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PubMed1991

Calcium-dependent inhibition of renin secretion: TMB-8 is a non-specific antagonist.

Intracellular Ca (Cai) is an inhibitory second messenger in renin secretion, and it has been hypothesized that some first messengers--especially angiotensin II [A-II] and antidiuretic hormone [ADH], and possibly A1-adenosine receptor antagonists as well--increase Cai and thereby inhibit renin secretion by causing the release or mobilization of Ca from intracellular sites of sequestration. The present experiments were designed to test this hypothesis, by using 3,4,5-trimethoxybenzoic acid 8-(diethylamino)-octyl ester (TMB-8), a putative antagonist of Ca release from intracellular sequestration sites. The rat renal cortical slices preparation was used. Basal renin secretory rate was unaffected by 1 and 10 microM TMB-8, but more than doubled in response to 100 microM TMB-8. Basal renin secretory rate was inhibited by A-II (1 microM), by ADH (200 units/1), by an A1-adenosine receptor agonist (N6-cyclohexyladenosine, or CHA; 0.5 microM), and by an alpha-adrenergic agonist (methoxamine; 10 microM). Only the inhibitory effect of methoxamine was blocked by 1 and 10 microM TMB-8, but these concentrations had no effect on basal secretory rate. At 100 microM, TMB-8 blocked the inhibitory effects of ADH as well as of methoxamine, but failed to block the inhibitory effects of CHA and A-II. However, these observations cannot be taken as evidence that methoxamine and ADH, but not CHA and A-II, inhibit renin secretion by a mechanism involving release of Ca from intracellular sequestration sites, because 100 microM TMB-8 clearly had non-specific effects. Among them, it completely blocked the inhibitory effect of K-depolarization on renin secretion. Collectively, at least three separate actions of TMB-8 must be invoked to explain the present results. Likely candidates are an Na-channel blocking effect and a Ca channel blocking effect in addition to antagonism of the release of Cai.

Adenosine↗
PubMed1987

Lipoxygenase inhibitors reduce insulin secretion without impairing calcium mobilization.

Inhibitors of pancreatic islet lipoxygenase (LPX) impair nutrient-induced insulin (I) release. To define the mechanism of action of these inhibitors, studies were carried out at subthreshold glucose concentrations (0-1.7 mM) in order to minimize any effects of LPX blockade on the potentiating effect of extracellular fuels. Barium chloride (Ba2+; 2 mM) increased 45Ca2+ release from prelabeled islets in Ca2+-free medium and, thus, is a model for the mobilization of intracellular Ca2+ stores. Inhibition of LPX (using nordihydroguaiaretic acid, BW755c [3-amino-1-(trifluomethyl-phenyl)2-pyrazoline] or butylated hydroxytoluene) did not have any consistent effect on the influx of Ba2+ (as assessed by 133Ba uptake) or on the consequent release of cellular Ca2+ stores; however, each LPX inhibitor vitiated Ba2+-induced I release. The LPX inhibitors were not merely acting as nonspecific antioxidants, since two inhibitors which do not act by scavenging hydroperoxides (5,8,11,14-eicosatetraynoic acid and 15-hydroxy-5,8,11,13-eicosatetraenoic acid) also impeded the effect of Ba2+ on I secretion; furthermore, a series of hydroxyl radical scavengers, reducing agents, or agents that block nonenzymatic and/or NADPH-activated lipid peroxidation did not inhibit I secretion. LPX inhibitors also blocked the residual I response to 16.7 mM glucose in Ca2+-free medium. Additionally, they reduced secretion induced by 46 mM K+ or 1 mM isobutylmethylxanthine (provided in the presence of extracellular Ca2+), without inhibiting K+- or isobutylmethylxanthine-induced Ca2+ fluxes. Stimuli sensitive to LPX blockade were also antagonized by antimycin A (an inhibitor of energy flux) or TMB-8 [8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride; which appeared to deplete critical intracellular Ca2+ stores]. In contrast, the effects of exogenous phospholipase C (and several other Ca2+-dependent membrane-active agonists) were resistant to the LPX inhibitors, TMB-8, and antimycin A; thus, LPX inhibitors are not nonspecific global poisons of all Ca2+-dependent exocytotic hormone release. We conclude that LPX (or a very similar enzyme) may modulate the effects (or redistribution) of an ATP-dependent trigger pool of Ca2+ at a site distal to and independent of its mobilization by primary islet agonists. LPX inhibitors also blocked secretion induced by 12-O-tetradecanoyl-phorbol-13-acetate; this effect may reflect an effect of LPX on the activation of protein kinase C or a modulation of its synergism with the same trigger Ca2+ pool(s).

