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PubMed1982

Amine modulation of the neurogenic Limulus heart.

(1) The biogenic amines octopamine (OCT), dopamine (DA), epinephrine (E), and norepinephrine (NE) cause dose-dependent increases in both the rate and amplitude of contractions of the isolated Limulus heart-cardiac ganglion. Their relative ability to produce this excitation is OCT greater than DA approximately the same as E greater than NE. (2) The excitatory effects of all these amines are antagonized by the alpha-adrenergic blocker phentolamine and the dopaminergic antagonist haloperidol. The beta-adrenergic antagonist dichloroisoproterenol slightly reduces amine excitation, but is also a partial agonist. The beta-adrenergic antagonist propanolol, the alpha-blocker phenoxybenzamine, and the serotonin antagonist metergoline are ineffective. (3) In addition to their excitatory effects, DA and, to a lesser extent, NE initially reduce contraction rate and amplitude. (4) The transient inhibition is eliminated selectively by metergoline and is unaffected by the other antagonists. (5) The amines all increase the frequency of cardiac ganglion electrical bursting activity, whether ganglia are isolated or attached to cardiac muscle. Dopamine and NE also transiently inhibit the cardiac ganglion. (6) The amines do not alter myocardial resting tension, contractility, or membrane potential. (7) These amines appear to exert their modulatory effects on Limulus heart by altering the properties of the neurons which comprise its cardiac ganglion.

Animals↗
PubMed1998

Reactions of hypochlorous acid with biological substrates are activated catalytically by tertiary amines.

The activation of reactions of HOCl with a variety of model substrates by tertiary amines was investigated spectroscopically by tandem-mix and stopped-flow techniques. HOCl-induced chlorination of salicylate can be sped up by several orders of magnitude by catalytic amounts of trimethylamine (TMN). The effect is obviously due to the fast generation of reactive quarternary chloramonium ions, TMN+ Cl, which act as chain carrier in a catalytic reaction cycle. Of various catalysts tested, quinine shows the highest activity; this is attributable to the quinuclidine (QN) substituent, a bicyclic tertiary amine, forming a particularly reactive chloro derivative, QN+ Cl, which does not decompose autocatalytically. The rate of catalytic salicylate chlorination as a function of pH (around pH 7) depends not at least on the basicity of the tertiary amine; the rate increases with pH in the cases of TMN and quinuclidine (high basicity), but decreases with pH in the case of MES (low basicity). Tertiary amines also catalyze the interaction between HOCl and alkenes, as shown using sorbate as model. Reaction of HOCl with the nucleotides GMP and CMP is sped up remarkably by catalytic amounts of tertiary amines. In the case of GMP the same product spectrum is produced by HOCl in absence and presence of catalyst, but a change in the product spectra is obtained when AMP and CMP are reacted with HOCl in presence of catalyst. Using poly(dA-dT).poly(dA-dT) as DNA model, it is shown that HOCl primarily induces an absorbance increase at 263 nm, which indicates unfolding of the double strand due to fast chlorination of thymidine; a subsequent secondary absorbance decrease can be explained by slow chlorination of adenosine. Both the primary and secondary processes are activated by catalytic amounts of quinine. No evidence was found for a radical pathway in TMN-mediated oxidation of formate by HOCl. The present results suggest that low concentrations of certain tertiary amines have the potential of modifying the spectrum of target molecules which can be damaged by HOCl in biological systems.

Amines↗
PubMed2002

Detection and determination of aromatic amines as products of reductive splitting from selected azo dyes.

The current environment-friendly regulations concerning textile products ban the marketing of textiles dyed with azo dyes capable of reductively splitting carcinogenic aromatic amines. The study analyzes seven azo dyes whose chemical structure determines various quantities of splitting aromatic amines, such as benzidine. For tests, seven commercially available azo dyes with aromatic amines in their structure were selected. These included two hazardous dyes: Acid Red 85 and Direct Blue 6, both capable of reductively splitting carcinogenic benzidine. Of the remaining five azo dyes, three--Ponceau SS, Sudan II, and Disperse Yellow 7--are capable of splitting p-phenylenediamine and aniline, while Mordant Orange 1 and Disperse Orange 3 can split only p-phenylenediamine. For Acid Red 85 and Direct Blue 6, the quantity of benzidine split from them was analyzed, depending on the conditions of the reduction process (e.g., in the HPLC method, 104 g/kg of dye for reduction in NaOH, and 41 g/kg of dye for reduction in acetate buffer). The spectrophotometric method proved useful for preliminary analysis of amine content in examined samples. Spectrophotometric analysis may be used to determine the total content of amines counted as aniline. A full qualitative and quantitative analysis of amines released from azo dyes is possible using high-performance liquid chromatography (HPLC).

