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PubMed1992

Radiosensitization and hypoxic cell toxicity of NLA-1 and NLA-2, two new bioreductive compounds.

Two new bioreductive compounds, 9-[3-(2-nitro-1-imidazolyl)propylamino]acridine hydrochloride (NLA-1) and 9-[2-(2-nitro-1-imidazolyl)ethylamino]acridine hydrochloride (NLA-2), have been prepared. They feature an acridine ring to intercalate with DNA, a 2-nitroimidazole ring as the radiosensitizing moiety and an amino functionality for increased DNA-binding and hydrophilicity. Time and concentration dependent cytotoxicity as well as radiosensitization efficacy of the two compounds under hypoxic or aerobic conditions were determined in vitro using V-79 cells and an MTT colorimetric or clonogenic assay. The isosensitization point (ISP), defined as that drug concentration which results in the same survival decrement upon exposure of hypoxic or oxygenated cells to a given radiation dose, has been determined for both compounds at 7.5 Gy and the values are significantly lower than the ISPs of 5-[3-(2-nitro-1-imidazolyl)propyl]phenanthridinium bromide, 2-(2-nitro-1-imidazolyl)ethylamine or misonidazole (MISO). NLA-1 and NLA-2 are potent hypoxic cytotoxins and on a concentration basis, more potent than MISO as radiosensitizers in vitro. The sensitization enhancement ratios were significantly increased when 1 h drug preincubation under hypoxia at 37 degrees C was applied, before irradiation at room temperature.

Aminoacridines↗
PubMed1995

A comparison of the contractile effects of 5-hydroxytryptamine, sumatriptan and MK-462 on human coronary artery in vitro.

1. MK-462 (N,N-dimethyl-2-[5-(1,2,4-triazol-1-ylmethyl)-1H- indol-3-yl]ethylamine) is a novel selective 5-HT1D-receptor agonist which in clinical trials has been shown to be an effective antimigraine agent. As angiographic studies have shown that sumatriptan (an established 5-HT1D-receptor agonist) can cause coronary artery vasoconstriction in patients, we compared the effects of MK-462 with those of 5-HT and those of sumatriptan, on isolated segments of human coronary artery in vitro. 2. Coronary arteries were obtained from explanted hearts from patients (n = 22, 2 females, 20 males, aged 21-60 years) undergoing cardiac transplantation. Endothelium-denuded ring segments of coronary artery, 2mm long were mounted in organbaths for isometric tension recording. For each arterial ring segment, a cumulative concentration-effect curve to either 5-HT, sumatriptan or MK-462 was determined. After maximal response to each agonist had been obtained, ketanserin (a 5-HT2 receptor antagonist) 0.6 microM was added to the tissue bath, followed by methiotepin (0.6 microM) and the reduction in tension produced by the addition of each antagonist was determined. 3. Out of 22 coronary arteries studied, only 10 showed any response (contraction) to 5-HT. Not all arteries which responded to 5-HT contracted in response to both sumatriptan and MK-462 (one ring from each artery being exposed to a single agonist in each case).(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Vessels↗
PubMed1975

A kinetic study of mitochondrial calcium transport.

This report describes a kinetic analysis of energy-linked Ca2+ transport in rat liver mitochondria, in which a ruthenium red/EGTA [ethanedioxy-bis(ethylamine)-tetraacetic acid] quenching technique has been used to measure rates of 45Ca2+ transport. Accurately known concentrations of free 45Ca2+ were generated with Ca2+/nitrilotriacetic acids buffers for the determination of substrate/velocity relationships. The results show that the initial velocity of transport is a sigmoidal function of Ca2+ concentration (Hill coefficient = 1.7), the Km being 4 muM Ca4 at 0 degrees C and pH 7.4. These values for the Hill coefficient and the Km remain constant in the presence of up to 2 mM phosphate, but with 10 mM acetate both parameters are increased slightly. Both permeant acids increase the maximum velocity to an extent dependent on their concentration. The Ca2+-binding site(s) of the carrier contains a group ionizing at pH approximately 7.5 at 0 degrees C, which is functional in the dissociated state. The stimulatory effect of permeant acids is ascribed to their facilitating the release of Ca2+ from the carrier to the internal phase, an interpretation which is strengthened by the lack of effect of the permeant anion SCN- on Ca2+ transport. Studies on the time-course of Ca2+ uptake and of EFTA-induced Ca2+ efflux from pre-loaded mitochondria demonstrate the reversibility of the carrier in respiring mitochondria and the extent to which this property is influenced by permeant acids. These data are accommodated in a carrier mechanism based on electrophoretic transport of Ca2+ bound to pairs of interacting acidic sites.