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1989

Characterization of a novel inhibitor of human DNA polymerases: 3,4,5-tri-O-galloylquinic acid.

Various galloyl derivatives of quinic acid were found to be inhibitors of human DNA polymerases. Among them, 3,4,5-tri-O-galloylquinic acid (TGQA) was the most potent inhibitor of DNA polymerase alpha. Under identical conditions, this compound was 60-fold more potent than aphidicolin as an inhibitor of DNA polymerase alpha. The inhibition of DNA polymerase alpha by this compound was not competitive with either the template or any of the deoxynucleoside triphosphates with a Ki of 0.28 microM. Under similar reaction conditions, DNA polymerases beta and gamma were much less sensitive to the effects of these compounds and, in contrast to the effect seen with DNA polymerase alpha, the inhibition of DNA polymerases beta and gamma by TGQA was competitive with respect to the template with Ki values of 44.4 and 7.5 microM respectively. The potency of these compounds against DNA polymerase gamma varied according to the assay conditions used. The inhibition of DNA polymerase gamma by TGQA could be increased substantially by using MnCl2 in place of MgCl2 and by including 50 mM potassium phosphate, pH 7.5, in the assay mixture. DNA polymerase beta was also more sensitive to TGQA when measured with MnCl2. However, potassium phosphate had little, if any, effect on the inhibition by TGQA of either DNA polymerase alpha or beta. DNA polymerase alpha was less sensitive to TGQA when assayed with MnCl2. TGQA was not a potent inhibitor of human KB cell growth in culture, which could be due to its degradation or poor uptake. Nevertheless, this compound could serve as a model for developing antitumor drugs targeted at DNA polymerases.

Cell Line↗
PubMed1997

Effects of erythropoietin on endothelin-1 synthesis and the cellular calcium messenger system in vascular endothelial cells.

A rise in blood pressure is the main side effect of erythropoietin (EPO) treatment in patients with renal anemia. The mechanisms, however, by which EPO may cause hypertension are still unclear. We therefore investigated the effects of EPO on endothelin (ET) synthesis and cytosolic free calcium concentration ([Ca2+]i) in vascular endothelial cells. Porcine endothelial cells were isolated from thoracic aorta, pulmonary artery, and vena cava. Studies were performed with cells of the first subculture. ET concentrations were measured radioimmunologically. Changes in [Ca2+]i were determined with the fluorescent probe fura-2. Cytotoxicity was assessed by sodium 3'-[1-(phenyl-amino-carbonyl)-3,4-tetrazolium]-bis(4-methoxy-6-nitro)ben zene sulfonic acid hydrate (XTT) assay. ET synthesis was similar in cells of different vascular origins and was time-dependent, reaching approximately 2 pmol ET/mg protein within 12 h of incubation. EPO (12 to 200 U/mL) stimulated ET release time- and dose-dependently by up to 83.2% (P < .01) within 12 h in the absence of fetal calf serum and heparin. EPO induced an immediate significant rise in [Ca2+]i from 58 +/- 12 nmol/L to 495 +/- 85 nmol/L (P < .01) with a subsequent slow return to 257 +/- 3 nmol/L. During 2 h of incubation, the Ca-ionophore A 23187 (10(-8) mol/L) moderately but significantly stimulated endothelial ET synthesis. However, the Ca-channel blocker verapamil, the intracellular Ca-release blocker TMB-8, and nickel, an unspecific calcium channel blocker, had no consistent effects on [Ca2+]i or ET synthesis. The protein kinase C inhibitor H-7 stimulated basal [Ca2+]i and cellular ET synthesis. The tyrosine kinase inhibitor genistein suppressed the EPO-induced rise in [Ca2+]i and cellular ET synthesis. From these data we conclude that EPO may stimulate ET synthesis in vascular endothelial cells by activation of an EPO-receptor and via intracellular signalling mechanisms that comprise tyrosine kinase activation and a rise in [Ca2+]i. Therefore, the systemic hypertensive effects of EPO may be due at least in part to local stimulation of vascular endothelial ET synthesis via calcium mobilization.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1999

