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Biomedical subjects

V Glover

Publications and source records attributed to V Glover.

At least 145 records · Page 8Linked to original sources
PubMed1984

The prevalence of diet-induced migraine.

Nineteen percent of about 490 patients with classical or common migraine reported that headaches can be precipitated by chocolate, 18% by cheese and 11% by citrus fruit, and a highly significant majority of these patients were sensitive to all three foods. Twenty-nine percent of the patients reported sensitivity to alcohol; again this was significantly associated with sensitivity to the three food stuffs, though a substantial number of patients were sensitive to alcohol but not foods. Thirty-one percent of 331 female patients believed that oral contraceptives precipitated headaches, but this could not be related to any dietary response. Patients with affected relatives were significantly more likely to report sensitivity to alcohol and chocolate; sensitivity to cheese and citrus fruit was less strongly related, and there was no relationship at all for oral contraceptives. These correlations suggest that food induced headaches are mediated by chemical constituents common to these foods.

Alcoholic Beverages↗
PubMed1984

Characterization of human brain phenolsulphotransferase.

Both human phenolsulphotransferase M (for monoamines) and P (for phenol) were detected in eight out of twelve brains examined postmortem. Activity values were low compared with those in other human tissues and in brains from other species. The activity of both forms was unevenly distributed in different brain regions in a pattern different from that of the monoamines. From a study of substrate specificity, Km values, and inhibitor sensitivity, the two forms of the human brain enzyme did not appear to differ from their counterparts in platelet.

Adult↗
PubMed1984

Low platelet monoamine oxidase activity in headache: no correlation with phenolsulphotransferase, succinate dehydrogenase, platelet preparation method or smoking.

Platelet monoamine oxidase activity in male migrainous and cluster headache patients was significantly lower than in male controls, confirming our previous study. The activity range showed a normal distribution and low mean values could not be attributed to a subgroup with particularly low activity. When Corash 's platelet preparation method was used, with its high platelet yield, specific enzyme activities of a similar order were obtained. Thus, the low values encountered were not due to abnormal recovery within the platelet population. Two other enzyme activities, phenolsulphotransferase M and succinate dehydrogenase, were also measured in the same platelet samples. Although low succinate dehydrogenase activity was identified in the headache groups, it appeared to represent a separate phenomenon and there was no significant correlation between activity of either enzyme and that of monoamine oxidase. This shows that the low activity of platelet monoamine oxidase in headache is not related to a generalised platelet enzyme deficit. It was also shown that the low monoamine oxidase activity in the headache patients could not be attributed to smoking.

Arylsulfotransferase↗
PubMed1983

New endogenous benzodiazepine receptor ligand in human urine: identity with endogenous monoamine oxidase inhibitor?

Normal human urine contains both monoamine oxidase-inhibiting and benzodiazepine receptor-binding material. Each was extracted into ethyl acetate at pH 1 and subjected to high performance liquid chromatography: they ran similarly, showing three major peaks. The correlation coefficient between the pattern of MAO inhibition and inhibition of 3H-flunitrazepam binding to benzodiazepine receptors in the second half of the elution process was 0.78 (p less than 0.001): most UV-absorbing material present was eluted earlier in the run. These results are compatible with, although they do not prove, the hypothesis that the endogenous MAO inhibitor, previously shown to be increased in stress, is also an endogenous inhibitor of 3H-flunitrazepam binding to the benzodiazepine receptor. This material is different from other putative endogenous ligands: it migrates more rapidly than the potent but artefactual beta-carboline-3-carboxylic acid ethyl ester previously isolated from human urine; nor can the effect we have identified derive from harmane, inosine, hypoxanthine or nicotinamide which fail to extract into ethyl acetate at pH 1.

Adult↗
PubMed1983

Output of endogenous monoamine oxidase inhibitor in rats: effect of ethanol, tryptamine and tryptophan.

Contrary to prediction, loading rats with tryptamine, tryptophan or methanol failed to produce any rise in endogenous monoamine oxidase inhibitor output, whilst ethanol administration resulted in a significantly decreased excretion. These findings, which provide no support for the hypothesis that the inhibitor is a beta-carboline, may shed some light on the tranquilizing effect of ethanol in man.

