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S C Hong

Publications and source records attributed to S C Hong.

64 records · Page 4Linked to original sources
PubMed1986

Identification of new metabolites of phosphoramide and nor-nitrogen mustards and cyclophosphamide in rat urine using ion cluster techniques.

The metabolism of nor-nitrogen (NNM) and phosphoramide mustards (PM) and cyclophosphamide (CP) was investigated in the Sprague-Dawley rat using chemical ionization mass spectrometry and ion cluster techniques. Following administrations of a 1:1 mixture of the non-labeled and the corresponding side-chain deuterium-labeled compounds to separate rats, the urinary extracts were screened for cluster ions which were characteristic of the administered compounds and their derived metabolites, and on this basis, tentative identifications of known and new metabolites were accomplished. Combining derivatization, deuterium labeling on strategic locations, gas chromatography/mass spectrometry, and chemical synthesis in some cases, 3-(2-chloroethyl)-1,3-oxazolidin-2-one was identified as a major metabolite for NNM, PM and CP and 3-(2-chloroethyl)-4-hydroxy-1,3-oxazolidin-2-one was identified as a major metabolite for NNM and PM, but a minor metabolite for CP. A new dechlorinated metabolite for CP, 3-(2-hydroxyethyl)-1,3-oxazolidin-2-one, was also identified.

Amides↗
PubMed1985

Ketamine metabolism: identification and synthesis of a deaminated product.

During attempts to synthesize 2-amino-2-(2-chlorophenyl)-6-hydroxycyclohexanone (6), a ketamine metabolite, an unexpected product, 3-(2-chlorophenyl)-2-hydroxy-2-cyclohexenone (4) was obtained as the major product. This compound apparently was formed by rearrangement and deamination of 6 during the isolation and purification procedures. This same compound was found in plasma and urine extracts obtained from mice and rats that had been treated with either ketamine or norketamine. It is suggested that 3-(2-chlorophenyl)-2-hydroxy-2-cyclohexenone (4), isolated from these biological samples, probably arose from decomposition of the 6-hydroxylated metabolite of ketamine or norketamine and is itself not a true metabolite.

Animals↗
PubMed1984

Effects of cinepazide on the purinergic responses in the dog cerebral artery.

The effects of cinepazide, 1-[(1-pyrrolidinylcarbonyl)methyl]-4-(3,4,5-trimethoxycinnamoyl )piperazine hydrogen maleate, were studied in isolated dog cerebral arteries. Cinepazide in concentrations ranging from 10(-6) to 10(-5) M augmented the relaxing responses to ATP, adenosine and cAMP. However, this agent did not affect the relaxations induced by isoproterenol and papaverine and the contractions induced by 5-HT, prostaglandin F2 alpha and ATP. In the basilar artery preloaded with 3H-norepinephrine or 3H-adenosine, electrical transmural stimulation resulted in a marked increase in 3H-efflux. This efflux accompanied an initial transient contraction followed by a relaxation. Cinepazide slightly reduced the 3H-efflux evoked by electrical stimulation. However, the relaxing response was mostly augmented by the treatment with cinepazide. The relaxing responses to ATP, adenosine, cAMP and electrical transmural stimulation were attenuated by theophylline. These results suggest that cinepazide selectively potentiates the relaxing response mediated through purinergic P1-receptors.

Adenosine↗
PubMed1982

Stereochemical studies of demethylated ketamine enantiomers.

The enantiomorphs of norketamine, 2-(o-chlorophenyl)-2-aminocyclohexanone, were synthesized and screened for biological activity. Resolution was achieved by fractional crystallization of the tartrate salts. Stereochemical purity was determined using standard GC or GC-MS analysis. Preliminary pharmacological evaluations revealed that intraperitoneally injected dextrorotatory norketamine caused a greater duration of loss of righting reflex in mice than the levorotatory isomer.

Anesthetics↗
PubMed1982

Effects of goniopora toxin on non-adrenergic, non-cholinergic response and purine nucleotide release in guinea-pig taenia coli.

1. Effects of goniopora toxin (GPT) on non-adrenergic, non-cholinergic inhibitory responses were examined in isolated guinea-pig taenia coli and the transmission mechanism was analysed.2. GPT (20-50 nM) gradually augmented the relaxation and rebound contraction induced by electrical transmural stimulation in the presence of guanethidine and atropine. These effects were abolished by tetrodotoxin.3. The resting tension and the response to exogenously applied ATP were little affected by GPT.4. The action potentials and the electrotonic potentials recorded by a double sucrose-gap method were little affected by GPT.5. These results indicate that the augmentation is elicited by a direct action of GPT on the non-adrenergic, non-cholinergic neurones, rather than on the smooth muscles per se.6. GPT augmented the amplitude of the inhibitory junction potential (i.j.p.) recorded in the presence of guanethidine and atropine. GPT also enhanced the (3)H efflux in response to electrical transmural stimulation of preparations pre-loaded with [(3)H] adenosine. Tetrodotoxin markedly inhibited or abolished the i.j.p. and (3)H efflux.7. These results would suggest that augmentation of the non-adrenergic, non-cholinergic responses is due to increased transmitter release from the nerve. Under conditions in which the transmitter release was augmented, the non-adrenergic, non-cholinergic response showed an essentially similar pattern to that obtained under normal conditions; therefore the inhibitory response is probably due to a putative transmitter, possibly ATP or a related nucleotide.

Adenosine Triphosphate↗
PubMed1977

Relationships, among the steroids, of anti-inflammatory properties and inhibition of prostaglandin production and arachidonic acid release by transformed mouse fibroblasts.

Anti-inflammatory steroids inhibit the serum-stimulated prostaglandin synthesis and release of [3H]arachidonic acid by methylcholanthrene-transformed mouse fibroblast, MC5-5. The half-maximal concentration for inhibition of both effects parallels the relative anti-inflammatory potencies of these steroids. The fatty acid cyclooxygenase activities of microsomal fractions isolated from cells that had been pretreated with dexamethasone were similar to the activities of microsomal fractions isolated from untreated cells. Intracellular as well as extracellular levels of prostaglandins in dexamethasone inhibited cells were decreased. The anti-inflammatory steroids seem to be blocking deacylation of the phospholipids or transport of the arachidonic acid, after deacylation to the cyclooxygenase.

Animals↗