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L C Tang

Publications and source records attributed to L C Tang.

15 recordsLinked to original sources
PubMed1991

Linking phospholipase A2 to phospholipid turnover and prostaglandin synthesis in mast cell granules.

Rapid incorporation of exogenous arachidonic acid into phospholipid has been detected in conjunction with eicosanoid synthesis by purified mast cell granules [Chock, S. P. & Schmauder-Chock, E. A. (1988) Biochem. Biophys. Res. Commun. 156, 1308-1315]. The species of phospholipid formed has now been identified primarily as phosphatidylinositol. A calcium-dependent phospholipase A2 has also been detected in the secretory granule. This enzyme, like the cyclooxygenase [Schmauder-Chock, E. A. & Chock, S. P. (1989) J. Histochem. Cytochem. 37, 1319-1328], appears to bind tightly to the granule matrix components. It is heat resistant and requires millimolar concentrations of calcium for optimal activity. It prefers phosphatidylinositol over phosphatidylcholine as substrate. Since the granule contains a large amount of phospholipid, the action of this phospholipase A2 can provide the required substrate for the arachidonic acid cascade. These findings provide the basis for linking phospholipase A2 to the production of eicosanoids during granule exocytosis. Since the granule also contains both an active acylating system that can rapidly reacylate lysophosphatidylinositol to form phosphatidylinositol, and an active phospholipase A2 which hydrolyzes phosphatidylinositol, a rapid turnover involving the fatty acid at the sn-2 position of phosphatidylinositol may occur. These findings are consistent with our postulation that the secretory granule is the source and/or the cause of many of the early biochemical events associated with the process of stimulus-secretion coupling.

Animals↗
PubMed1991

Human erythrocyte as a model for investigating muscarinic agonists and antagonists.

1. Human erythrocyte muscarinic receptor is further classified as M1 subtype by its binding of [3H]pirenzepine (a specific M1 antagonist). Conversely, binding of [3H]piperidinyl AF-DX116 (a specific M2 antagonist) is not detected. 2. There are high correlations between the binding efficacies of 25 known or putative cholinergic agents using either human erythrocyte membrane or mouse caudate homogenate. Also the in vitro data corresponds satisfactorily with in vivo data measuring the protective effect of these compounds against organophosphate poisoning. 3. The human erythrocyte membrane is an efficient model for investigating cholinergic agonists and antagonists.

Animals↗
PubMed1979

The beta-adrenergic responses in isolated splenic capsule area of several species of animals.

In isolated splenic capsules of mouse, rat, guinea pig, rabbit, cat and dog, either a single or a cumulative dose of l- and dl-isoproterenol at a concentration higher than l0(-9) M, induced a relaxation which was inhibited or blocked with pretreatment of 10(-5) M propranolol. At a concentration of 5 x 10(-6) M to 10(-5) M 1- and dl-isoproterenol, an inverse contraction was induced, and such response was prevented or reversed to one of relaxation in the presence of 10(-5) M phentolamine. Application of 10(-5) M epinephrine produced a strong contraction and such was reversed to one of relaxation after addition of 10(-4) M phentolamine. This relaxation was reduced or blocked with pretreatment of 10(-5) M propranolol. Thus, it was confirmed that both alpha- and beta-receptors exist in the splenic capsule area of these different species.

Animals↗
PubMed1978

Morphine sulfate stimulates the adenylate cyclase in mouse caudate nuclei.

The effect of several concentrations of morphine on the activity of adenylate cyclase [ATP pyrophosphate-lyase (cyclizing): EC 4.6.1.1.] was measured in homogenates of caudate nuclei of mice. Morphine stimulated the enzyme at 500 micron and inhibited slightly at 5 micron. Morphine stimulation was blocked by naloxone. Depending on its dose, morphine also increased or decreased the stimulating effect of dopamine on the dopamine-sensitive adenylate cyclase activity of caudate homogenate. Like dopamine, morphine'e effect on the adenylate cyclase activity was increased or decreased, respectively, by pretreating the animals with poly(I).poly(C) or with chloramphenicol. Thus, both dopamine and morphine appear to act on the same receptor. This "new" receptor differs from the one described by Snyder et al. and others, who demonstrated only binding affinity and no enzymatic activity. These data indicate that certain functions of the opiates might be mediated through the dopamine-sensitive adenylate cyclase of the caudate nuclei, which are the dopamine receptors in the brain.

Adenylyl Cyclases↗
PubMed1977

Levodopa, fertility, and longevity.

High concentrations of the dopaminergic drug levodopa (L-dopa, L-3,4-dihydroxphenylalanine) administered to mice in their diet affected fertility to a moderate degree and prolonged the mean life-span by a maximum of 50 percent.

Animals↗
PubMed1977

Opposing effects of dopaminergic to cholinergic compounds on a cerebral dopamine-activated adenylate cyclase.

In contrast to antipsychosis drugs which inhibit the dopamine-activated adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] of caudate nucleus, dopaminergic drugs for treatment of Parkinson's disease stimulate this cyclase. Stimulants and inhibitors of cholinergic neurons inhibited this adenylate cyclase activity competitively and specifically. Thus, the mechanism by which dopaminergic medications ameliorate the effects of Parkinson's disease includes activation of the dopamine-sensitive adenylate cyclase. Excessive activation might be present during the psychotic episodes seen in patients with parkinsonism who are overtreated. The enzymatic effects of the drugs that affect cholinergic mechanisms seem to be generally in keeping with the pharmacological reciprocity between psychoses and extrapyramidal function, except for the anticholinergic ones which inhibited this cyclase although they can be hallucinogenic.

