Linked Life Data

10378480

Source:http://linkedlifedata.com/resource/pubmed/id/10378480

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2-3
pubmed:dateCreated
1999-7-6
pubmed:abstractText
Recent investigations suggest that Ca2(+)-ATPase from fish gills is very sensitive to Zn2+ (Hogstrand et al., 1996. Am. J. Physiol. 270, R1141-R1147). The effect of free Zn2+ ion on the human erythrocyte plasma membrane Ca2(+)-ATPase was investigated to explore the possible extension of this finding to humans. Membrane vesicles were prepared and the Ca2(+)-ATPase activity was measured as Ca2(+)-stimulated ATP hydrolysis and as ATP-dependent Ca2+ transport. The Zn2+ ion inhibited the erythrocyte Ca2(+)-ATPase by reducing Vmax and increasing the K0.5. While in the Ca2+ transport assay only the Vmax was affected at lower Zn2+ concentrations (50-100 pM), reduction of Vmax was always accompanied by an affinity decrease in the ATP hydrolysis assay. The Ca2(+)-ATPase was found to be inhibited by Zn2+ at extremely low concentrations. The IC10 and IC50 for Zn2+, at a Ca2+ concentration of 1.0 microM, were estimated at 4 and 80 pM, respectively. Although the Ca2(+)-ATPase might be more sensitive in vitro than in vivo conditions, the results suggest that physiological concentrations of Zn2+ may reduce the activity of the erythrocyte Ca2(+)-ATPase. Furthermore, disturbance of Ca homeostasis may be a mechanism causing Zn toxicity during exposure.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0300-483X
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
133
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
139-45
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Inhibition of human erythrocyte Ca2+-ATPase by Zn2+.
pubmed:affiliation
T.H. Morgan School of Biological Sciences, University of Kentucky, Lexington 40506-0225, USA. hogstra@pop.uky.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't