Red wine contains a potent inhibitor of phenolsulphotransferase.

Littlewood, JT; Glover, Vivette; Sandler, M.

doi:10.1111/j.1365-2125.1985.tb02644.x

Cited by 35 publications

(18 citation statements)

References 18 publications

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“…Our finding of a lower activity of platelet phenol sulphotransferase P in susceptible subjects [10] has been confirmed by Launay et al [11], whereas platelet monoamine oxidase is not lower in diet-sensitive patients [12]. Littlewood et al [13] demonstrated an inhibition of phenol sulphotransferase in vitro by red wine, consistent with the consumption in vivo of a single glass. Jarman et al [14] showed that serotonin could be released from pre-loaded platelets by red wine, which could also be demonstrated in vivo [15,16].…”

Section: Red Wine Sensitivitysupporting

confidence: 77%

Pharmacological analysis of red-wine-induced migrainous headaches

Peatfield¹,

Fletcher

Rhodes

et al. 2003

J Headache Pain

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IntroductionCheese, chocolate and red wine are the most publicised triggers for migrainous headaches, at least in English speaking countries. Systematic surveys of patients attending the Princess Margaret Migraine Clinic at Charing Cross Hospital have established that about 18%-19% of patients report sensitivity to cheese or chocolate, and usually to both [1]. In a more recent epidemiological survey [2] the 18% of migrainous patients sensitive to all alcoholic drinks were distinguished from a further 12% sensitive only to red wine, but not to white wine or clear spirits. There was a statistically significant but by no means absolute correlation between red wine and food sensitivity, though it was extremely rare for a diet-sensitive patient to be tolerant of all forms of alcohol [2]. We also found very few patients with tension or cluster headache to be sensitive to food or Abstract We describe a series of experiments designed to investigate the mechanisms by which headaches can be triggered by red wine in a small minority of migraine patients. Some red wines are particularly potent releasers of serotonin from platelet stores, but these are no more effective as triggers of headache in sensitive patients. Both the selective 5-HT 2A antagonist ketanserin and the non-selective 5-HT2ABC antagonist pizotifen blocked the majority of headaches, and we then thought the antihistamine properties of these two drugs might be important. In a third experiment, however, the H1 antagonist mepyramine did not convincingly antagonise the response to red wine. Plasma levels of the enzyme diamine oxidase, which metabolises histamine, were lower in all migraine patients, whether or not they were sensitive to red wine. The results reported here do not permit making firm conclusions; nevertheless it seems that different pharmacological receptors may be responsible in different patients.

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Section: Red Wine Sensitivitysupporting

confidence: 77%

Pharmacological analysis of red-wine-induced migrainous headaches

Peatfield¹,

Fletcher

Rhodes

et al. 2003

J Headache Pain

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“…Ethyl acetate extracts of red wine inhibit human phenol sulfating phenol SULT (P-PST) by 90-100% at a dilution of 1/75, and monoamine sulfating phenol SULT (M-PST) by 100% at a dilution of 1/10 [85]. Similarly, Jones et al found that the dealcoholised red wine inhibited human platelet P-PST activity by 50% in a 2,000-fold dilution [38].…”

Section: Dietary Chemicalsmentioning

confidence: 92%

“…It was shown that the central region spanning amino acid residues 102-164 in rat hydroxysteroid SULT are essential for the activity [52]. Studies using (HUMAN)SULT1A1 and 1A3, which are 93% identical but exhibit distinct substrate specificity and other enzymatic properties, have revealed that region I (84)(85)(86)(87)(88)(89) and region II (143)(144)(145)(146)(147)(148) were responsible for its substrate specificity [53]. A chimeric construct of (HUMAN)SULT 1A1 with region I replaced with region II showed (HUMAN) SULT1A3 specificity, and vice versa [53].…”

Section: Structure Of Sultsmentioning

confidence: 98%

Inhibition of Sulfotransferases by Xenobiotics

Wang

James²

2006

CDM

130

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The sulfotransferase (SULT) family comprises important phase II conjugation enzymes for the detoxification of xenobiotics and modulation of the activity of physiologically important endobiotics such as thyroid hormones, steroids, and neurotransmitters. SULT enzymes catalyze the transfer of a sulfuryl group, donated by 3'-phosphoadenosine-5'-phosphosulfate (PAPS), to an acceptor substrate that may be a hydroxy group or an amine group in a process originally called sulfation, but more correctly referred to as sulfonation or sulfurylation. SULT activity may be inhibited when humans are exposed to certain xenobiotics including drugs (mefenamic acid, salicylic acid, clomiphene, danazol etc.), dietary chemicals (catechins, food colorants, flavonoids and phytoestrogens etc.), and environmental chemicals (hydroxylated polychlorinated biphenyls, hydroxylated polyhalogenated aromatic hydrocarbons, pentachlorophenol, triclosan and bisphenol A, etc.). Inhibition of individual SULT isoforms may cause adverse effects on human health. For example, hydroxylated polychlorinated biphenyls have been shown to interfere with the transport of thyroid hormones, inhibit estradiol sulfonation, and inhibit thyroid hormone sulfonation, thereby potentially disrupting the thyroid hormone system. Formation of sulfate conjugates of toxic xenobiotics usually decreases their toxicity, so inhibition of this pathway may lead to prolonged exposure to the compounds. Conversely, some sulfate conjugates are chemically reactive, inhibition of their formation may protect from toxicity. This manuscript will review the literature concerning the inhibition of SULTs by xenobiotics including isoform-selective effects, inhibition kinetics and health effects resulting from the inhibition.

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“…First, the duration of direct effects of alcoholic drinks are unknown, as are the long-term effects of alcohol congeners on other body systems which may influence tyramine conjugation. Littlewood, Glover and Sandler (1985) showed that red wine potently inhibits PST, although via substances other than alcohol. Whilst every attempt was made to exclude patients whose metabolism was substantially distorted by recent drinking, in terms of markedly elevated liver function tests, more subtle effects on tyramine conjugation may still have been present.…”

Section: Discussionmentioning

confidence: 98%

Detoxified alcoholics, major depressives and tyramine sulphate excretion

Hale

Hannah²,

Sandler³

et al. 1995

J Psychopharmacol

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The excretion of tyramine sulphate after challenge with an oral load of tyramine was assessed in recently detoxified, clinically depressed alcoholics and a matched group of major depressives. Tyramine excretion in the alcohol group (mean 5.95 ± 3.28 mg/3 h SD) was in the range previously observed in controls and was significantly higher than in the matched depressives (mean 3.43 ± 2.37 mg/3 h SD). Tyramine sulphate excretion has been suggested as a genetic vulnerability marker for major depression. This study suggests that depression associated with alcohol withdrawal is not characterised by decreased tyramine sulphate excretion after oral tyramine challenge, such decreased conjugation only being present, perhaps, in those patients with pre- existing endogenous depressive vulnerability. Although a genetic link between alcoholism and depression exists, these results support the absence of such a link to major depression.

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Red wine contains a potent inhibitor of phenolsulphotransferase.

Cited by 35 publications

References 18 publications

Pharmacological analysis of red-wine-induced migrainous headaches

Pharmacological analysis of red-wine-induced migrainous headaches

Inhibition of Sulfotransferases by Xenobiotics

Detoxified alcoholics, major depressives and tyramine sulphate excretion

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