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PubMed1984

Effect of trifluoperazine, compound 48/80, TMB-8 and verapamil on ionophore A23187 induced calcium transients in human red cells.

A transient increase of cellular calcium was induced by addition of the divalent cation ionophore A23187 to human red cells in the absence or presence of drugs. The peak height of the calcium transient was increased about five times at pH 6.9 and up to eighteen times at pH 7.4 by trifluoperazine (0.30 mM), and two to three times at pH 6.9 by compound 48/80 (0.89 mg/ml), 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8, 2.13 mM) and verapamil (1.81 mM). The time-dependent changes of cellular calcium were analysed by the aid of a pump-leak model based partly on the calcium dependent parameters obtained from calcium ATPase experiments, partly on the A23187 induced calcium fluxes determined in experiments with ATP depleted cells. The transient increase of cellular calcium induced within few minutes after the addition of ionophore A23187 could be explained satisfactorily by the model both in the absence and presence of the four drugs, whereas the final level of cellular calcium in the drug experiments was more difficult to predict from the pump-leak model. Comparison of experimental and model calcium transients suggested that trifluoperazine and TMB-8 affected both pump and leak, whereas compound 48/80, probably due to low membrane-permeability, mainly affected the leak and verapamil affected the pump only.

Biological Transport, Active↗
PubMed1985

Effects of Quin-2, an intracellular Ca chelator, and TMB-8, an intracellular Ca antagonist, on the short-term desensitization to histamine in guinea pig taenia caecum.

The effects of Quin-2-acetoxylmethylester, an intracellular Ca ion chelator, and 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate-HCl (TMB-8), an intracellular Ca antagonist, on short-term desensitization to histamine were tested in guinea pig taenia caecum. Desensitization was induced by incubating the muscle with 10(-4) M histamine for 30 min and the recovery from the desensitization needed ca. 90 min. Both Quin-2-acetoxylmethylester (50 microM for 120 min) and TMB-8 (5 microM for 20 min) suppressed the desensitization. Modes of action and structures of both agents are quite different but both may reduce the availability of intracellular Ca ion. It is possible that reduction of intracellular Ca ion suppressed the desensitization.

Aminoquinolines↗
PubMed2000

Either desipramine or TMB-8 suppresses cyanide-induced norepinephrine efflux from in vivo cardiac sympathetic nerves of cats.

To investigate the effect of hypoxia on endogenous norepinephrine (NE) release from cardiac sympathetic nerve ending, we administered sodium cyanide (NaCN) for 30 min into the myocardial interstitial space through a dialysis probe and measured dialysate NE levels. During the NaCN perfusion, a marked and concentration-dependent increase in dialysate NE was observed. This cyanide-induced NE response was suppressed by pretreatment with despiramine (a membraneous NE transport inhibitor). Furthermore, the cyanide-induced NE response was suppressed by pretreatment with TMB-8 (intracellular Ca(2+) antagonist) but unaffected by omega-conotoxin GVIA (NE releasing inhibitor). Our data suggest that two (desipramine or TMB-8 suppressive) mechanisms contributed to the amount of NE efflux induced by cyanide in in vivo cardiac sympathetic nerve.

Animals↗
PubMed1994

Calcium antagonist, TMB-8, prevents the induction of adaptive response by hydrogen peroxide or X-rays in human lymphocytes.

Treatment of human lymphocytes with hydrogen peroxide (10 microM, 30 min, 37 degrees C in PBS) or with 1 cGy X-rays evoked about a 30% decrease in the frequency of micronuclei upon subsequent X-irradiation (1.5 Gy). In addition to a lower micronuclei frequency, we also found an increase in the sedimentation distance of the nucleoids, when measured 90 min (duration of the isolation procedure carried out at 4 degrees C) after the adaptive dose (hydrogen peroxide or X-rays) and preceding the challenge dose. To test whether Ca2+ is involved in the induction of the adaptive response pathway, we treated cells with the calcium chelator, EGTA. When EGTA was given at the same time as the adaptive dose, it prevented the development of the adaptive response. In addition, the calcium antagonist, TMB-8, also prevented the development of the adaptive response as it prevented the reduction of both micronuclei and increased nucleoid sedimentation. Cellular treatment with TMB-8 increased the free [Ca2+] by 40%, when given together with hydrogen peroxide. The faster sedimenting nucleoids from adapted cells were also examined by ethidium bromide titration; there was no indication of any change in supercoil density or loop size. Psi-tectorigenin, an inhibitor of phosphatidylinositol turnover, did not modify the adaptive response, indicating that inositol (1,4,5)-trisphosphate is not involved in the induction of the adaptive response, but free Ca2+ ions are.

