Catabolism of aromatic compounds by micro-organisms.
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Aerobiosis↗
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Modification of cements containing vanillate or syringate esters.
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Chemical Phenomena↗
Synergistic effect of bismuth subgallate and borneol, the major components of Sulbogin, on the healing of skin wound.
Most skin lesions heal delay and even heal efficiently within 1-2 weeks, the healed tissue is neither aesthetically nor functionally perfect. Therefore, facilitating skin healing rate and controlling healed skin quality are major aims of drug treatment for a wound event. Bismuth subgallate (BS) and Borneol (BO) are the two components of Sulbogin, a new Vaseline-based wound healing ointment, one for treating skin wounds. Although BO has antibiotic function, while BS is widely used clinically, neither has been used specifically for wound healing. The experiment described here aimed to study the effect of BS and BO on the healing of skin wounds. This study also compared the effects of BS and BO with Flamazine cream, which is currently the most popular drug for wound healing in hospitals. Full-thickness wounds (3 cm x 3 cm x 0.2 cm) were created on the back of adult male Sprague-Dawley rats. BS, BO, BS+BO, and Flamazine were then evenly applied to cheesecloth and placed over the lesion areas. The drug patches were replaced every 2-3 days until the wound areas were completely covered by epidermis in any kinds of drug treatment. The combined BS and BO treatment had the best effect on healing by decreasing lesion area, while increasing granulation tissue formation, re-epithelialization, eating behavior and reconstitution of skin appendages. This investigation showed that BS and BO have a synergistic effect on the skin wound restoration.
Administration, Topical↗
Coordination of aluminium with purpurogallin and theaflavin digallate.
Polyphenols are antioxidants, which are known to influence bioavailability of metals in the body. The theaflavins of black tea are important members of this family, which have been sparsely investigated. The complexation of aluminium with purpurogallin (2,3,4,6-tetrahydroxy-5H-benzocyclohepten-5-one) has been investigated using nuclear magnetic resonance (NMR) spectroscopy, liquid chromatography-mass spectroscopy (LC-MS) and Fourier transform infrared (FT-IR) spectroscopy. 1H NMR was used to determine the coordination site of the aluminium ion and LC-MS to determine the stoichiometry and molecular weight of the major complex formed in solution. FT-IR spectral comparisons were used to corroborate the proposed chelating moiety. The complexation of aluminium with the high-molecular-weight, tea polyphenol theaflavin digallate was also investigated using 1H NMR and heteronuclear multiple quantum coherence experiments. Structures of the major aluminium purpurogallin and aluminium theaflavin digallate complexes are proposed.
Aluminum↗
Influence of probes for calcium-calmodulin and protein kinase C signalling on the plasma membrane Ca2+-ATPase activity of rat synaptosomes and leukocyte membranes.
The influence of selected inhibitors of calcium signalling on the plasma membrane Ca2+-ATPase activity of rat synaptosomes and peritoneal leukocyte membranes was studied. The calmodulin inhibitor calmidazolium was an efficient inhibitor (50%) of the synaptosomal Ca2+-ATPase activity in a manner competitive with phosphatidylserine. The inhibition by CGS 9343B (30%) was not counteracted by phosphatidylserine. The intracellular calcium antagonist TMB-8 and the protein kinase inhibitor staurosporine and the derivatives CGP 41251 and CGP 42700 hardly affected the synaptosomal Ca2+-ATPase activity. The flavonoid quercetin was a more effective inhibitor of the ATPase activity of synaptosomal than of leukocyte membranes. Phloretin, at relatively high concentrations, caused only a modest inhibition of synaptosomes. The protein kinase C inhibitor sphingosine was a weak inhibitor of the synaptosomal but an effective inhibitor of the leukocyte membrane Ca2+-ATPase activity. The antineoplastic ether phospholipids BM 41.440 (ilmofosine) and ET-18-OCH3 (edelfosine) effectively inhibited the leukocyte membranes whereas the ATPase activity of synaptosomes was significantly increased by 20 microM and slightly inhibited by higher concentrations of these agents. The analogue hexadecylphosphocholine (miltefosine) did not affect the ATPase activity of the synaptosomes and only inhibited that of the leukocyte membranes at concentrations above 20 microM. These results show that several test substances of current interest affect the activity of the plasma membrane Ca2+-ATPase. The effects depend on the origin of the membranes. The investigation does not permit a distinction between direct effects on the enzyme and an interference with its membrane environment although the latter is indicated for the ether phospholipids.