Animals↗
PubMed1994

Expression of the mau genes involved in methylamine metabolism in Paracoccus denitrificans is under control of a LysR-type transcriptional activator.

Expression of methylamine dehydrogenase in Paracoccus denitrificans and its concomitant ability to grow on methylamine is regulated by a substrate-induction mechanism as well as by a catabolite-repression-like mechanism. Methylamine dehydrogenase is synthesized in cells growing on either methylamine or ethylamine, but not during growth on succinate, methanol or choline as sole sources of carbon and energy. The synthesis of methylamine dehydrogenase is repressed when succinate is added to the growth medium in addition to methylamine. Repression is not observed when the growth medium contains methylamine and either choline or methanol. Induction of the mau genes encoding methylamine dehydrogenase is under control of the mauR gene. This regulatory gene is located directly in front of, but with the transcription direction opposite to that of, the structural genes in the mau cluster. The mauR gene encodes a LysR-type transcriptional activator. Inactivation of the gene results in loss of the ability to synthesize methylamine dehydrogenase and amicyanin, and loss of the ability to grow on methylamine. The mutation is completely restored when the mauR gene is supplied in trans. The first gene of the cluster of mau genes that is under control of MauR is mauF, which encodes a putative membrane-embedded protein. Inactivation of the gene results in the inability of cells to grow on methylamine. Downstream from mauF and in the same transcription direction, mauB is located. This gene encodes the large subunit of methylamine dehydrogenase.

Amino Acid Sequence↗
PubMedDate not supplied

Species difference in the beta1/beta2-adrenoceptor selectivity of SM220CL in the cat and guinea-pig.

The beta-receptor stimulant effects of Sm220Cl, dl-N-(1,1-dimethyl-3-phenylpropyl)-2-hydroxy-2-(3,4-dihydroxy-2-methoxyphenyl)ethylamine, and (-)-isoprenaline have been compared in isolated atrial (beta1) and tracheal (beta2) preparations from guinea-pigs and cats. 2. The compounds were also tested for their ability to increase the heart rate (beta1), reduce serotonin-induced increases in pulmonary resistance (beta2), and decrease soleus muscle contractility (beta2) in vivo in the two species. 3. In all experiments cumulative concentration or dose-effect curves were established, EC50 or ED50 values obtained and molar activity-ratios (Sm220Cl: (-)-isoprenaline) calculated. 4. Calculated selectivity ratios [activity-ratio (heart):activity-ratio (bronchial smooth muscle)] from the in vitro experiments showed that Sm220Cl possessed beta2-receptor selectivity. This was more marked in guinea-pig than in cat preparations. 5. In the anaesthetized animals this species difference was more apparent; in cats Sm220Cl was non-selective in its actions for beta1- and beta2-receptor mediated responses, while marked beta2-receptor selectivity was obtained in the guinea-pig. 6. Since in both species the activity-ratios for beta2-receptor mediated actions are similar, the differences in the beta1/beta2-receptor selectivity of Sm220Cl are caused by the divergent cardiac effects produced by the drug.

Airway Resistance↗
PubMed1985

Measurement of platelet monoamine oxidase using three different substrates in patients with alcoholism and schizophrenia.

The platelet monoamine oxidase (MAO) activities in alcoholism and schizophrenia were investigated by means of simultaneous determination, using beta-phenyl-ethylamine, tryptamine and serotonin as substrates. No significant difference was found between the MAO levels in the alcoholic and schizophrenic groups, when tryptamine was used as a substrate, but both groups showed lower values than the controls. On the other hand, beta-phenylethylamine, a specific substrate for MAO B used as a substrate, showed no significant difference between the alcoholic and control groups in the activities. These two groups showed higher values in MAO activity than the schizophrenic group, whereas when MAO activity was estimated using serotonin, platelet enzyme was found to be inhibited significantly in alcoholism, and the level of activities in the schizophrenics was similar to that of the controls. Moreover, the beta-phenylethylamine inhibition curve obtained serotonin as the substrate in the pooled platelets of 50 normal human subjects, and the MAO activity could not be inhibited by higher concentrations than the Km value of serotonin. These findings suggested that there might be two interacting catabolic sites having different substrate affinities in blood platelet MAO. Thus, it could be speculated that serotonergic catabolic sites of MAO in the platelets are disturbed in the alcoholics, while beta-phenylethylaminergic catabolic sites of platelet MAO are inherently vulnerable in schizophrenia.