Animals↗
PubMed1983

Platelet phenolsulphotransferase activity in Parkinson's disease.

Mean platelet phenolsulphotransferase activity was significantly increased in L-dopa-treated parkinsonian patients compared with controls. The degree of rise was associated with dose of and duration of treatment with L-dopa and may thus represent an adaptive increase to circulating dopamine. Alternatively, the increase may reflect changes supervening with duration of illness.

Age Factors↗
PubMed1983

Human platelet phenolsulphotransferase M and P: substrate specificities and correlation with in vivo sulphoconjugation of paracetamol and salicylamide.

Human platelet phenolsulphotransferase exists in two functional forms. M and P. In this study the substrate specificity of the two forms has been further delineated by correlating activities in different individuals with various substrates. m-Tyramine, noradrenaline, adrenaline, 5-hydroxytryptamine, p-hydroxyamphetamine, isoprenaline, salbutamol and l-naphthol were all specific substrates for the M form of the enzyme. Paracetamol, a mixed substrate, was predominantly metabolized by the M form. Salicylamide at 5 microM was a substrate for the P form but became and M substrate at higher concentration. Phenol itself, a specific substrate for phenolsulphotransferase P at 10 microM, also became an M substrate at 1 mM concentration. These substrate specificities were confirmed with the selective inhibitor, dichloronitrophenol. In this study, we measured phenolsulphotransferase activity in platelets from 13 individuals selected on the basis of their wide variation in ability to sulphoconjugate paracetamol and salicylamide in vivo. There was no significant relationship between the in vivo pattern with either drug and the activity of platelet phenolsulphotransferase assayed with paracetamol or salicylamide respectively.

Acetaminophen↗
PubMed1983

Tyramine-induced noradrenaline release from rat brain slices: prevention by (-)-deprenyl.

Clorgyline (1 and 10 microM) and (+)-deprenyl (10 microM) both significantly potentiated the tyramine (100 microM)-induced release of [3H]-noradrenaline from rat cerebral cortex slices. (-)-Deprenyl (50 microM) significantly reduced it, while lower concentrations had no effect on noradrenaline release. However, in combination, 1 microM (-)-deprenyl blocked the release-facilitating action of 1 microM clorgyline, and 10 microM (-)-deprenyl that of 10 microM (+)-deprenyl. Low concentrations of (+)- and (-)-deprenyl (1 and 10 microM), both selectively inhibited phenylethylamine oxidation by monoamine oxidase B. Higher concentrations of (-)-deprenyl (20 and 50 microM) also inhibited 5-hydroxytryptamine oxidation by monoamine oxidase A. Clorgyline (1 and 10 microM) inhibited both enzymes. Thus, the effects of these drugs on noradrenaline-release cannot be explained solely in terms of irreversible inhibition of monoamine oxidase A and B, and other possible mechanisms are discussed. If the brain-slice model faithfully mirrors the sequence of events manifesting peripherally as the tyramine hypertensive response ('cheese effect'), then it is possible that low doses of (-)-deprenyl, administered with antidepressant monoamine oxidase inhibitors, can prevent this adverse reaction.

Animals↗
PubMed1983

Pressor sensitivity to tyramine in patients with headache: relationship to platelet monoamine oxidase and to dietary provocation.

The pressor responses to oral and intravenous tyramine were not different from controls in migrainous patients with or without a history of attacks triggered by foods. However, patients who reported a dietary trigger were more likely to develop headache after tyramine administration than those without such a dietary history. Pressor responses to intravenous tyramine in patients with cluster headache were indistinguishable from controls. A group of five males with platelet monoamine oxidase activity one standard deviation or more below that of male controls required less intravenous tyramine to raise blood pressure by 30 mm Hg than males with monoamine oxidase levels within one standard deviation of the controls. This finding suggests that platelet monoamine oxidase activity to some extent reflects that of total body monoamine oxidase A plus B.

Administration, Oral↗