Adaptation, Physiological↗
PubMed2005

TMB-Hunt: an amino acid composition based method to screen proteomes for beta-barrel transmembrane proteins.

BACKGROUND: Beta-barrel transmembrane (bbtm) proteins are a functionally important and diverse group of proteins expressed in the outer membranes of bacteria (both gram negative and acid fast gram positive), mitochondria and chloroplasts. Despite recent publications describing reasonable levels of accuracy for discriminating between bbtm proteins and other proteins, screening of entire genomes remains troublesome as these molecules only constitute a small fraction of the sequences screened. Therefore, novel methods are still required capable of detecting new families of bbtm protein in diverse genomes. RESULTS: We present TMB-Hunt, a program that uses a k-Nearest Neighbour (k-NN) algorithm to discriminate between bbtm and non-bbtm proteins on the basis of their amino acid composition. By including differentially weighted amino acids, evolutionary information and by calibrating the scoring, an accuracy of 92.5% was achieved, with 91% sensitivity and 93.8% positive predictive value (PPV), using a rigorous cross-validation procedure. A major advantage of this approach is that because it does not rely on beta-strand detection, it does not require resolved structures and thus larger, more representative, training sets could be used. It is therefore believed that this approach will be invaluable in complementing other, physicochemical and homology based methods. This was demonstrated by the correct reassignment of a number of proteins which other predictors failed to classify. We have used the algorithm to screen several genomes and have discussed our findings. CONCLUSION: TMB-Hunt achieves a prediction accuracy level better than other approaches published to date. Results were significantly enhanced by use of evolutionary information and a system for calibrating k-NN scoring. Because the program uses a distinct approach to that of other discriminators and thus suffers different liabilities, we believe it will make a significant contribution to the development of a consensus approach for bbtm protein detection.

Algorithms↗
PubMed1985

Effects of TMB-8, an intracellular calcium antagonist, and W-7, a calmodulin antagonist, on prostaglandin output from the guinea-pig uterus.

TMB-8, an intracellular Ca2+ antagonist, inhibited the A23187-induced increase in outputs of prostaglandin (PG) F-2 alpha and 6-keto-PGF-1 alpha from the guinea-pig uterus superfused in vitro. The high basal output of PGF-2 alpha from the Day-15 guinea-pig uterus was not inhibited by TMB-8, indicating that a maintained high intracellular free Ca2+ concentration is not necessary for maintaining this high output of PGF-2 alpha. W-7, a calmodulin antagonist, had similar actions except that PGF-2 alpha output from the Day-15 uterus was reduced 20-30 min after the W-7 treatment had stopped. Overall, these findings suggest that, in the guinea-pig, oestradiol acting on a progesterone-primed uterus causes a prolonged stimulation of endometrial phospholipase A-2 in the absence of a maintained high Ca2+ concentration, thus providing a continuous release of arachidonic acid for increased endometrial PGF-2 alpha synthesis during the last third of the oestrous cycle.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

[Heightened anticholinesterase activity of chlorophos in its interaction with the TMB-4 reactivator in vitro].

Experiments in vitro demonstrated that a thermostatic treatment of an aqueous chlorophos solution at 38 degrees is attended by its increased cholinesterase activity. The speed of the process is much higher in an alkaline medium. A joint incubation of chlorophos with the TMB-4 reactivator of pH of 7.5 and 38 degrees not only fails to result in decomposition of the poison, but on the contrary, tends to speed up the progressive accretion of the inhibitory properties of this organophosphorus compound. The author considers the data obtained as one of the proofs pointing to the formation during direct interaction of TMB-4 with chlorophos or the product of its transformation of a stable complex appearing to be a powerful anticholinesterase agent.

Cholinesterase Inhibitors↗
PubMed1986

The effect of altering the external Ca++ concentration and TMB-8 on noradrenaline-induced contractions of the rat anococcygeus muscle.

The effect of varying external Ca++ concentration and 8(-N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) on noradrenaline-induced contractions of the rat anococcygeus muscle was studied. The contractile response to NA was not significantly altered when the external Ca++ concentration was reduced by 50% and 75%. The contractions were however reduced to approximately 10% of the control on complete withdrawal of extracellular Ca++. The loss of contractile response to NA in O-Ca++ was time-dependent and the rate was not modified by EGTA (0.1 mM). There was a rapid restoration of NA responses on re-introducing Ca++. NA-induced contractions were concentration-dependently antagonized by TMB-8, an intracellular Ca++ antagonist. The results are interpreted to suggest that alpha 1-adrenoceptor activation in the rat anococcygeus muscle releases Ca++ from intracellular stores.

