PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 6712147

Interference by thimerosal in cholesterol estimation by the CHOD-PAP method.

C J Briggs·D Anderson·R A Muirhead
View original source ↗Export metadata ↓

Abstract

We report that interference with the cholesterol assay using the cholesterol oxidase: p-aminophenazone method which is observed during lipoprotein preparation, is caused by the anti-bacterial agent thimerosol used in the preparation. We suggest that an alternative anti-bacterial agent should be used in these circumstances.

Explore related subjects

AminopyrineCholesterolCholesterol OxidaseEthylmercury CompoundsHumansThimerosalUltracentrifugationJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

C J Briggs, D Anderson, R A Muirhead. 1984. Interference by thimerosal in cholesterol estimation by the CHOD-PAP method.. https://doi.org/10.1177/000456328402100213

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1995

Epidermal growth factor induces H+,K+-ATPase alpha-subunit gene expression through an element homologous to the 3' half-site of the c-fos serum response element.

Epidermal growth factor (EGF) acutely inhibits acid secretion; however, prolonged administration of EGF has been reported to increase acid production. We undertook these studies to examine whether the physiological effects of EGF on acid secretion are mediated by regulation of gastric H+,K+-ATPase, the principle enzyme responsible for acid secretion. EGF in concentrations equivalent to those in plasma increased H+,K(+)-ATPase alpha-subunit mRNA levels. Using H+,K(+)-ATPase-luciferase constructs transfected into primary cultured parietal cells, a significant step up in EGF inducibility was observed between bases -162 and -156 (5'-GACATGG-3') relative to the cap site. This EGF response element (ERE) conferred EGF inducibility when linked to homologous and heterologous promoters. The ERE is homologous to the 3' half-site of the c-fos serum response element to which rNFIL-6, rE12, and SRE-ZBP bind. Electrophoretic mobility shift assays using an ERE probe and parietal cell nuclear extracts revealed a specific DNA-protein complex, the formation of which was changed by neither E12 and NFIL-6 consensus oligonucleotides nor antibodies for NFIL-6, SRE-ZBP, and E12. Our studies indicate that EGF induces gastric H+,K(+)-ATPase alpha-subunit gene expression via an interaction between a specific ERE and a novel transcriptional factor and that this may be a physiologic mechanism by which EGF regulates acid secretion.

Aminopyrine↗
PubMed1995

A role for calcineurin (protein phosphatase-2B) in the regulation of glutamate release.

Previous studies have shown that 4-aminopyridine (4AP) induced Ca-influx effects the release of glutamate from nerve terminals (synaptosomes) isolated from rat cerebral cortex. We now show that the Ca-dependent component of this release is potentiated by preincubation of the synaptosomes with the immunosuppressant, FK506, an inhibitor of protein phosphatase-2B (calcineurin). FK506 did not inhibit the Ca-independent release of glutamate from a cytosolic pool. Examination of the effect of FK506 on the influx of Ca elicited by 4AP indicated that inhibition of calcineurin activity resulted in an increase of voltage-dependent Ca-influx. Based on these results, we suggest that protein dephosphorylation effected by calcineurin may suppress voltage-dependent Ca-channel activity and in so doing inhibits evoked glutamate release. Activation of calcineurin produced by initial Ca-entry may represent a negative feedback to limit the activity of Ca-channels coupled to the release of glutamate.

Aminopyrine↗