Linked Life Data

8510014

Source:http://linkedlifedata.com/resource/pubmed/id/8510014

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-7-14
pubmed:abstractText
The effect of extracellular acidosis on different types of cell injury and death was examined using suspensions of rabbit renal proximal tubules. Cell death produced by the mitochondrial inhibitors rotenone, antimycin A, carbonyl cyanide p-trifluoromethoxyphenylhydrazone and oligomycin and by the ion exchangers valinomycin, nigericin and monensin was ameliorated by reducing extracellular pH (pHe) from 7.4 to 6.4. The protection lasted for more than 5 hr and was not due to the release of mitochondrial inhibition or to the maintenance of tubular ATP levels. In contrast, extracellular acidosis potentiated the cell injury and death produced by the oxidants t-butyl hydroperoxide, H2O2 and ochratoxin A. Because a decrease in pHe resulted in an increase in lipid peroxidation and in glutathione disulfide formation, and caused a decrease in glutathione peroxidase and glutathione reductase activities, the mechanism of this potentiation is most likely the result of an increase in free-radical production or a decrease in free-radical detoxification. The findings with the oxidants are in marked contrast to those in hepatocytes. These results show that renal cell death as a consequence of mitochondrial inhibition is sensitive to the protective effects of extracellular acidosis and that the effects of extracellular acidosis on cell death are dependent on the mechanism of injury.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
265
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1355-60
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Extracellular acidosis ameliorates metabolic-inhibitor-induced and potentiates oxidant-induced cell death in renal proximal tubules.
pubmed:affiliation
Department of Physiology and Pharmacology, College of Veterinary Medicine, University of Georgia, Athens.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't