Animals↗
Caffeine decreases intracellular free Mg2+ in isolated adult rat ventricular myocytes.
Caffeine has been extensively used to study intracellular Ca2+ control and contraction-relaxation in cardiomyocytes. The effects of caffeine on intracellular free Mg2+ concentration, [Mg2+]i, were studied in isolated adult rat ventricular myocytes by fluorescent techniques using mag-fura-2. Basal [Mg2+]i was 0.62 +/- 0.02 mM, n = 54, in quiescent cells and 0.73 +/- 0.02 mM, n = 23, in electrically-stimulated adult rat ventricular myocytes. Caffeine, 20 mM, significantly decreased [Mg2+] in both quiescent (-0.17 +/- 0.01 mM) and electrically-stimulated (-0.16 +/- 0.01 mM) adult ventricular myocytes. Ryanodine, a blocker for Ca(2+)-release channels of the sarcoplasmic reticulum, did not have any effect on basal [Mg2+]i, 0.67 +/- 0.02 mM nor on caffeine-induced reduction in [Mg2+]i, -0.16 +/- 0.01 mM in quiescent cardiomyocytes or electrically-stimulated cells; 0.74 +/- 0.03 mM and -0.11 +/- 0.03 mM, respectively. Ruthenium red, an inhibitor of mitochondrial Ca2+ uptake, also failed to alter basal [Mg2+]i, or caffeine-induced reduction in [Mg2+], in either quiescent or electrically-stimulated cells. The effects of caffeine on [Mg2+]i, may be important in considering the use of this drug to study contraction/function studies in heart cells.
Animals↗
Mastoparan induces an increase in cytosolic calcium ion concentration and subsequent activation of protein kinases in tobacco suspension culture cells.
Mastoparan induced a transient elevation of cytosolic free Ca2+ concentration ([Ca2+]cyt) in tobacco suspension culture cells. The mastoparan-induced [Ca2+]cyt elevation was inhibited by 8-(N,N-diethylamino)-octyl 3,4,5-trimethoxybenzoate-HCl and neomycin but not by depletion of extracellular Ca2+, suggesting that the elevation was the result of Ca2+ release from the intracellular stores caused by stimulation of phosphoinositide turnover. Hydrogen peroxide which has been shown to induce an oxidative burst in soybean cells by mastoparan treatment [L. Legendre, P.F. Heinstein, P.S. Low, Evidence for participation of GTP-binding proteins in elicitation of the rapid oxidative burst in cultured soybean cells, J. Biol. Chem., 267 (1992) 20140-20147], also induced a transient [Ca2+]cyt elevation in the tobacco cells. However, mastoparan did not induce an oxidative burst in the tobacco cells. Activation of a 50, a 75 and a 80 kDa protein kinases after the mastoparan-induced [Ca2+]cyt elevation was shown by an in-gel protein kinase assay. This activation was inhibited by neomycin, suggesting that the [Ca2+]cyt elevation is necessary for the mastoparan-induced activation of the protein kinases. The activation was inhibited also by pretreatment with staurosporine and was sustained by pretreatment with calyculin A, suggesting that the protein kinase activity is regulated by protein phosphorylation/dephosphorylation. The present report shows that mastoparan induces an increase in [Ca2+]cyt without oxidative burst and subsequent activation of protein kinases in tobacco cells.
Aequorin↗
A novel colorimetric method to quantify tannase activity of viable bacteria.
A novel colorimetric method to quantify tannase activity of viable tannase-producing bacterial strains was developed through application of a visual reading method that was to detect the activity qualitatively. The novel method was sensitive enough to quantify the marginal tannase activity of strains that could not be otherwise measured by conventional spectrophotometric or colorimetric methods.
Bacteria↗
Antifungal activity of octyl gallate.
