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Biomedical subjects

A K Cho

Publications and source records attributed to A K Cho.

At least 91 records · Page 5Linked to original sources
PubMed1978

Test dose response in schizophrenia: chlorpromazine blood and saliva levels.

A gas chromatographic/mass spectrometric method for measuring chlorpromazine using 2H6--labeled chlorpromazine as an internal standard has the potential for considerable precision and specificity. Results are reported of chlorpromazine levels in plasma and saliva after administration of a single test dose to 13 schizophrenic patients in a tightly designed experiment. There was a clear and substantive relationship between blood and saliva levels of chlorpromazine, both following a typical decay curve. Saliva and plasma levels were strongly associated for a particular patient, and there was even a strong consistency in saliva-plasma ratios between patients, with an overall statistically significant correlation between plasma and saliva levels for all measurement on all 13 patients. In general, it seems that saliva sampling has great potential as a simple noninvasive technique for investigation of chlorpromazine and other antipsychotic drugs in psychotic patients. Nevertheless, for the moment, it should be regarded as strictly experimental and not suitable for immediate clinical application.

Adult↗
PubMed1978

Folate and pterin metabolism by cancer cells in culture.

Malignant cells grown in culture excrete into their growth medium a folate catabolite that can be seen as a blue-fluorescent region on paper chromatograms of such media. This folate catabolite has now been identified by paper chromatography, thin-layer chromatography, and combined gas chromatography-mass spectrometry as 6- hydroxymethylpterin and not as pterin-6-carboxaldehyde as previously reported. Moreover, when pterin-6-carboxaldehyde was added to the growth medium of logarithmically growing malignant cells, it was primarily reduced to 6-hydroxymethylpterin. In contrast pterin-6-carboxylate was the principal product formed from added pterin-6-carboxaldehyde by normal established cell lines in culture. These results have been interpreted as indicative of a possible mechanism of folate catabolism in malignant cells. Folic acid or another folate derivative is oxidatively cleaved at the C-9-N-10 bond to yield pterin-6-carboxaldehyde as one of the products. This derivative is subsequently reduced to 6-hydroxymethylpterin, which is excreted into the growth medium.

Cells, Cultured↗
PubMed1977

Neuronal accumulation and metabolism of 3H-1-norepinephrine in rat portal vein: evidence in relation to possible uneven alpha receptor distribution.

The rate of accumulation and metabolism of 3H-1-norepinephrine in the neuronal plexus of rat portal vein produces a small transmitter concentration gradient across the longitudinal smooth muscle layer which cannot account for the prejunctional supersensitivity observed and suggests localization of the alpha-adrenergic receptors adjacent to the nerve plexus.

Animals↗
PubMed1977

Pharmacokinetics of methylphenidate in the rat using single-ion monitoring GLC-mass spectrometry.

A GLC-mass spectrometric assay for methylphenidate in biological fluids was developed using the ethyl ester homolog of the drug as the internal standard. The procedure has a lower level of sensitivity of 1.2 ng/ml and is based on GLC-mass spectrometic monitoring of the m/e 180 ion common to the mass spectra of the N-trifluoroacetyl derivatives of the drug and internal standard. The brain and plasma levels of methylphenidate in rats were determined after intravenous administration of 0.5 mg/kg of the drug. The two-compartment open pharmacokinetic model fit the data.

Animals↗
PubMed1977

The metabolism of amphetamine in vitro by rabbit liver preparations: a comparison of R(-) and S(+) enantiomers.

1. Incubation of R(-), S(+) and RS(+/-) amphetamines with rabbit liver 9000 g supernatant indicated that R(-) was metabolized at a faster rate than S(+), but that racemic amphetamine was metabolized at the same rate as S(+) during one hour incubations. 2. N-Hydroxyamphetamine and 1-phenyl-2-propranol were the major compounds detected in both R(-) and S(+) amphetamine incubations. 3. Phenylacetone oxime was detected in significant quantities after 3 h incubations of R(-) amphetamine, but only in minor quantities from S(+). 4. A fall in the amount of N-hydroxyamphetamine present in R(-) amphetamine incubations after a 3 h period as compared to a 1 h incubation, paralleled by a rise in the amount of phenylacetone oxime during 3 h suggested that the oxime was derived as a secondary metabolics from N-hydroxyamphetamine. 5. R(-) and S(+) N-hydroxyamphetamines were both metabolized to phenylacetone oxime by rabbit liver 9000 g supernatant, but the R(-) enantiomer was converted at a faster rate than S(+).

Amphetamine↗
PubMed1977

Metabolism of 2-nitro-1-phenylpropane to phenylacetone by rabbit liver microsomes.

Phenylacetone was found to be the major metabolite formed when 2-nitro-1-phenylpropane was incubated with rabbit liver microsomes. The enzymatic character of the reaction was demonstrated by the increase of product with microsomal protein and dependency on NADPH and oxygen. Furthermore, phenobarbital induction markedly increased the formation of phenylacetone. Carbon monoxide decreased the reaction indicating the involvement of a metalloenzyme. Experiments with H218O indicated that the carbonyl oxygen originated from water. It is suggested that the microsomal metabolism of 2-nitro-1-phenylpropane involves an enzymatic step followed by chemical hydrolysis of an intermediate, possibly a secondary nitronic acid.

Acetone↗