Amines↗
PubMed1986

Oxidation of amines by yeasts grown on 1-aminoalkanes or putrescine as the sole source of carbon, nitrogen and energy.

The maximum growth rate of Trichosporon cutaneum CBS 8111 in chemostat cultures was 0.185 h-1 on ethylamine and 0.21 h-1 on butylamine, that of Candida famata CBS 8109 was 0.32 h-1 on putrescine. The amine oxidation pattern of the ascomycetous strains studied, viz. Candida famata CBS 8109, Stephanoascus ciferrii CBS 4856 and Trichosporon adeninovorans CBS 8244 was independent of the amine that had been used as the growth substrate. It resembled that of benzylamine/putrescine oxidase found in other ascomycetous yeasts. However, differences in pH optimum and substrate specificity were observed between the amine-oxidizing systems of these three species. The amine oxidation pattern of cell-free extracts of Trichosporon cutaneum CBS 8111 varied with the amine that was used as growth substrate. The enzyme system produced by Cryptococcus laurentii CBS 7140 failed to oxidize isobutylamine and benzylamine, and showed a high pH optimum. The synthesis of amine oxidase in the four yeast strains studied was not repressed by ammonium chloride and was weakly repressed by glucose but was strongly repressed if both compounds were present in the growth medium.

Amines↗
PubMed1988

Kinetics of intraventricularly injected trace amines and their deuterated isotopomers.

Intraventricular injection into the rat brain of four trace amines and a catecholamine resulted in rapid exponential loss of the amines in the first 30 minutes after injection. The half-lives were: phenylethylamine 3.8 min, para-tyramine 5.1 min, meta-tyramine 7.4 min and dopamine 8.0 min. Tryptamine showed a biphasic loss with half-lives of 4.7 min (over the 5 to 10 min period) and 14.1 min (10 to 30 min). The half-lives were substantially increased by deuterium labeling at the alpha carbon position: phenylethylamine 4.8 min, para-tyramine 8.8 min, meta-tyramine 14.1 min, dopamine 13.0 min and tryptamine 6.0 min (5 to 10 min period) and 28.7 min (10 to 20 min). The loss of the amines was reduced by monoamine oxidase inhibition by pargyline hydrochloride and the deuterium isotope effect was abolished. It is noteworthy that the half-life of dopamine was similar to those of the trace amines in this time period and that the trace amine half-lives after i.v. injection was longer than those obtained from measurements of increases of concentrations of endogenous amines after MAOI in vivo and that of dopamine shorter than values calculated from turnover measurements.

Animals↗
PubMed1993

Analysis of biogenic amines in plasma of hypertensive patients and a control group.

Procedures were developed for the determination of 17 circulating amines using gas chromatography-negative ion chemical ionisation mass spectrometry. The amines were quantified against their appropriate deuterated isotopomers. The mean concentrations and ranges of catecholamines and trace amines were high compared with previous studies. In comparison with nonhypertensives, plasma from hypertensives had higher concentrations of the following amines: noradrenaline (t = 4.0%); normetanephrine (t = 6.1%) and metanephrine (t = 1.9%). There were no significant differences between 5HT levels in plasma from hypertensives and controls. The following trace amines could be detected in variable amounts in plasma: p-tyramine, m-tyramine, p-octopamine, m-octopamine, p-synephrine, m-synephrine, and salsolinol. The trace amines melatonin, N-acetyl 5HT, tryptamine, 6-hydroxymelatonin and 5-methoxytryptamine could not be detected in plasma with limits of detection lying in the range 20-100 pg ml-1.

Biogenic Amines↗
PubMed2003

The vesicular amine transporter family (SLC18): amine/proton antiporters required for vesicular accumulation and regulated exocytotic secretion of monoamines and acetylcholine.