Animals↗
PubMed1980

[Thrombocyte counts in TMB (Tryon Maze Brights) and TMD (Tryon Maze Dulls) rats following warfarin (author's transl)].

A dosage of 3 mg Warfarin/kg body weight causes a highly significant increase in the number of platelets both in TMB (Tryon maze brights) and TMD (Tryon maze dulls) rats. Different "intelligence levels" show no effect on this increase. In condition of rest the number of platelets is significantly higher in TMD rats than in TMB animals. With regard to a hypothetical relationship between the number of platelets and the amount of circulating and urinary catecholamines the results suggest a similar relationship in conditions of rest as can be shown in emotive (e+) and nonemotive (e--) Wistar rats as well as a varying reaction to stress -- different levels of "intelligence" and anxiety provided.

Animals↗
PubMed1993

TMB-8 and thapsigargin modulate purine release from dissociated primary cultures of rat brain astrocytes.

In our previous studies, the evoked purine outflow from rat brain cultured astrocytes was reported to be Na+ independent and K+ and [Ca2+]e partially dependent. Thus, the eventual [Ca2+]i influence on purine astrocyte release was investigated in an attempt to better characterize the ionic requirements of this mechanism in cells which serve many complex and still partly unknown functions within the CNS. TMB-8 and Thapsigargin (drugs described as able to inhibit and increase the ion efflux from its internal stores respectively) and BAPTA/AM (able to chelate the cytoplasmic free Ca2+), were used. TMB-8 and BAPTA/AM decreased, whereas Thapsigargin enhanced glial purine outflow. These findings suggest a significant [Ca2+]i dependence of the electrically evoked purine efflux from cultured astrocytes even though further investigations using fluorescent probes are needed.

Adenosine↗
PubMed1982

Connections between the frontal eye field and pretectum in the monkey: an anterograde/retrograde study using HRP gel and TMB neurohistochemistry.

Horseradish peroxidase (HRP) gel implants in the frontal eye field (FEF) of macaque monkeys, processed with tetramethylbenzidine (TMB) neurohistochemistry and studied with darkfield microscopy, demonstrated bidirectional HRP labeling of the afferents and efferents of this cortical area. It was evident that among the entire scope of its inputs, the FEF received a prominent afferent projection from the nucleus of the optic tract (NOT, nucleus limitans) and the suprageniculate nucleus, and projected to a medial subdivision of NOT, sublentiform nucleus, nucleus of the pretectal area, nucleus of the posterior commissure, and the rostral periaqueductal gray. The direct afferent projections to FEF from NOT could provide a route for visual input to reach FEF via the pretectum without first going to the visual cortex. The efferents probably represent the pathway through which FEF influences pupillary dynamics known to accompany, or occur independently of, eye movements.

Animals↗
PubMed1985

An HRP-TMB ultrastructural study of rubral afferents in the rat.

The projections from the deep cerebellar nuclei and the sensorimotor cortex to the red nucleus were studied in the rat using anterograde transport of horseradish peroxidase conjugated with wheat germ agglutinin (HRP-WGA). The anterogradely transported HRP-WGA was visualized ultrastructurally by using a modification of the tetramethylbenzidine (TMB) histochemical technique of Carson and Mesulam ('82). Following injection of HRP-WGA into the sensorimotor cortex, ultrastructural examination of anterograde labeling in the ipsilateral red nucleus revealed labeled synaptic terminals located on small-diameter dendrites of the parvocellular region. These terminals made asymmetrical contacts and contained round vesicles. HRP-WGA placement in the nucleus lateralis resulted in anterograde labeling of synaptic terminals which made asymmetrical contacts with small- to medium-sized dendrites of the parvocellular red nucleus. Similar placements in the nucleus interpositus gave rise to anterograde labeling of synaptic terminals which made asymmetrical contacts with somata and proximal dendrites of magnocellular neurons. In addition, retrograde labeling of magnocellular neurons was also observed following HRP-WGA placements in the nucleus interpositus. Anterogradely labeled interpositorubral synaptic terminals were located on retrogradely labeled rubrocerebellar neurons. The rat red nucleus thus receives topographically organized afferents which are characterized by their specificity in location at the cellular level.

Afferent Pathways↗
PubMed1985

Diacylglycerol downregulates junctional membrane permeability. TMB-8 blocks this effect.