Antifungal activities of propyl (C3), octyl (C8) and dodecyl (C12) gallates (3,4,5-trihydroxybenzoate) were tested against Saccharomyces cerevisiae ATCC7754 and Zygosaccharomyces bailii ATCC 60483. Octyl gallate was found to be the only active compound with the minimum fungicidal concentration of 25 microg/ml (89 microM) against S. cerevisiae and of 50 microg/ml (177 microM) against Z. bailii, respectively. The inactivation study showed that octyl gallate was fungicidal against both S. cerevisiae and Z. bailii at any stage of growth. These fungicidal activities were not influenced by pH values. Octyl gallate at 100 microg /ml reduced plasma membrane fluidity to 48% of control. On the other hand, dodecyl gallate at the same concentration reduced it to 76% of control. Only octyl gallate inhibited glucose-induced medium acidification, indicating direct or indirect inhibition of plasma membrane H +-ATPase. The primary fungicidal activity of octyl gallate comes from its ability to act as a nonionic surface-active agent (surfactant), though it can not be inferred that membrane damage, such as a decrease in the membrane fluidity, is the only cause of the lethal effect.
Antifungal Agents↗
Safety of propyl gallate in topical products.
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Administration, Topical↗
Mechanism of thymocyte apoptosis induced by serum of tumor-bearing host: the molecular events involved and their inhibition by thymosin alpha-1.
The observations presented in this paper indicate that serum of Dalton's lymphoma (DL) bearing mice contained certain soluble factor(s) that augmented the induction of apoptosis in thymocytes in a time- and dose-dependent manner. DL-ascitic fluid and DL-conditioned medium could also induce apoptosis of thymocytes in vitro, though the magnitude of the same was consistently lower than that induced by serum of DL-bearing mice. It was observed that the interaction of FasL and TNFalpha with their respective receptors could trigger apoptosis in thymocytes. Elucidation of the signal transduction mechanism revealed involvement of protein tyrosine kinase, protein kinase C and ser/thr phosphatases with concomitant increase in the level of protein products of apoptosis associated genes p53, bax, bad, fas and fas ligand and cleavage of N-terminal 23 kDa fragment of Bcl-2 that exhibited Bax-like death effector properties. Further, we report, for the first time, the ability of thymosin alpha-1, an immunopotentiating thymic hormone, to antagonize apoptosis in thymocytes induced by factors present in serum of DL-bearing mice. The underlying mechanism of tumor serum induced apoptosis inhibition by thymosin alpha-1 was also analyzed. The signal transduction cascade evoked by thymosin alpha-1 involves activation of protein kinase C with a decrease in the level of protein products of proapoptotic genes like bax and bad and increase in the protein products of bcl-2 gene.
Animals↗
Nimodipine and TMB-8 potentiate the AMPA-induced lesion in the basal ganglia.
Acute injection of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) into the rat globus pallidus leads to calcium precipitation, neuronal death and gliosis. In order to determine whether L-type calcium channels and/or release of Ca(2+) from intracellular stores contribute to the effects of AMPA, nimodipine and 8-(N,N-diethylamino) octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8) were administered in combination with AMPA. Nimodipine, but not TMB-8, tended to exacerbate the calcification process initiated by AMPA; the AMPA/nimodipine/TMB-8 combination produced much more calcium deposition than AMPA (+62%, P<0.05). AMPA alone induced a slight but not significant astroglial reaction. Nimodipine slightly enhanced the astroglial reaction triggered by AMPA, whereas TMB-8 doubled it (P<0.001 versus AMPA). These data suggest that blockade of L-type calcium channels by nimodipine enhances calcium imbalance triggered by AMPA, and the calcium release from the endoplasmic reticulum does not participate in the AMPA-induced calcification.
Animals↗
Enteral absorption and biotransformation of the food additive octyl gallate in the rat.
Following oral administration of 14C-labelled octyl gallate in a single dose of 15 mg/kg to female rats, only 20-30% of the radioactivity administered was detected in the tissues, while 60-80% of the dose was found in the contents of the gastro-intestinal tract up to 12 hr after administration. Isotope dilution analysis demonstrated the presence of the unchanged ester in the tissues. In the liver, the highest concentration of the ester demonstrated was 1.6 micrograms/g. in a rat killed 10 min after treatment. In the 24 hr following ip administration of labelled octyl gallate, about 91% of the administered radioactivity was recovered. Most of this was in the form of metabolites, only 9% being accounted for as unchanged ester.