Effect of 3,4,5-trimethoxybenzoic acid 8-diethylamino-octyl ester (TMB-8) on neuronal calcium homeostasis, protein synthesis, and energy metabolism.

It has been suggested recently that disturbances of endoplasmic reticulum calcium homeostasis plays a major role in ischaemic cell injury of the brain. Depletion of endoplasmic reticulum calcium stores induces suppression of the initiation process of protein synthesis, a prominent feature of ischaemic cell damage. The benzoic acid derivative 3,4,5-trimethoxybenzoic acid 8-diethylamino-octyl ester (TMB-8), an established inhibitor of calcium release from endoplasmic reticulum, would be an ideal tool for elucidating the role of endoplasmic reticulum dysfunction in this pathological process. The present investigation was performed to study the effects of TMB-8 on neuronal metabolism (cytoplasmic calcium activity, ATP levels and protein synthesis) using hippocampal slices and primary neuronal cell cultures. In addition, we investigated whether the rise in cytoplasmic calcium activity and the suppression of protein synthesis induced by endoplasmic reticulum calcium pool depletion, is reversed by this agent. Exposure of neurones to TMB-8 (100 microM) induced a small transient increase in cytoplasmic calcium activity ([Ca2+]i), whereas a second dose of TMB-8 (200 microM) produced a marked and sustained rise in [Ca2+]i. The increase in [Ca2+]i evoked by blocking endoplasmic reticulum Ca(2+)-ATPase was only transiently suppressed and then aggravated by TMB-8. The dose-dependent suppression of protein synthesis by TMB-8, observed both in neuronal cultures and hippocampal slices, indicates that TMB-8 has a pathological effect on neuronal metabolism. This inhibition was not reversed after washing-off of the drug. TMB-8 did not reverse the inhibition of protein synthesis evoked by caffeine, which depletes endoplasmic reticulum calcium stores by activating the ryanodine receptor. The results indicate that TMB-8 is not a suitable investigative tool for blocking in neuronal cell cultures the depletion of endoplasmic reticulum calcium stores and the suppression of protein synthesis induced by endoplasmic reticulum calcium pool depletion.

Adenosine Triphosphate↗
PubMed1982

Transfer of radiation-induced spins from deoxyribonucleic and thymidylic acids to propyl gallate.

When calf thymus deoxyribonucleic acid (DNA), propyl gallate (PG) and their five molecular mixtures (with PG content of 1, 2, 5, 10 and 20%) are irradiated with gamma-rays in dry state in vacuum at 296 degrees K, the ESR spectra of all molecular mixtures differ strikingly from those of DNA, but bear a close resemblance to those of PG. The spin yield in the PG contained in these mixtures is two to three orders of magnitude higher than that in the case of PG irradiated separately. Furthermore, on the basis of the relative saturation characteristics of ESR spectra, these molecular mixtures behave more like PG than like DNA. It may be inferred that the radiation-induced spins could be transferred from DNA to PG. With r representing the molar ratio of nucleotides to PG, we have found a good linear correlation between the transfer ratio (TR) and square root of r. One PG molecule could protect at least 68 nucleotides in the duplex DNA chain, and thereby the minimal range of spin transfer is estimated at 115 A. Results obtained from irradiation at 77 degrees K show that PG exerts no protective effect on DNA, so DNA sustains an irreversible damage. It is thought that the spin transfer from DNA to PG is exclusively due to a hydrogen transfer mechanism. We have also demonstrated the transfer of radiation-induced spins from both thermally denatured DNA and TMP to PG. The former process can be ascribed primarily to the hydrogen transfer mechanism, whereas the latter, as in the case of native DNA, exclusively to this mechanism.

