Linked Life Data

3263555

Source:http://linkedlifedata.com/resource/pubmed/id/3263555

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1988-12-22
pubmed:abstractText
Effects of nickel and magnesium on the responsiveness of BALB/c mouse spleen lymphocytes to a mitogen, concanavalin A (Con A), were studied using the in vitro 3H-thymidine (TdR) incorporation test. Nickel chloride (NiCl2) and nickel subsulfide (Ni3S2) were found to suppress this response. The control level of TdR incorporation from a magnesium-free medium containing 0.625 microgram Con A/ml into trichloroacetic-acid-precipitable nucleoprotein was depressed by both nickel compounds in a dose-dependent manner to 3% of its original value by 0.25 mumol NiCl2/ml or 0.33 mumol Ni3S2/ml (5 micron particles). Magnesium stimulated TdR incorporation up to a maximum of 200% of the control level at concentrations greater than 2.0 mumol MgCl2/ml. Also, gradual increase of magnesium concentration in the culture medium up to 2.0 mumol/ml attenuated the effects of nickel, restoring the lymphocyte response to Con A to 43% of the control level at 0.25 mumol NiCl2/ml or to 30% at 0.33 mumol Ni3S2/ml. Higher concentrations of magnesium did not further enhance this responsiveness. These data suggest that the effect of magnesium upon early cellular response to nickel observed in vivo [Kasprzak et al.: Carcinogenesis 6: 1161-1166, 1985], which eventually results in a decreased tumor incidence, may be due in part to antagonism by magnesium of nickel suppression of the activity of T lymphocytes.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0252-1156
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
166-72
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Magnesium counteracts nickel-induced suppression of T lymphocyte response to concanavalin A.
pubmed:affiliation
Inorganic Carcinogenesis Section, National Cancer Institute, Frederick, Md.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.