We tested the question whether junctional cell-to-cell communication is regulated by the diacylglycerol branch of the phosphoinositide transmembrane signal pathway. Cultured epithelial rat liver cells were treated with the synthetic diacylglycerol 1-oleoyl-2-acetyl glycerol, while their junctional permeability was probed with the microinjected 443-dalton fluorescent tracer Lucifer Yellow. The treatment reduced junctional permeability (without affecting Lucifer permeability of nonjunctional cell membrane). The effect was dose dependent, with a threshold of about 25 micrograms diacylglycerol/ml in sparse cultures and about 50 micrograms/ml in confluent cultures. The reduction of junctional permeability began within 3 min of diacylglycerol application, peaked within 20 min, and reversed spontaneously within 90 min. The phorbol ester TPA mimicked the diacylglycerol effect, but the (spontaneous) reversal was slower. We propose that cell-to-cell communication is under dual physiological control: an up-regulatory one, as exerted by the cyclic AMP signal route (Loewenstein, W.R., 1985, Biochem. Soc. Symp. London, 50: 43-58), and a downregulatory one, by the diacylglycerol signal route. TMB-8 (54-70 microM)--a blocker of intracellular Ca2+ mobilization--impeded the diacylglycerol action on junctional permeability. It prevented the effect of low diacylglycerol doses completely and it markedly reduced the effect of high doses. (It also counteracted the effect of TPA.) Ca2+ thus emerges as a possible candidate for a role in the junctional downregulation by the diacylglycerol signal route. We tentatively advance two models. In one, leaning closely on the Calcium Hypothesis of cell-to-cell channel regulation (Loewenstein, W.R., 1966, Ann. N.Y. Acad. Sci. 137:441-472), Ca2+ mediates the action of the route on the channel. In the other, Ca2+ acts farther removed from the channel, on protein kinase C. Calmidazolium (5-10 microM)--an inhibitor of calmodulinactivated proteins--did not prevent the diacylglycerol-induced reduction of junctional permeability. Nor did sodium orthovanadate (25 or 50 microM)--an inhibitor of tyrosyl phosphatase--prevent the reversal of diacylglycerol-induced (or TPA-induced) reduction of junctional permeability.

Animals↗
PubMed1990

Influence of TMB-8 and calmidazolium on phorbol ester promoted histamine release from isolated rat mast cells.

The effects of TMB-8 and calmidazolium were investigated on mast cell responses believed to be mediated by protein kinase C, i.e. histamine release induced by TPA (tetradecanoyl-phorbol-acetate) in combination with sub-threshold concentrations of the ionophore A23187 and with antigen. Inhibition with both drugs was found in the same concentration range as observed earlier and could be counteracted by glucose, indicating an impaired oxidative energy production. Hence, the test drugs do not reveal protein kinase C selectivity.

Animals↗
PubMed1985

Desaggregation of PAF-acether-aggregated platelets by verapamil and TMB-8 with reversal of phosphorylation of 40K and 20K proteins.

Verapamil at a concentration of 10(-4) M inhibited aggregation and release of [3H]5HT induced by platelet activating factor (PAF-acether, PAF) in rabbit platelet-rich plasma and washed labelled platelets. When added to platelets previously aggregated by PAF-acether verapamil caused them to desaggregate at doses as low as 2 X 10(-6) M. The desaggregated platelets were refractory to further additions of similar doses of PAF-acether but could further be aggregated by A23187. Simultaneous to full aggregation PAF-acether caused phosphorylation of 40K and 20K proteins in particular. Addition of verapamil at the concentration of 2 X 10(-6) M to platelets already aggregated by PAF-acether resulted in dephosphorylation of 40K protein and reduction of phosphorylation of 20K protein to the level of control parallel to desaggregation. TMB-8 (10(-3) M) also caused desaggregation and reversal of phosphorylation of 40K and 20K proteins. When A23187 was added to verapamil desaggregated platelets, 40K and 20K proteins were rephosphorylated. The extracellular calcium antagonists EGTA or La3+, when added to PAF-acether aggregated platelets, did not abolish the phosphorylation of 40K and 20K proteins. The experiments suggest that inhibition of intracellular calcium-dependent reactions is involved in the desaggregatory action of verapamil.

Animals↗
PubMed1984

Inhibition of cyclic GMP formation and aggregation in Dictyostelium by the intracellular Ca2+ antagonist TMB-8.

Aggregation in Dictyostelium discoideum was shown in previous studies employing EGTA to require Ca2+, but the intra- or extracellular site of action of this ion and its role in chemotaxis were not determined [1]. In this investigation we show that the intracellular Ca2+ immobilising agent TMB-8 does not affect binding of the signalling nucleotide, cAMP, to the cell surface receptors but abolishes the rapid accumulation of intracellular cGMP and subsequent chemotactic aggregation. We infer that movement of Ca2+ from membrane-bound stores is triggered by binding of cAMP to the cell-surface receptor and that this plays a primary role in stimulating cGMP formation and chemotaxis.

Journal Article↗