Animals↗
Novel, thapsigargin-insensitive intracellular Ca(2+) stores control growth hormone release from goldfish pituitary cells.
The relative contribution of intracellular Ca(2+) stores to basal and agonist-stimulated hormone release in pituitary cells is still not well understood, especially in non-mammalian vertebrates. Using ratiometric Ca(2+) imaging of single identified goldfish somatotropes, along with time-resolved measurements of growth hormone (GH) secretion, we investigated the Ca(2+)-dependent signal transduction of two endogenous regulators of GH release from the goldfish pituitary. Two gonadotropin-releasing hormones (sGnRH and cGnRH-II) initiated GH release in nominally Ca(2+) free conditions. GnRH-evoked GH release was additive to KCl-stimulated GH responses. Ca(2+) signals and GH release elicited by both GnRHs were abolished by pretreatment with TMB-8, which blocks the release of Ca(2+) from intracellular stores. GnRH-stimulated GH secretion is mediated by caffeine-sensitive intracellular Ca(2+) stores that are functionally independent from those sensitive to thapsigargin and other inhibitors of SERCA-type Ca(2+)/ATPases. The caffeine/TMB-8-sensitive Ca(2+) stores are also involved in spontaneous Ca(2+) signalling and the maintenance of prolonged GH release.
Animals↗
Do ryanodine receptors regulate transmitter release at the neuromuscular junction of rat?
It has been suggested that calcium that is stored in nerve terminals can be released via activation of ryanodine receptors and this source of calcium could serve to modulate evoked transmitter release. Calcium influx via voltage dependent calcium channels could lead to calcium induced calcium release via ryanodine receptors in neuronal tissue. This additional source of calcium could contribute to the total calcium that is available for transmitter release or it could result in having a negative feedback action on calcium influx and transmitter release. We examined the effect of blocking and activating the ryanodine receptors on quantal transmitter release at the rat neuromuscular junction. Intracellular recording techniques were used to monitor end-plate potentials and miniature end-plate potentials. The data supports the view that intracellular calcium released via ryanodine receptors suppresses calcium influx leading to depressed quantal release.
Animals↗
Defibrotide augments the anticandidial activity of NK cells.
1. The mechanism of action of Defibrotide, a fibrinolytic agent on Natural Killer (NK) cell cytotoxicity, was investigated through verapamil, TMB-8 cells and pertussis toxin. 2. Defibrotide increased the activity against Candida albicans cells (anticandidial activity), and it is determined that the calcium channels have a role in this effect. 3. Blockage of calcium channels reduced the anticandidial effect by 39.2%. Pertussis toxin led to a 10.7% inhibition, whereas the application of TMB-8 resulted in the stimulation of anticandidial activity. 4. It is concluded that defibrotide is a potent activator of NK cells.
Animals↗
An in vitro study of theaflavins extracted from black tea to neutralize bovine rotavirus and bovine coronavirus infections.
Crude theaflavin was extracted from black tea and then fractionated by HPLC into five components (initial peaks (IP), TF1, TF2A, TF2B, and TF3). The crude extract and the various fractions of theaflavin were collected and tested, individually and in combination, for antirotaviral activity. The mean effective concentration (EC50) was calculated and compared. Activity varied from the most active being the uncharacterized theaflavin-like initial peaks (IP) with an EC50 of 0.125 microgram/ml to the least active being theaflavin-3 monogallate (TF2A) with an EC50 of 251.39 micrograms/ ml. The combination of TF1 + TF2A + TF2B + TF3 was more active than the sum of the activities of these four fractions individually, indicating synergism among the peaks. Only the crude extract was assayed for activity against coronavirus; the EC50 was 34.7 micrograms/ml.
Animals↗
[Probable hepatoxicity from epigallocatecol gallate used for phytotherapy].
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Anti-Obesity Agents↗