Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1998-7-30
pubmed:abstractText
Solid tumours develop an acidic extracellular environment with high concentration of lactic acid, and lactic acid produced by glycolysis has been assumed to be the major cause of tumour acidity. Experiments using lactate dehydrogenase (LDH)-deficient ras-transfected Chinese hamster ovarian cells have been undertaken to address directly the hypothesis that lactic acid production is responsible for tumour acidification. The variant cells produce negligible quantities of lactic acid and consume minimal amounts of glucose compared with parental cells. Lactate-producing parental cells acidified lightly-buffered medium but variant cells did not. Tumours derived from parental and variant cells implanted into nude mice were found to have mean values of extracellular pH (pHe) of 7.03 +/- 0.03 and 7.03 +/- 0.05, respectively, both of which were significantly lower than that of normal muscle (pHe = 7.43 +/- 0.03; P < 0.001). Lactic acid concentration in variant tumours (450 +/- 90 microg g(-1) wet weight) was much lower than that in parental tumours (1880 +/- 140 microg/g(-1)) and similar to that in serum (400 +/- 35 microg/g(-1)). These data show discordance between mean levels of pHe and lactate content in tumours; the results support those of Newell et al (1993) and suggest that the production of lactic acid via glycolysis causes acidification of culture medium, but is not the only mechanism, and is probably not the major mechanism responsible for the development of an acidic environment within solid tumours.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-1333263, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-14190544, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-1789823, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-1835627, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-2684393, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-2910882, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-3179183, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-3392744, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-341374, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-3558049, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-5660132, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-6097949, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-6428413, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-7060023, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-7923215, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-8430084, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-9018236, http://linkedlifedata.com/resource/pubmed/commentcorrection/9667639-9020474
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0007-0920
pubmed:author
pubmed:issnType
Print
pubmed:volume
77
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1726-31
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
The contribution of lactic acid to acidification of tumours: studies of variant cells lacking lactate dehydrogenase.
pubmed:affiliation
Department of Medicine and Medical Biophysics, Ontario Cancer Institute/Princess Margaret Hospital, Toronto, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't