Animals↗
PubMed2005

Differentiation of androgen-independent prostate cancer PC-3 cells is associated with increased nuclear factor-kappaB activity.

Recently, we have reported that inosine 5'-monophosphate dehydrogenase inhibitors, such as mycophenolic acid (MPA), induce the differentiation of PC-3 cells, which are derived from a human androgen-independent prostate cancer, into cells with a phenotype resembling maturing prostate secretory cells. Here, we describe such differentiation induced by the histone deacetylase inhibitor tributyrin. The maturation was defined by cytoplasmic vacuole production and induction of CD10, CD46, CD55, GRP78, keratin 17, and zinc-alpha-2-glycoprotein. To identify additional genes associated with tributyrin-induced PC-3 cell differentiation and to gain some insight into the mechanism that underlies this differentiation, we have, by means of microarray analyses, compared tributyrin-induced gene expression patterns with those of MPA, which initiates PC-3 cell differentiation by a dissimilar mode of action. We suggested that genes induced by both tributyrin and MPA would be most likely associated with differentiation rather than with the unique action of each particular inducer. Our results indicated that tributyrin or MPA induced the expression of a large number of common genes, including genes known or assumed to be NF-kappaB dependent. The NF-kappaB dependency of a group of these genes, which included the PC-3 cell differentiation marker keratin 17, was confirmed by using two common NF-kappaB activation inhibitors, Bay11-082 and TMB-8, and p65 subunit of NF-kappaB complex specific small interfering RNA. Taken together, our results implicate both NF-kappaB-dependent and NF-kappaB-independent genes in the processes leading to PC-3 cell differentiation induced by tributyrin and MPA.

Androgens↗
PubMed1998

[Development of antiviral therapeutic agents from traditional medicines].

Traditional medicines contain various metabolites derived from nucleic acid, protein, and lipid metabolism. Some of these specific metabolites may recognize the differences between viral and host metabolism resulting in anti-viral activity; hence traditional medicines may be useful sources for new antiviral agents. Traditional medicines can be cheaply obtained and have been orally administered as hot-water extracts. Therefore, they may be used for the prophylactic and therapeutic treatment of viral infection by drinking them, such as coffee or tea. Here we describe how the antiviral activity of traditional medicines was screened in vitro and how their therapeutic antiviral activities were verified in vivo, to obtain traditional antiviral medicines that can be clinically used. Therefore, we have selected 12 herbal extracts, from more than 250 herbal medicines, that exhibit therapeutic activities against cutaneous herpes simplex virus (HSV) type 1 (HSV-1) infection in mice. Four of the 12 augmented the therapeutic efficacy of acyclovir (ACV) in mice and showed potent anti-HSV activity against infection with ACV-resistant HSV-1 mutants in mice. These herbal extracts selectively inhibited viral DNA synthesis and showed a different mode of anti-HSV-1 action from that of ACV. They were also effective against both recurrent HSV and cytomegalovirus infections, without toxicity. Such prophylactic and therapeutic antiviral activities of the traditional medicines were verified by the purification of major active compounds. We could show new indications of traditional medicines as antiviral agents. Thus, the drinking of the extracts, in a daily tea or coffee, may be used for prophylaxis and therapy of diseases caused by herpes virus infection and improve the quality of life.

Animals↗
PubMed1999

Avoidance of primary post-tonsillectomy hemorrhage in a teaching program.

