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Biomedical subjects

C Dalton

Publications and source records attributed to C Dalton.

At least 55 records · Page 3Linked to original sources
PubMed1977

Serum lipid-lowering properties of 6-chloro-9-[2-(6-methyl-3-pyridyl)ethyl]-1,2,3,4-tetrahydrocarbazole-2-carboxylic acid.

6-Chloro-9-[2-(6-methyl-3-pyridyl)ethyl]-1,2,3,4-tetrahydrocarbazole-2-carboxylic acid hydrochloride lowered serum cholesterol, triglyceride, phospholipid, and free fatty acid levels in normal rats. The compound appeared to have a low toxicity and to be well tolerated in mice, adult and neonatal rats, and rabbits. At hypolipidemic doses, it caused a slight hepatomegaly associated with an increase in liver phospholipid and protein content. Liver N-demethylase and catalase activities were increased by the drug treatment. This acid had no in vitro antilipolytic activity and did not affect serum desmosterol-cholesterol ratios. The results indicate that it has a mechanism of action similar to clofibrate.

Adipose Tissue↗
PubMed1975

Influence of dietary vitamin E on prostaglandin biosynthesis in rat blood.

A vitamin E (alpha-tocopherol) deficient diet stimulated prostaglandin biosynthesis in coagulating rat blood. Prostaglandins were extracted from serum, purified and bioassayed. The identity of prostaglandin E2 was confirmed by gas chromatography-mass spectrometry. Withholding vitamin E from the diet caused a marked increase in PGE2 and a lesser increase in PGF2alpha production in serum. In rats maintained on diets containing different concentrations of vitamin E, serum concentrations of PGE2 and PGF2alpha were inversely related to serum concentrations of alpha-tocopherol. These data suggest that in vitro alpha-tocopherol inhibits the endogenous conversion of arachidonic acid into PGE2 and PGF2alpha. The possibility that alpha-tocopherol may inhibit the formation of endoperoxide intermediates of PGE2 and PGF2alpha biosynthesis and subsequent induction of platelet aggregation is discussed.

Animals↗
PubMed1973

Adenosine-mediated elevation of cyclic 3':5'-adenosine monophosphate concentrations in cultured mouse neuroblastoma cells.

Adenosine causes an increase in the concentration of cyclic AMP in mouse neuroblastoma cells. The amount of increase observed in intracellular cyclic AMP levels due to exogenous adenosine depends greatly on the concentration of a specific cyclic AMP phosphodiesterase inhibitor, 4-(-3-butoxy-4-methoxybenzyl)-2-imidazolidinone. Unstimulated concentrations of cyclic AMP were 29-40 pmol/mg of protein, and concentrations after addition of 0.2 mM adenosine were usually twice as high. The presence of 0.7 mM inhibitor along with 0.2 mM adenosine caused an increase in cyclic AMP levels up to 1000-2000 pmol/mg of protein. In the presence of 0.7 mM inhibitor, 2 muM adenosine gives a half-maximal cyclic AMP elevation. Theophylline blocked the elevation of cyclic AMP concentrations caused by exogenous adenosine. The data show that the cyclic AMP system of mouse neuroblastoma has the necessary receptor components to respond positively to exogenous adenosine. The results presented support a direct effect of adenosine, mediated through its control of intracellular levels, on neuronal elements of the nervous system.

Acetylcholine↗