The vesicular amine transporters (VATs) are expressed as integral proteins of the lipid bilayer membrane of secretory vesicles in neuronal and endocrine cells. Their function is to allow the transport of acetylcholine (by the vesicular acetylcholine transporter VAChT; SLC18A3) and biogenic amines (by the vesicular monoamine transporters VMAT1 and VMAT2; SLC18A1 and SLC18A2) into secretory vesicles, which then discharge them into the extracellular space by exocytosis. Transport of positively charged amines by members of the SLC18 family in all cases utilizes an electrochemical gradient across the vesicular membrane established by proton pumping into the vesicle via a vacuolar ATPase; the amine is accumulated in the vesicle at the expense of the proton gradient, at a ratio of one translocated amine per two translocated protons. The members of the SLC18 family have become important histochemical markers for chemical coding in neuroendocrine tissues and cells. The structural basis of their remarkable ability to transport positively charged amines against a very large concentration gradient, as well as potential disease association with impaired transporter function and expression, are under intense investigation.

Acetylcholine↗
PubMed1996

Effect of alkalinization of cytosolic pH by amines on intracellular Ca2+ activity in HT29 cells.

The effect of secondary, tertiary and quaternary methyl- and ethylamines on intracellular pH (pHi) and intracellular Ca2+ activity ([Ca2+]i) of HT29 cells was investigated microspectrofluorimetrically using pH- and Ca2+- sensitive fluorescent indicators, [i.e. 2', 7'-biscarboxyethyl-5(6)-carboxyfluorescein (BCECF) and fura-2 respectively]. Membrane voltage (Vm) was studied by the patch-clamp technique. Secondary and tertiary amines led to a rapid and stable concentration-dependent alkalinization which was independent of their pKa value. Trimethylamine (20 mmol/l) increased pHi by 0.78 +/- 0.03 pH units (n = 9) and pH remained stable for the application time. Removal led to an undershoot of pHi and a slow and incomplete recovery: pHi stayed 0.26 +/- 0.06 pH units more acid than the resting value. The quaternary amines, tetramethyl- and tetraethylamine were without influence on pHi. All tested secondary and tertiary amines (dimethyl-, diethyl-, trimethyl-, and triethyl-amine) induced a [Ca2+]i transient which reached a peak value within 10-25 s and then slowly declined to a [Ca2+]i plateau. The initial Delta[Ca2+]i induced by trimethylamine (20 mmol/l) was 160 +/- 15 nmol/l (n = 17). The [Ca2+]i peak was independent of the Ca2+ activity in the bath solution, but the [Ca2+]i plateau was significantly lower under Ca2+-free conditions and could be immediately interrupted by application of CO2 (10%; n = 6), a manoeuvre to acidify pHi in HT29 cells. Emptying of the carbachol- or neurotensin-sensitive intracellular Ca2+ stores completely abolished this [Ca2+]i transient. Tetramethylamine led to higher [Ca2+]i changes than the other amines tested and only this transient could be completely blocked by atropine (10(-6) mol/l). Trimethylamine (20 mmol/l) hyperpolarized Vm by 22.5 +/- 3.7 mV (n = 16) and increased the whole-cell conductance by 2.3 +/- 0.5 nS (n = 16). We conclude that secondary and tertiary amines induce stable alkaline pHi changes, release Ca2+ from intracellular, inositol-1,4, 5-trisphosphate-sensitive Ca2+ stores and increase Ca2+ influx into HT29 cells. The latter may be related to both the store depletion and the hyperpolarization.

Alkalies↗
PubMed1991

Sequence analysis of end-labeled DNA fragments by solvolysis in aqueous solutions of different amines.

Cleavage of 3'-end-labeled DNA in hot aqueous solutions of different amines is comparatively examined for overall rate of DNA scission as well as for potential differences in the preference of the various amines for cleavage at the different bases. Under comparable conditions (0.5 M amine, 0.3 M NaCl, 90 degrees C), piperidine, diethylamine, morpholine, and ethylenediamine produce the same set of labeled fragments, at approximately equal overall cleavage rates. The same set of fragments is also obtained with diisopropylamine, triethylamine, and 1,4-diazabicyclo[2.2.2]octane, but at markedly lower overall cleavage rates. Solvolysis in aqueous piperidine or aqueous diethylamine leads to DNA scission predominantly at A sites, followed by G and C sites, and least frequently at T sites. In contrast, morpholine, ethylenediamine, diisopropylamine, triethylamine, and diazabicyclo[2.2.2]octane cleave the DNA predominantly at G sites. Therefore, use of one of the latter amines allows clear distinction of G bands and C bands, which could not be distinguished by the criterion of band intensity in the original one-lane sequencing method based on cleavage in hot aqueous piperidine (B. Ambrose and R. Pless (1985) Biochemistry 24, 6194-6200). The effect of varying the salt concentration on the cleavage distribution obtained with various amines is also examined, and a rationale is given for the influence of salt concentration and amine basicity on the relative rate of cleavage at G sites.