OBJECTIVE: To determine the incidence of primary post-tonsillectomy hemorrhage in a teaching institution by using a uniform technique, including a 3-minute relaxation of retraction before case termination and the use of bismuth subgallate. DESIGN: Case series. SETTING: Tertiary care academic pediatric center. PATIENTS: A 7-year retrospective study was performed by using the medical records of 1286 children without a bleeding abnormality who underwent tonsillectomy (with or without adenoidectomy). A uniform technique, proposed to reduce hemorrhage, was used for 705 children and was not used for 581 children. RESULTS: No episodes of primary hemorrhage (onset < or = 24 hours after surgery) occurred, and the incidence of delayed hemorrhage (onset >24 hours after surgery) was 1.1% in the study group. The primary hemorrhage rate of the study group was significantly lower (P = .007) than the rate for the reference group (0.0% vs 1.0%), as was the total hemorrhage rate (1.1% vs 4.1%) and the delayed hemorrhage rate (1.1% vs 3.1%). CONCLUSION: A uniform technique including the use of bismuth subgallate and reassessment of the tonsillar fossae after a 3-minute observation period reduces the incidence of primary tonsillar hemorrhage in a teaching institution setting.

Academic Medical Centers↗
PubMed2000

Respiratory difficulty following bismuth subgallate aspiration.

Bismuth subgallate, an agent that initiates clotting via activation of factor XII, has been advocated for use in controlling bleeding during tonsillectomy and adenoidectomy. Direct aspiration of bismuth has produced pulmonary complications in laboratory animals, but no clinical correlation in humans has been previously described. We report 2 cases of bismuth aspiration that resulted in respiratory difficulty after tonsillectomy and adenoidectomy. Neither child's respiratory compromise required airway intubation. This report of pulmonary complications secondary to bismuth aspiration should alert surgeons to the potential for airway problems when using bismuth as a hemostatic agent for tonsillectomy and adenoidectomy.

Adenoidectomy↗
PubMed1989

Adenotonsillectomy. A safe outpatient procedure.

Traditionally, adenotonsillectomy in children and tonsillectomy in adults have been performed as inpatient procedures. Our experience with this procedure as outpatient started in 1975 at the University of Miami-Jackson Memorial Medical Center. From 1975 to 1987, 1428 cases performed in Florida and Cleveland were reviewed to evaluate the safety and efficacy of the technique used. Bismuth subgallate and epinephrine mixture for hemostasis is used without relying on electrocautery, ties, or suture technique to control bleeding. The incidence of immediate and delayed postoperative bleeding in a series of patients was extremely low (four [0.28%] of 1428 cases). Our technique has good hemostatic properties allowing vessels to contract and retract into the muscle of the tonsillar fossae and adenoid bed. Bismuth subgallate activates factor XII (Hageman factor) and, therefore, markedly accelerates the cascade of blood clotting. Outpatient adenotonsillectomy is safe, cost-effective, and minimizes psychologic implications, which may be an important factor, especially in children. Ambulatory adenotonsillectomy has not been well emphasized in the literature.

Adenoidectomy↗
PubMed1996

Light-sensitive response in melanophores of Xenopus laevis: I. Spectral characteristics of melanophore response in isolated tail fin of Xenopus tadpole.

Melanophores in the isolated tail from the amphibian larvae Xenopus laevis, Hyla japonicus, Rana pirica, and Hynobius retardatus aggregated melanin granules in response to light and dispersed them when placed in darkness. The spectral characteristics for the melanin-aggregation response were examined by irradiating the Xenopus tail-fin locally (diameter, 2.1 mm) with monochromatic light (380-1,020 nm). The spectral region of wave length which induced melanosome aggregation depended on the light intensity but was limited to the visible spectrum. At low light intensity (1.59 microW/cm2, delta lambda = 5 nm), the aggregation response occurred in the spectral region between 400 and 600 nm and the maximum response was observed at 500 nm. This range is very close to the absorption spectrum of rhodopsin in the visual rod cell. Hypodermic injection of cGMP into isolated tail-fin induced a marked melanin-dispersion in spite of light-stimuli. When the tail-fin was treated with isobutylmethylxanthine (IBMX; phosophodiesterase inhibitor) in darkness and then was re-exposed to light, the aggregation response was inhibited. The photo-sensitive melanin aggregation was independent of a requirement for Ca2+ ions but melanosome dispersion in darkness was Ca(2+)-dependent. K(+)-rich Hanks' solution, ouabain (inhibitor of Na(+)-K(+)-ATPase) or nonactin (cation ionophore), which induced a change of the membrane potential of melanophores, inhibited the aggregation response when the melanophores were re-exposed to light after a period in darkness. These results suggest that the molecular mechanism of photoreception in melanophores of amphibian tadpoles is similar to that in visual cells.