Adult↗
PubMed1980

Catecholamine-sensitive guanylate cyclase from human caudate nucleus.

Partial purification of soluble guanylate cyclase on DEAE-Sephacel yields two separate peaks of guanylate cyclase activity. After 10-fold purification of the soluble enzyme, guanylate cyclase is markedly inhibited by micromolar concentrations of dopamine (I50 = 0.2 microM). Dopamine inhibition is observed whether the reaction is conducted with Mn2+ or with Mg2+, under atmosphere or N2(g), and using enzyme from either peak from the DEAE-Sephacel column. Other catecholamines also inhibit partially purified guanylate cyclase with an order of potency at 1 microM of: dopamine = L-DOPA > norepinephrine = isoproterenol = adrenochrome > epinephrine. The structural requirements for inhibition are two free hydroxyl groups on the phenyl ring and an ethylamine side chain. Dopamine also inhibits the Triton X-100-solubilized microsomal guanylate cyclase after partial purification on DEAE-Sephacel. Neither chlorpromazine, propranolol, nor phentolamine at 20 microM effectively block the dopamine inhibition of partially purified soluble guanylate cyclase. Micromolar concentrations of the reducing agents dithiothreitol and glutathione also inhibit partially purified guanylate cyclase, but unlike these agents, catecholamines can inhibit whether added in the reduced or the oxidized forms. Inhibition of enzyme activity by micromolar concentrations of dopamine, adrenochrome, or dithiothreitol is rapidly reversed by dilution and the dopamine inhibition is competitive with MgGTP. Inhibition does not appear to involve covalent binding or to result from the ability of catecholamines to reduce the concentrations of oxygen or free radicals in solution.

Adrenochrome↗
PubMed1985

Effect of the cerebral tryptaminergic system on the turnover of dopamine in the striatum of the rat.

The effect of the cerebral 5-hydroxytryptamine system on the turnover of striatal 3,4-dihydroxyphenyl-ethylamine (dopamine) was investigated by measuring the level of dopamine and one of its metabolites in rats depleted of cerebral 5-hydroxytryptamine or treated with a 5-hydroxytryptamine receptor blocker. Treatment with p-chlorophenylalanine induced, in addition to a reduction in striatal 5-hydroxytryptamine and 5-hydroxyindol-3-ylacetic acid, an increase in the striatal concentration of dopamine, a diminution in the concentration of homovanillic acid in the same cerebral area, and a reduction in the rise of this acid after the administration of a butyrophenone derivative or tetrabenazine. Treatment with methysergide also reduced the increase of homovanillic acid induced by the butyrophenone. When probenecid was given to rats treated with p-chlorophenylalanine, homovanillic acid failed to accumulate, whereas the accumulation of 5-hydroxyindol-3-ylacetic acid was unaffected. The decay of dopamine after alpha-methyl-p-tyrosine administration was normal for the first 6 h but was later reduced in rats given p-chlorophenylalanine or methysergide. The results suggest that the lack of activation of 5-hydroxytryptamine receptors leads to a reduction in the turnover of dopamine in the nigrostriatal pathway.

5-Hydroxytryptophan↗
PubMed2006

Evolution of malolactic bacteria and biogenic amines during spontaneous malolactic fermentations in a Greek winery.

AIMS: To study the population dynamics of indigenous malolactic bacteria in a Greek winery and to examine their potential to produce detrimental levels of biogenic amines (BA) under winemaking conditions. METHODS AND RESULTS: Although the wines studied were of different vintage, grape variety and enological characteristics, molecular typing of malolactic bacteria revealed only a low number of strains within the single-species populations of Oenococcus oeni that developed during spontaneous fermentations. Strain MF1, originating primarily from the vineyards surrounding the winery invariably predominated in almost all samples. HPLC analysis showed a slight increase in the BA, putrescine, tyramine and phenylethylamine after malolactic conversion, while histamine, methylamine and ethylamine remained unaffected. No correlation could be established between the BA profiles and the bacterial compositions or the amino acid concentrations in wine samples studied. CONCLUSIONS: A certain regional bacterial flora is established in the winery that prevails in spontaneous malolactic fermentations (MLF) irrespective of the wine characteristics. In all cases, the BA content of the wines after malolactic conversion was within enologically acceptable levels. SIGNIFICANCE AND IMPACT OF THE STUDY: This is the first report on the malolactic bacteria occurring naturally in spontaneous MLF in Greek red wines and a preliminary assessment of their impact on wine safety in relation to BA.