Adenylyl Cyclases↗
PubMed1977

Quantitative correlation of dopamine-dependent adenylate cyclase with responses to levodopa in various mice.

We obtained 12 groups of mice with widely different neurological responses to levodopa by selecting them from different strains and submitting some of them to pretreatments. We scored the symptoms evoked by a standardized dose of levodopa in one subgroup from each group. We tested another subgroup for activation of an adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] by a standardized dose of dopamine added to homogenates of the caudate nuclei of the brains of these mice. Both sets of tests were performed randomly. When the accruing two sets of data were plotted against each other there emerged a straight line which fitted the data with a coefficient of correlation of 0.97 (P less than 0.0001). The dopamine-dependent activity of the adenylate cyclase of the brain was thus shown to be a determinant of the neurological responses of intact animals to a dopaminergic drug.

Adenylyl Cyclases↗
PubMed1977

L-3,4-dihydroxyphenylalanine-induced hypersensitivity simulating features of denervation.

The manner in which dyskinesia and intermittency of neurological control had emerged late in the therapy of Parkinsonism with L-3,4-dihydroxyphenylalanine (levodopa) had suggested to us that this drug can imprint on the brain a chemical memory of its passage. The majority of authors ascribed these events to denervation hypersensitivity caused by the nigral and other lesions of the disease. By feeding levodopa to mice, however, we induced a state that simulated denervations hypersensitivity, including hyperreaction to single injections of levodopa and increased dopamine-stimulated adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] activity in homogenates of caudate nuclei. These phenomena were not caused by actual denervation, because the hypersensitivity declined and disappeared some weeks after the dietary levodopa was stopped.

Adenylyl Cyclases↗
PubMed1976

Modification of the actions of some neuroactive drugs by growth hormone.

The flat serum growth hormone (GH) patterns of untreated parkinsonian patients develop diurnal rises during treatment with levodopa. This chronic exposure to excesses of GH might lead to the eventual emergence of the "on-off" phenomenon, which would indicate a need for animal experiments. Pretreatment of mice with GH increased (1) cerebral dopa and dopamine concentrations in levodopa-treated mice, (2) cerebral accumulation of injected tritiated apomorphine and tritiated thymidine, and (3) behavioral responses to levodopa, L-m-tyrosine, apomorphine hydrochloride, and oxotremorine.

Animals↗
PubMed1975

Cholinergic effects of molecular segments of apomorphine and dopaminergic effects of N,N-dialkylated dopamines.

The hydrochlorides of molecular segments of apomorphine [2-(3',4'-dihydroxybenzyl)-1,2,3,4-tetrahydroisoquinoline, 2-(3'4'-dihydroxybenzyl)piperidine, and 1,2,3,4-tetrahydroisoquinoline with their respective N-methyl and N-n-propyl homologs] and N,N-dialkylated dopamine compounds were synthesized and studied for (1) LD50 in intact mice; (2) stereotypy in intact mice; (3) curving of the body in unilaterally caudectomized mice; (4) rotation in 6-hydroxydopamine-lesioned rats, and (5) activation of adenylate cyclase in homogenates of mouse caudate nuclei. Instead of dopaminergic effects 1-(3',4'-dihydroxybenzyl)-2-methyl-1,2,3,4-tetrahydroisoquinoline and 2-methyl-1,2,3,4-tetrahydroisoquinoline showed cholinergic ones. These effects were blocked in atropine-pretreated animals. Of the N,N-dialkylated dopamine compounds synthesized, the N-n-propyl-N-n-butyldopamine ranked in all tests as the strongest dopamine-receptor agonist and N-methyl-N-n-propyldopamine as the weakest. In contrast, N,N-dimethyldopamine and 1-(3,4-dihydroxyphenylethyl)piperidine showed no dopaminergic effects. The effectiveness of the dopaminergic agonists depended on the length of the N-alkyl substituents suggesting interactions with hydrophobic regions of the receptor site.

Adenylyl Cyclases↗
PubMedDate not supplied

Seminal plasma beta-human chorionic gonadotropin (beta-HCG): relationships with seminal characteristics and spermatozoal fertilizing capacity.

Seminal plasma beta-human chorionic gonadotropin (beta-HCG) levels were determined in 254 semen samples collected from fertile and suspected subfertile men, and their relationships with seminal characteristics and spermatozoal fertilizing capacity were evaluated. Radioimmunoassayable beta-HCG, as defined by greater than 5 mIU/ml concentration, was demonstrated in only 44.5% of all the samples studied. beta-HCG concentrations were similar in normospermic, oligospermic and azoospermic samples. There were no significant differences in beta-HCG concentration between high-motility and low-motility samples, between normal-morphology and abnormal-morphology samples, and between high-fertilizing capacity and low-fertilizing capacity samples. No significant correlations between the concentrations of beta-HCG and individual parameters of semen analysis and spermatozoal fertilizing capacity among the various groups of samples were observed. The physiological role of seminal plasma beta-HCG is presently uncertain and the relationship of its determination to male fertility requires further investigation.

Chorionic Gonadotropin↗