1-Methyl-3-isobutylxanthine↗
PubMed1998

Selective down-regulation of human papillomavirus transcription by 2-deoxyglucose.

The glycolytic pathway inhibitor 2-deoxyglucose (2-DG) is capable of suppressing the transcription of the human pathogenic papillomavirus type 18 (HPV 18) in cervical carcinoma cells and derived non-tumorigenic somatic cell hybrids at the level of transcription initiation. HPV down-regulation is selective, since other reference genes are not affected or even up-regulated under the same experimental conditions. Moreover, 2-DG appears to restore the normal half-life of the tumor suppressor gene product p53, because the protein is strongly up-regulated after HPV 18 E6/E7 suppression. The observed 2-DG-effect is not cytotoxic and is reversible after refeeding with fresh medium. HPV 18 suppression by 2-DG can be completely abrogated by simultaneous treatment with the intracellular Ca2+ antagonist TMB-8, indicating that Ca2+, a known intracellular "second messenger", is involved in this process. Elevated c-myc and p53 expression appears to be responsible for the time-dependent accumulation of apoptotic cells after prolonged 2-DG treatment. The finding that 2-DG acts selectively against the expression of a human pathogenic papillomavirus strongly suggests that an appropriate level of glycolysis is not only a peculiarity of growing tumors, but even may be an essential prerequisite for the maintenance of virus-specific E6/E7 gene expression. Our results may have substantial implications for the potential therapeutic application of 2-DG or other glucose derivatives in the treatment of precancerous and malignant HPV-associated lesions.

Adenosine Triphosphate↗
PubMed2000

[8-(Diethylamino)octyl-3,4,5-trimethoxybenzoate, HCl], the inhibitor of intracellular calcium mobilization, blocked mitogen-induced T cell proliferation by interfering with the sustained phase of protein kinase C activation.

The physiological role of IP(3)-dependent Ca(2+) release in T cell activation was in question due to the contradictory findings that [8-(Diethylamino)octyl-3,4,5-trimethoxybenzoate, HCl] (TMB-8), an inhibitor of intracellular Ca(2+) mobilization, blocked T cell proliferation, curtailing specifically the level of released Ca(2+) did not affect T cell activation and T cell line lacking IP(3) receptor was defective in IL-2 production in response to TCR/CD3 ligand. In the present study we found that TMB-8 inhibited Concanavalin A (Con A)- but not PMA/Ionomycin-induced T cell proliferation in a reversible and dose-dependent manner. The kinetic study revealed that TMB-8 exerted the inhibitory effect at a very early step of T cell activation. The Ca(2+) ionophore ionomycin augmented instead of overcoming the inhibitory effect of TMB-8, although the same doses of ionomycin alone had no effect on Con A-induced T cell proliferation. PMA the metabolically stable, but not diacylglycerol (DAG) the metabolically labile, activator of protein Kinase C (PKC) completely overcome the antiproliferative effect of TMB-8. A specific DAG lipase inhibitor RHC80267 also overcome the effect of TMB-8. Taken together, these results showed that the process of Ca(2+) release through IP(3) receptor, not the released Ca(2+), is essential for the sustained phase of PKC activation during T cell proliferation.

Animals↗
PubMed1999

Inhibitory effects of Indonesian medicinal plants on the infection of herpes simplex virus type 1.