Biogenic Amines↗
PubMed1971

Turning behaviour as an index of the action of amphetamines and ephedrines on central dopamine-containing neurones.

1. Rats lesioned unilaterally in the substantia nigra show no obvious abnormalities after recovery from the operation but rotate towards the lesioned side after administration of drugs of the amphetamine and ephedrine groups.2. (+)-Amphetamine and (-)-amphetamine are equally potent in producing turning behaviour but (+)-methylamphetamine is considerably more effective.3. (-)-Ephedrine (with a beta-OH group on the ethylamine side chain) induces turning but only in doses approximately 20 times greater than (+)-methylamphetamine.4. (+)-Norpseudoephedrine was the most effective of the ephedrine isomers tested followed by (-)-ephedrine and (+)-pseudoephedrine.5. Turning produced by (-)-ephedrine and (+)-methylamphetamine is not reduced by FLA63 (50 mg/kg) 4 h previously, but is almost completely inhibited by alpha-methyl-p-tyrosine (150 mg/kg) 12 h previously.6. Reserpine pretreatment potentiates turning produced by (-)-ephedrine.7. Chlorpromazine (5 mg/kg) completely blocks turning induced by (+)-methylamphetamine although it concurrently increases exploratory activity. The level of exploratory activity after the (+)-methylamphetamine-chlorpromazine combination is more than 3 times that attained after saline alone.

Amphetamine↗
PubMed1979

The effects of histamine on responses of the rabbit ear artery to electrical stimulation and to exogenous noradrenaline.

1 The effects of a subconstrictor dose of histamine (9 x 10(-7) mol/l) on the responses of the isolated perfused ear artery of the rabbit to electrical stimulation (E.S.) and to exogenous noradrenaline (NA) were investigated.2 Both intraluminal (I/L) and extraluminal (E/L) histamine potentiated responses to E.S. and to I/L NA to the same extent.3 Mepyramine alone (2.5 x 10(-6) mol/l) had no effect on the response of the ear artery to either stimulus, but in the presence of this concentration of mepyramine, the potentiation by histamine of the response to I/L NA was significantly decreased and that to E.S. was replaced by inhibition.4 The H(1)-receptor agonist, 2(2-pyridyl) ethylamine, applied I/L potentiated responses to I/L NA at both concentrations used (5.1 and 51 x 10(-7) mol/l), but only potentiated the effects of E.S. at the higher concentration.5 The H(2)-receptor antagonist, metiamide (4 x 10(-6) mol/l), alone did not alter the extent of potentiation of responses to either E.S. or I/L NA by histamine. This suggests relatively weak H(2)-receptor activity in the rabbit ear artery. In the presence, but not the absence of metiamide, the potentiation by histamine of the I/L NA response was reversible, an observation suggesting an interaction between metiamide and the non-reversible component of the potentiating effect of histamine.6 These results are interpreted in terms of postsynaptic H(1)-receptors which potentiate and presynaptic H(2)-receptors which inhibit contractile responses in the ear artery.

Animals↗
PubMed1979

Characterization of vascular histamine receptors in the rat.

1 In the rat the decrease in blood pressure caused by histamine involves activation of both H1- and H2-receptors. Since arterial pressure measurements alone do not permit the separation of responses into cardiac and vascular components, the following experiments were undertaken to study vascular histamine receptors. 2 Vascular responses were studied in the autoperfused hindquarters of anaesthetized rats. Intra-arterial histamine caused vasodilatation which was only partially attenuated by treatment with mepyramine, an H1-receptor antagonist. Treatment with metiamide, the H2-receptor antagonist, did not affect vasodilatation caused by histamine but did attenuate vasodilatation which persisted after mepyramine. 3 Intra-arterial 4-methylhistamine, an H2-receptor agonist, caused vasodilatation which was reduced by metiamide. The H1-receptor agonist, 2-(2-pyridyl)ethylamine also caused vasodilatation which was blocked by mepyramine. 4 It is concluded that in the rat, histamine causes vasodilatation mediated by both H1- and H2-receptors.

Animals↗
PubMed1982

Analysis of histamine receptors in the central thermoregulatory mechanism of Mastomys natalensis.

