Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1993-3-5
pubmed:abstractText
Isolated enterocytes were used as differential transporting cells to examine calcium homeostasis in control and vitamin B-6-deficient rats. Kinetic analysis of calcium fluxes, as well as biochemical determinations, indicated that enterocytes from control animals had high concentrations of cytosol ionized calcium (318.5 +/- 22.4 nmol/L) and a large pool of exchangeable calcium (2.72 nmol/mg protein, or 86% of total cell calcium). Vitamin B-6 deficiency resulted in a 44% reduction in total cellular calcium (1.71 +/- 0.24 vs. 3.07 +/- 0.29 nmol/mg protein), a 69% reduction in total exchangeable calcium (0.85 vs. 2.72 nmol/mg protein) and a 56% reduction in cytosol ionized calcium concentration (141.4 +/- 13.5 vs. 318.5 +/- 22.4 nmol/L). Calcium fluxes between all cellular compartments were markedly diminished as a result of vitamin B-6 deficiency. However, vitamin B-6 deficiency did not affect the basic morphological or functional features of the enterocytes, such as cell viability, cell volume, membrane permeability and protein content. Moreover, intestinal calcium transport in vivo was not affected during vitamin B-6 deficiency, perhaps due to the greater paracellular ion movement compensating for the lower transcellular transport.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-3166
pubmed:author
pubmed:issnType
Print
pubmed:volume
123
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
204-15
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Vitamin B-6 deficiency alters rat enterocyte calcium homeostasis but not duodenal transport.
pubmed:affiliation
Department of Biochemistry and Experimental Medicine, Child's Health Centre, Warsaw-Miedzylesie, Poland.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.