't