1 The effect of intracerebroventricular (i.c.v.) injection of histamine on the rectal temperature of Mastomys natalensis at ambient temperatures of 10, 24 and 33 degrees C has been studied. 2 Low doses (0.1-1.0 microgram) of histamine produced hypothermia while larger doses (5-20 micrograms) produced dose-dependent hyperthermia. The hypothermic effect was significantly antagonized by mepyramine while the hyperthermia was blocked by cimetidine. 3 Histamine H1-receptor agonists, 2-methyl-histamine and 2-pyridyl-ethylamine, also produced hypothermia which could be blocked by mepyramine. 4 Histamine H2-receptor agonists, impromidine and dimaprit, produced hyperthermia which was antagonized by cimetidine. 5 Pretreatment of the animals with a beta-adrenoceptor antagonist, MJ1999, did not affect the response to histamine. 6 The hyperthermic effect of histamine (10 micrograms) was most marked at 10 degrees C and was attenuated at 33 degrees C. 7 It is concluded that both H1 and H2-histamine receptors are present in the brain of Mastomys. The H1-receptors mediate hypothermia and H2-receptors hyperthermia.

Animals↗
PubMed1984

The antagonism of histamine-induced tracheal and bronchial muscle contraction by diphenhydramine: effect of maturation.

Airway reactivity in spontaneously breathing unanaesthetized female guinea-pigs was significantly reduced as a consequence of maturation. Threshold doses to histamine (% w/v base) were 0.08% +/- .01 and 0.27% +/- .04 in immature (110 g +/- 2; 1 week old) and mature (837 g +/- 29; 4 months old) animals, respectively. The potency of 2-(2-thiazolyl) ethylamine in tracheal tissues from mature animals was significantly less than that in tissues from immature animals (5.06 +/- .03 vs 5.26 +/- .07). There was no change in the potency of this agonist in bronchial tissues (5.0 +/- .09 vs 4.9 +/- .13). Diphenhydramine reduced tissue contractility in tracheal (30% at 0.1 microM; 50% at 3 microM) but not bronchial tissues. The antihistamine in concentrations ranging from 0.1 microM to 3 microM reduced the potency of histamine 2 to 50 fold in both tissues. Schild plots were linear but slopes were significantly less than unity. pA2 values +/- 95% fiducial limits derived from data from tracheal tissues of immature and mature animals using constrained Schild plots (unit slope) were 7.7 (7.6-7.7) and 7.1 (7.0-7.2), respectively (P less than 0.05). pA2 values for diphenhydramine in bronchial tissues using constrained Schild plots were 7.8 (7.7-7.9) and 7.5 (7.3-7.5), respectively (P less than 0.05). The data emphasize the unique nature of tracheal and bronchial tissues. We conclude that, with maturation, the characteristics of the histamine receptor change. We suggest that the remission of asthma which frequently occurs at puberty may be related to alteration in the properties of membrane receptors.

Aging↗
PubMed1986

Pharmacological investigation into the effects of histamine and histamine analogues on guinea-pig and rat colon in vitro.

The effects of histamine and specific histamine agonists has been examined on isolated longitudinal colon strips of guinea-pig and rat. Histamine and 2-pyridyl-ethylamine but not 4 methylhistamine produced a concentration-related contractile response in the guinea-pig colon. The H1-antagonist clemizole antagonized competitively the effect of histamine but the H2-antagonist ranitidine did not modify the dose-response curve to histamine in the guinea-pig colon. Atropine, hexamethonium, prazosin and propranolol failed to modify the contractile response to histamine. Tone induced with KCl in guinea-pig isolated colon was not modified by histamine agonists even in tissues pretreated with clemizole or ranitidine. Histamine and histamine analogues were without effect on the isolated longitudinal strip of the rat colon. It is concluded that histamine produced dose-dependent contractions of the guinea-pig colon due to direct activation of H1-histamine receptors. There is no evidence in favour of the existence of H2-histamine receptors in this preparation. The lack of effect of histamine agonists in rat colon strip argues against the existence of histamine receptors in this preparation.

Animals↗
PubMed1993

L-694,247: a potent 5-HT1D receptor agonist.

