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Biomedical subjects

M Hong

Publications and source records attributed to M Hong.

At least 181 records · Page 10Linked to original sources
PubMed1983

Elevation of circulating prolactin concentrations may not cause striatal dopamine receptor supersensitivity.

Neuroleptic drugs, on repeated administration, increase plasma prolactin levels and induce behavioural and biochemical changes suggesting supersensitivity of striatal dopamine receptors. It has been suggested that the increase in plasma prolactin is responsible for the change in striatal dopamine receptors. We now find that repeated administration of haloperidol (5 mg/kg i.p.) for 21 days, followed by a 3 day drug-washout period, caused a 12-fold increase in circulating prolactin concentration in samples taken 1 h after the last injection. Haloperidol treated animals also exhibited an exaggerated stereotyped response to apomorphine 0.0625-0.5 mg/kg s.c.) and an increase in striatal dopamine receptor numbers labelled by [3H]spiperone. Administration of the same dose of domperidone or sulpiride (5 mg/kg i.p., 21 days), compounds which penetrate poorly into brain, also elevated plasma prolactin levels, but failed to alter cerebral dopamine function. Our findings indicate that neuroleptic-induced elevations in plasma prolactin levels are not responsible for the induction of cerebral dopaminergic supersensitivity.

Animals↗
PubMed1982

Stereoselective formation of bromobenzene glutathione conjugates.

Two bromobenzene-glutathione conjugates have been detected as both in vivo and in vitro metabolites of bromobenzene. Separation and purification by high pressure liquid chromatography (HPLC) and analysis by 13C and 1H-NMR spectroscopy indicated that the metabolites are trans-3-bromo-6-(glutathion-S-yl)-cyclohexa-2,4-dien-1-ol and trans-4-bromo-6-(glutathion-S-yl)-cyclohexa-2,4-dien-1-ol. The two conjugates are formed in unequal amounts; over a dose range of 25-500 mg/kg the ratio of the two conjugates excreted into bile in 6 h was 1.6 +/- 0.1 (mean +/- S.E.). Pretreatment of rats with either phenobarbital or 3-methyl-cholanthrene did not significantly alter the ratio of the two conjugates excreted into bile. When bromobenzene was incubated with rat liver microsomes and glutathione, the same two conjugates were formed in the presence but not in the absence of 100 000 x g supernatant. Furthermore, in the presence of 100 000 x g supernatant from control animals, microsomes from rats treated with phenobarbital formed both conjugates 6 times more rapidly than did microsomes from control rats, whereas microsomes from rats treated with 3-methylcholanthrene formed both conjugates less rapidly than did those from control rats. Thus, the data suggest that both conjugates are formed via bromobenzene 3,4-oxide and that their formation requires in liver cytosol.

Animals↗
PubMedDate not supplied

Comparison of the acute actions of amine-depleting drugs and dopamine receptor antagonists on dopamine function in the brain in rats.

The effects of the monoamine depleting drugs oxypertine, tetrabenazine and reserpine were compared with those of the dopamine receptor antagonists, chlorpromazine and trifluoperazine, on behavioural and biochemical indices of dopamine function in the brain. Oxypertine (0.625-20 mg/kg, i.p.), chlorpromazine (0.625-20 mg/kg i.p.) and trifluoperazine (0.0625-2.0 mg/kg i.p.), administered to rats 1 hr previously, inhibited stereotyped behaviour induced by both amphetamine (5.0 mg/kg i.p.) and apomorphine (1.0 mg/kg, s.c.) in a dose-dependent manner. Tetrabenazine (0.625-20 mg/kg i.p., 1 hr previously) inhibited stereotypy induced by amphetamine but not that induced by apomorphine. Reserpine (0.1 10 mg/kg i.p., 6 hr previously) did not inhibit, but in larger doses, tended to enhance the stereotyped responses to both amphetamine and apomorphine. Oxypertine (10 mg/kg, i.p., 1 hr previously), tetrabenazine (5 mg/kg i.p., 1 hr previously) and reserpine (2.5 mg/kg i.p., 6 hr previously) reduced the content of dopamine in the striatum but increased the concentrations of homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC). Chlorpromazine (5 mg/kg i.p.) and trifluoperazine (0.5 mg/kg i.p.), given 1 hr previously, did not alter concentrations of dopamine in the striatum but increased those of HVA and DOPAC. Oxypertine, chlorpromazine and trifluoperazine weakly inhibited dopamine-stimulated adenylate cyclase in homogenates of the striatum in the rat. Tetrabenazine and reserpine had no effect. Similarly, trifluoperazine and chlorpromazine displaced the specific binding of [3H]piflutixol to membranes from the striatum. Oxypertine also was weakly effective, but tetrabenazine and reserpine were without effect. Trifluoperazine, chlorpromazine and oxypertine displaced specific binding of [3H]spiperone and [3H]N,n-propylnorapomorphine (NPA) to preparations of the striatum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Vasopressin elevates cytosolic calcium in small cell lung cancer cells.

The ability of vasopressin to elevate cytosolic Ca2+ in small cell lung cancer (SCLC) cells was investigated. Ten nanomolar vasopressin elevated the cytosolic Ca2+ in 6 of 8 SCLC cell lines that were loaded with Fura-2 AM. Using SCLC cell line NCI-H345, the effect of vasopressin was dose dependent, being maximal at 100 nM, where the cytosolic Ca2+ was elevated from 150 to 210 nM. Because addition of 1 mM EGTA had no effect on the vasopressin response, vasopressin released Ca2+ from intracellular pools. Also, oxytocin weakly elevated the cytosolic Ca2+. The response to vasopressin was strongly blocked by [(beta-mercapto-beta,beta-cyclopentamethylene propionic acid)1,O-MeTyr2,Arg8]vasopressin and weakly blocked by [(beta-mercapto-beta,beta-cyclopentamethylene propionic acid)1,O-MeTyr2,Orn8]vasotocin. These data suggest that V1 vasopressin receptors are present on SCLC cells.

Arginine Vasopressin↗
PubMedDate not supplied

The decline of atrial natriuretic peptide (ANP) gene expression in older rats and the effects of ginsenoside on ANP gene expression.

1. The levels of atrial natriuretic peptide(ANP) gene expression in rat atria at 2-3 and 14-18 months of age and the effects of ginsenosides on r-ANP gene expression by determining the concentration of ANP-mRNA were investigated. The male and female rats were abdominally (i.p.) injected with aqueous solution of ginsenosides prepared from ginseng stems and leaves (G-PSL) and ginseng roots (G-PR), 50 mg/kg body wt, once a day for 7 days. Atria total RNA was extracted by the cold phenol method. The ANP-mRNA contents were determined using the Northern blot and dot blot hybridization technique with alpha-32*P-labelled r-prepro-ANP-cDNA probe. 2. The ANP-mRNA contents of 14-18 month rats were remarkably less than that of 2-3 month rats. The levels of male and female rats' atria at 14-18 months were about 15 and 60%, the content of male and female rats at 2-3 months respectively. 3. G-PSL and G-PR increased the ANP-mRNA content of male rats at 14-18 months 1- and 2-fold, respectively, whereas G-PSL and G-PR decreased the ANP-mRNA content in male rats of age 2-3 months. 4. These results revealed that the ANP gene expression declined during ontogenic ageing development and ginsenosides possessed anti-ageing effects in the heart endocrineous function aspect.

Aging↗