Amines↗
PubMed1989

Sidedness of the effect of amines on the steady-state phosphorylation level of reconstituted Na+/K+-ATPase.

The sidedness of the effects of several amines on the steady-state phosphorylation level of rabbit kidney Na+/K+-ATPase has been studied with the enzyme incorporated in phosphatidylcholine-cholesterol containing proteoliposomes. The presence of ouabain prevented phosphorylation of non-incorporated or rightside-out incorporated enzyme, so that only the inside-out incorporated Na+/K+-ATPase molecules were studied. Addition of either Na+ or several amines to the extracellular side of the enzyme led to an enhancement of the steady-state phosphorylation level obtained with optimal concentrations of Na+, Mg2+ and ATP at the cytosolic side. The series imidazole greater than Na+ greater than triallylamine greater than Tris greater than ethylenediamine showed a decrease in affinity. Histidine, sorbitol and choline chloride had no effect at the extracellular side. This means that in addition to the well-known cytosolic ligands either Na+ or a positively charged amine buffer has to be present extracellularly in order to obtain an optimal phosphorylation level. At the cytoplasmic side the tested amines exerted different effects. (i) Imidazole and triallylamine enhanced the steady-state phosphorylation level when the extracellular conditions were optimal (saturating amine concentration). (ii) Tris and ethylenediamine decreased the steady-state phosphorylation level and (iii) histidine had no effect. The cytoplasmic effects of the amine compounds correlate with those described by Schuurmans Stekhoven et al. (Biochim. Biophys. Acta 937 (1988) 161-171) for the unsided preparation. The extracellular effects, however, are apparently masked in experiments with fragmented enzyme preparations and are assumed to be potentiating effects which make the enzyme ready for phosphorylation upon a cytoplasmic trigger (e.g. Na+).

Adenosine Triphosphate↗
PubMed1992

N-and O-acetylation of aromatic and heterocyclic amine carcinogens by human monomorphic and polymorphic acetyltransferases expressed in COS-1 cells.

Human monomorphic and polymorphic arylamine acetyltransferases (EC 2.3.1.5) were expressed in monkey kidney COS-1 cells and used to study the N- and O-acetylation of a number of carcinogenic amines and their N-hydroxy metabolites. The monomorphic enzyme N-acetylated the aromatic amines, 2-aminofluorene and 4-aminobiphenyl, and also O-acetylated their N-hydroxy derivatives. None of the food-derived heterocyclic amines (Glu-P-1, PhIP, IQ, MeIQx) were substrates and their N-hydroxy metabolites were poorly O-acetylated by this isozyme. By contrast, the polymorphic acetyltransferase catalyzed the N-acetylation of both aromatic amines, and to a lesser extent, Glu-P-1 and PhIP. However, all six N-hydroxy amine substrates were readily O-acetylated to form DNA-bound adducts by the polymorphic isozyme. These data suggest that, for the heterocyclic amine carcinogens, rapid acetylator individuals will be predisposed to their genotoxicity.

Acetylation↗
PubMed1992

Improvement of extraction procedure for biogenic amines in foods and their high-performance liquid chromatographic determination.

A high-performance liquid chromatography method is described for the simultaneous determination of the biogenic amines tryptamine, 2-phenylethylamine, putrescine, cadaverine, histamine, tyramine, spermidine, and spermine in cheese. The optimization of the procedure for the extraction of amines from the matrix is described. The separation of dansyl derivatives of the amines was achieved by reversed-phase liquid chromatography with gradient elution, followed by UV detection at 254 nm. The mobile phase was acetonitrile-0.01 M phosphate buffer (pH 7)-water. Under these conditions, rapid elution of the amines in less than 13 min was obtained. Validation of the method included calibration experiments, addition of standard amines for the determination of amine recoveries and repeatability tests.