1. The 5-hydroxytryptamine (5-HT) receptor binding selectivity profile of a novel, potent 5-HT1D receptor agonist, L-694,247 (2-[5-[3-(4-methylsulphonylamino)benzyl-1,2,4-oxadiazol-5-yl ]- 1H-indole-3-yl]ethylamine) was assessed and compared with that of the 5-HT1-like receptor agonist, sumatriptan. 2. L-694,247 had an affinity (pIC50) of 10.03 at the 5-HT1D binding site and 9.08 at the 5-HT1B binding site (sumatriptan: pIC50 values 8.22 and 5.94 respectively). L-694,247 retained good selectivity with respect to the 5-HT1A binding site (pIC50 = 8.64), the 5-HT1C binding site (6.42), the 5-HT2 binding site (6.50) and the 5-HT1E binding site (5.66). The pIC50 values for sumatriptan at these radioligand binding sites were 6.14, 5.0, < 5.0 and 5.64 respectively. Both L-694,247 and sumatriptan were essentially inactive at the 5-HT3 recognition site. 3. L-694,247, like sumatriptan, displayed a similar efficacy to 5-HT in inhibiting forskolin-stimulated adenylyl cyclase in guinea-pig substantia nigra although L-694,247 (pEC50 = 9.1) was more potent than sumatriptan (6.2) in this 5-HT1D receptor mediated functional response. L-694,247 (pEC50 = 9.4) was also more potent than sumatriptan (6.5) in a second 5-HT1D receptor mediated functional response, the inhibition of K(+)-evoked [3H]-5-HT release from guinea-pig frontal cortex slices. 4. The excellent agreement observed for L-694,247 between the 5-HTlD radioligand binding affinity and the functional potency confirm that the two functional models (the inhibition of forskolin-stimulated adenylyl cyclase in guinea-pig substantia nigra and the inhibition of K+-evoked [3H]-5-HT release from guinea-pig frontal cortex) do indeed reflect 5-HTID-mediated events.5. L-694,247 is a novel, highly potent 5-HTID/5-HTIB receptor ligand which should prove useful for the exploration of the physiological role of these receptors in animals.

Adenylyl Cyclases↗
PubMed1993

Reaction of acetaldehyde with proteins: formation of stable fluorescent adducts.

The properties of stable acetaldehyde-protein adducts, using bovine serum albumin as a model protein, were investigated. Upon prolonged incubation at 37 degrees C and pH 7.4, the reaction of acetaldehyde and albumin yielded stable adducts that exhibited fluorescent properties. Reaction mixtures of acetaldehyde with polylysine or ethylamine also formed fluorescent products with similar fluorescent spectral properties like acetaldehyde-albumin adducts, indicating that the amino groups of protein alone can generate fluorescent products on reaction with acetaldehyde. When reactions of acetaldehyde with albumin or polylysine were conducted at 22 degrees C, stable binding reached a maximum after 24 hr of incubation and essentially remained at this level during the remaining 216 hr of incubation, and minimal-to-no fluorescence was associated with this binding. At 37 degrees C, stable binding was greater and increased continuously over the entire 216 hr of incubation. After an initial lag period of 24 to 48 hr, increases in fluorescence intensity paralleled the increases in stable binding. The presence of sodium cyanoborohydride, which reduces Schiff bases, in the reaction mixtures prevented fluorescence, indicating that Schiff bases are intermediates in the formation of fluorescent products. Both stable binding and fluorescence intensities were minimally affected by exhaustive dialysis (up to 144 hr), indicating that the fluorescent products were quite stable. These results suggest that an initial reaction of a Schiff base with another acetaldehyde molecule via an aldol condensation reaction gives rise to the formation of a crotonaldehyde Schiff base derivative. This reactive intermediate could then undergo further condensation reactions and form advanced conjugated products, some of which could be fluorescent.

Acetaldehyde↗
PubMed1995

The clinical effect of percutaneous histamine on allergic contact dermatitis elicited to fragrance mix.

Histamine (2-(4-imidazol)ethylamine) has been shown to downregulate cell-mediated reactions in vitro. However, the rôle of such downregulation in vivo has not yet extensively been studied in humans. In an attempt to gain more insight into this, we studied in vivo the effect of percutaneous histamine on an allergic contact reaction elicited to fragrance mix in 28 human volunteers with previously-known sensitization (patch tests) to this allergen. Histamine (0.1 mg/ml) was administered either via subcutaneous injections or by scratching at the site of patch tests to one concentration (8% pet.) of fragrance mix at different times. Histamine and control solution were administered immediately before patch testing (0 hours) or 2x at 0 and 24 h (after application). No significant differences were observed in the grade of delayed-type hypersensitivity reaction (DTHR) to fragrance mix (8% pet.) by visual reading when histamine or control solution was administered. This study did not exclude the possibility that histamine could inhibit DTHR to lower concentrations of the allergen used, and therefore additional in vivo studies are required.

Administration, Cutaneous↗