Biomedical subjects

J Edelson

Publications and source records attributed to J Edelson.

At least 73 records · Page 4Linked to original sources

PubMed1976

Interactions of chlorphenesin and divalent metal ions with phosphodiesterase.

Chlorphenesin inhibition of the hydrolysis of cyclic AMP by guinea-pig lung phosphodiesterase was reversed by the addition of exogenous magnesium ions. Chlorphenesin and theophylline inhibition of this enzyme was shown to be noncompetitive when the substrate concentration was low. Kinetic studies of the inhibition of beef heart phosphodiesterase by chlorphenesin and theophylline indicated that the substrate concentration was a factor in determining whether inhibition was competitive or noncompetitive. Calcium, cobalt and copper ions were inhibitory to guinea-pig lung phosphodiesterase. The inhibition due to chlorphenesin was partially reversed by low (40 mM or less) concentrations of barium ions; high concentrations of barium ions, or manganese ions, were inhibitory. The concentration of the divalent cation did not affect the type of inhibition that was observed.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1976

Hexachlorophene metabolism in rats: the hepatic route.

The terminal elimination rate of radioactivity from the bile of bile-duct cannulated rats, that had received hexachlorophene-14C via the hepatic portal vein, had an apparent first-order half-life of about 10 hr. Tissue distribution studies in these rats indicated that 35-47% of the carbon-14 of the dose was eliminated through the bile within 24 hr. Significant amounts of radioactivity were also found in the liver and carcass at that time; the brain was the only tissue that did not consistently have much higher concentrations of carbon-14 than the blood. The rate limiting step in the disposition of hexachlorophene may be excretion into the bile. A bile-feeding technique demonstrated enterohepatic circulation.

Animals↗

PubMed1975

Absorption, distribution, and metabolic fate of 7-chloro-3,3a-dihydro-2-methyl-2H,9H-isoxazolo-(3,2-b)(1,3)-benzoxazin-9-one in rats, dogs, and humans.

The absorption and metabolic fate of 7-chloro-3,3a-dihydro-2-methyl-2H,9H-isoxazolo-(3,2-b)(1,3)-benzoxazin-9-one (I) was studied in rats, dogs, and humans. Orally administered I was readily absorbed by all species. In the rat, orally administered I was converted to its metabolite, 5-chlorosalicylic acid, by the intestinal wall. The half-lives of blood radioactivity, after the oral administration of I-9-14C, were about 18 and 12 hr in the rat and beagle hound, respectively. In human subjects, no intact I was detected in the bloodstream; however, the clearance of the metabolite, 5-chlorosalicylic acid, had a half-life of about 33 hr. Cleavage of the oxazine ring of I generated 5-chlorosalicylic acid, which was excreted both in the free form and conjugated with glycine and glucuronic acid. The isoxazole moiety was converted to beta-hydroxybutyric acid and its metabolites carbon dioxide and fumaric, citric, alpha-ketoglutaric, succinic, and malic acids. Binding of I to plasma proteins was extensive but was less than that of 5-chlorosalicylic acid.

Animals↗

PubMed1974