Biogenic Amines↗
PubMed1981

Use of nitrous acid-dependent decrease in mutagenicity as an indication of the presence of mutagenic primary aromatic amines. Non-specific reactions with phenols and benzo[alpha]pyrene.

Treatment of mutagenic primary aromatic amines with nitrous acid is known to decrease their mutagenicity. We examined some factors concerning the validity of using decreases in mutagenicity due to nitrous acid treatment as an indication of the presence of mutagenic primary aromatic amines in complex mixtures. We found that treatment of benzo[alpha]pyrene with nitrous acid for the extended periods of time previously employed leads to formation of three nitrobenzo[alpha]pyrene isomers. Some of the isomers are direct-acting mutagens for S. typhimurium with considerably greater mutagenicity than benzo[alpha]pyrene isomers. In attempts to minimize reaction of chemicals other than aromatic amines, we found that only very brief reaction periods are required for complete reaction of nitrous acid with representative aromatic amines, essentially eliminating their mutagenicity. During such brief reaction periods modification of benzo[alpha]pyrene is negligible, but phenols react readily. Chromatographic analysis indicated that reaction of nitrous acid with aromatic amines leads to the formation of families of products, thereby increasing the complexity of the mixtures in which the amines may occur. Thus, experiments examining the effects of nitrous acid on the mutagenic activity of complex mixtures must be carefully designed, and the results must be interpreted cautiously.

Amines↗
PubMed1991

QSARs for selected aliphatic and aromatic amines.

The relative toxicity of 24 selected amines was evaluated in the 48 h Tetrahymena pyriformis static population growth impairment assay and compared with literature data for the 96 h Pimephales promelas flow-through mortality assay. Chemicals selected included normal and branched aliphatic primary amines, 4-position alkyl-substituted primary aromatic amines, as well as secondary and tertiary amines. Three amines were not toxic at saturation in the Tetrahymena system, whereas one amine was not toxic at saturation in the Pimephales system. Due to the aberrantly high toxicity of aniline observed in the Tetrahymena system, this chemical was not included in the analyses. For QSAR development, toxicity measured as log IGC50(-1) and log LC50(-1), respectively, was regressed against the log of the 1-octanol/water partition coefficient (log KOW). Both toxicity and hydrophobicity varied over five orders of magnitude. The model, log IGC50(-1) = 0.72(log KOW) - 1.64 (n = 20, r2 = 0.92) (1), was found to be a good predictor of toxicity in the Tetrahymena system. Similarly, the model, log LC50(-1) = 0.80(log KOW) - 1.80 (n = 23, r2 = 0.96) (2), was found to be a good predictor of toxicity in the Pimephales system. A comparison of Eqns (1) and (2) showed the models to be very similar. Therefore, as seen by the model, log LC50(-1) = 1.11(log IGC50(-1] - 0.01 (n = 20, r2 = 0.93) (3), a regression of the log toxicities gave a slope of one, an intercept of zero and a high correlation.

Amines↗
PubMed1987

Mutagenicity modulating effect of quercetin on aromatic amines and acetamides.

The effect of quercetin on the mutagenicity of 32 kinds of aromatic amines and their acetamides were investigated using Salmonella typhimurium TA98 with a mammalian metabolic activation system (S9 mix). Quercetin enhanced the mutagenicity of the tricyclic aromatic amines (aminofluorene, aminoanthracene and aminophenanthrene) and their acetamides by 1.2-5.9-fold. Whereas, quercetin depressed the mutagenicity of aniline derivatives, biphenyl derivatives, and bi- and tetra-cyclic amino derivatives. The modulation of mutagenicity of Trp-P-1, Trp-P-2, Glu-P-1 and Glu-P-2 (heterocyclic amines) by quercetin were liable to be affected by the content of S9 in the S9 mix. It seems that quercetin does not have the same effect as norharman, because quercetin did not enhance the mutagenicity of aniline. It is suggested that the modulation of the mutagenicity of aromatic amines and acetamides is caused by the modulation of the balance between the mutagenic activation and inactivation in the metabolism of these amines and acetamides in the presence of quercetin. In this modulation, quercetin may participate through its effects on the promotion of N-hydroxylation and the inhibition of arylhydroxylation and transacylation. The presence of tricyclic aromatic rings of amines and acetamides is a structural requirement for the mutagenicity enhancement by quercetin.

Amides↗
PubMed1995

Heterocyclic amine content in fast-food meat products.

Heterocyclic aromatic amines are sometimes formed during the cooking of muscle meats, and their mutagenic and carcinogenic effects are of potential concern in the aetiology of human cancer. In a large survey of the heterocyclic amine content of foods, fried or charbroiled hamburgers, fried chicken, chicken breast sandwiches, fish sandwiches and breakfast sausages were purchased from fast-food restaurants. At least three different chains were visited per product and samples from five stores from each chain were pooled. The solid-phase extraction and HPLC method was used to analyse pooled samples for heterocyclic amine content and mutagenic activity with the Ames/Salmonella assay. Samples were analysed in a blind study which also contained quality control samples of two types, one high and one low in heterocyclic amine content and mutagenic activity. Results from the fast-food products showed undetectable levels of heterocyclic amines in 10 of 17 samples and only low levels [< or = 1 ng/g total of 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (DiMeIQx)] in the remaining samples. Compared with literature values based primarily on laboratory and home cooking conditions, fast-food meat products appear to contribute only a small percentage of the estimated daily dietary intake of heterocyclic amines.

Amines↗
PubMed1994

Aminated fucoidan promotes the invasion of 3 LL cells through reconstituted basement membrane: its possible mechanism of action.

Fucoidan is reported to have an antimetastatic activity. In the present study, we prepared an amino group-introduced derivative of fucoidan and examined its effect on the invasion of 3 LL cells through a reconstituted basement membrane (MatrigelTM). Unlike native fucoidan, the aminated derivative promoted the tumor cell invasion: maximal promotion (240% of control invasion) was obtained with 5 micrograms/ml. However, with higher concentrations (10-30 micrograms/ml) of the fucoidan derivative, the promotion was gradually reduced to 130% of control. Both native and aminated fucoidans inhibited specifically the attachment of 3 LL cells to laminin. Interestingly, aminated fucoidan, unlike the native one, promoted the tumor cell adhesion to immobilized synthetic laminin B 1 chain peptide, YIGSR, over a concentration range of 0.5-5 micrograms/ml. Higher concentrations (7-20 micrograms/ml) of the aminated derivative suppressed the adhesive ability of 3 LL cells to YIGSR. 3 LL cells secreted a 50-kDa form of urokinase-type plasminogen activator (u-PA) in the culture medium. Addition of aminated fucoidan (5 micrograms/ml) or YIGSR (10 micrograms/ml) resulted in a 1.7-fold increase in u-PA activity. This effect was enhanced up to 3.5-fold when both substances were simultaneously added. The addition of native fucoidan had no effect. The present results suggest that the 67-kDa receptor-mediated binding of 3 LL cells to laminin activates their invasiveness, especially by enhancing the extracellular u-PA levels. Aminated, but not native, fucoidan may act to enhance the laminin-receptor interaction at the limited concentration range.

Amination↗
PubMed2005

Regeneration and inhibition of proton pumping activity of bacteriorhodopsin blue membrane by cationic amine anesthetics.

Bacteriorhodopsin (bR) is the prototype of an integral membrane protein with seven membrane-spanning alpha-helices and serves as a model of the G-protein-coupled drug receptors. This study is aimed at reaching a greater understanding of the role of amine local anesthetic cations on the proton transport in the bR protein, and furthermore, the functional role of "the cation" in the proton pumping mechanism. The effect of the amine anesthetic cations on the proton pump in the bR blue membrane was compared with those by divalent (Ca2+, Mg2+ and Mn2+) and monovalent metal cations (Li+, Na+, K+ and Cs+), which are essential for the correct functioning of the proton pumping of the bR protein. The results suggest that the interacting site of the divalent cation to the bR membrane may differ from that of the monovalent metal cation. The electric current profile of the bR blue membrane in the presence of the amine anesthetic cations was biphasic, involving the generation and inhibition of the proton pumping activity in a concentration-dependent manner. The extent of the regeneration of the proton pump by the additives increased in the order of monovalent metal cation<monovalent amine anesthetic cation<divalent metal cation. We found that organic cations such as the amine anesthetics can also regenerate the proton pump in the bR protein. The inhibition of proton transport in the bR protein by the anesthetic cations was elucidated using the wild type, the E204Q and the D96N mutated bRs. The hydrophobic interaction of the amine anesthetics with the bR protein plays an important part in inhibiting the bR proton pump.

Amines↗