Water and methanol extracts of 30 traditional medicinal plants, collected in Indonesia, were tested for their anti HSV-1 activity. The extracts of eight plant species showed potent activity on the plaque assay at a concentration of 100 micrograms/mL. The therapeutic efficacy of seven selected plants was demonstrated by using a mouse HSV-1 infection assay, both the methanol extracts of the fruit of Melaleuca leucadendron (Myrtaceae) and the pericarp of Nephelium lappaceum (Sapindaceae) significantly prolonged the development of skin lesions and reduced the mortality.

Animals↗
PubMed2002

Regulation of activation-induced receptor activator of NF-kappaB ligand (RANKL) expression in T cells.

Receptor activator of NF-kappaB ligand (RANKL) is a type II membrane protein of the TNF family and plays a critical role in the regulation of osteoclastogenesis. RANKL expressed on osteoblastic stromal cells has been shown to support osteoclast differentiation originated from hematopoietic precursors. Interestingly, RANKL is also expressed on cells of the immune system including T cells and dendritic cells. We have shown that anti-CD3 could induce RANKL expression in T cell hybridoma A1.1 cells and splenic T cells. RANKL expressed on T cells could effectively induce osteoclast formation from the whole population of murine splenocytes. Furthermore, we have found that the induction of RANKL expression is solely dependent on TCR activation-induced Ca2+ mobilization since its expression can be blocked by cyclosporine A and TMB-8, a Ca2+ mobilization inhibitor. Additionally, treatment of A1.1 cells with ionomycin alone also strongly induces RANKL expression, while phorbol myristate acetate by itself does not. Moreover, although inhibition of c-myc has significant effects on anti-CD3-induced Fas ligand (FasL) expression, we have found that the anti-CD3-induced RANKL expression is independent of c-myc. Surprisingly, in contrast to its inhibitory effect on FasL expression, TGF-beta dramatically increased the expression of anti-CD3-induced RANKL expression. In addition to its potential role in immune responses, RANKL expressed on activated T lymphocytes may provide a mechanism for the communication between the immune and skeletal systems during immune responses and disease states such as rheumatoid arthritis.

Animals↗
PubMedDate not supplied

Chemiluminescence and reactive oxygen scavenging activities of the hydrogen peroxide/gallic acid/lactoperoxidase system.

Photon emission in the hydrogen peroxide/gallic acid/lactoperoxidase system was studied using visible region chemiluminescence. The photon emission intensity showed a pH-dependence curve with a maximum at pH 4.5-5.0. The spectral analysis showed to be at 510 nm and its energy was 61.0 kcal/mol at either pH 4.5 or pH 7.0. In addition, near-infrared spectral analysis at 1270 nm suggested that this photon emission from the hydrogen peroxide/gallic acid/lactoperoxidase system was produced without generation of (1)O(2). The gallic acid/lactoperoxidase system, based on the chemiluminescence system, has superoxide-, hydroxyl radical-scavenging activities and antioxidative activity. These results are strong evidence that the gallic acid/lactoperoxidase system is one of the reactive oxygen scavenging systems.

Animals↗
PubMed2005

Laccase-catalysed iodide oxidation in presence of methyl syringate.

The kinetics of potassium triiodide (KI(3)) formation during fungal laccase action was investigated in presence of methyl syringate (MS). The recombinant forms of Polyporus pinsitus (rPpL), Myceliophthora thermophila (rMtL), Coprinus cinereus (rCcL), and Rhizoctonia solani (rRsL) laccases were used. The triiodide formation rate reached 6.1, 5.5, 6.0, and 2.1 microM/min at saturated rPpL, rCcL, rRsL, and rMtL concentration, respectively, in acetate buffer solution pH 5.5 and in presence of 10 microM of MS and 1 mM of potassium iodide. The triiodide formation rate increased if pH decreased from 6.5 to 4.5. The scheme of laccase-catalysed iodide oxidation includes stadium of MS interaction with oxidized laccase with concomitant production of MS(ox). The reaction of MS(ox) with iodide produced triiodide. The turnover number of MS was 93 and 44 at pH 5.5 for rPpL and rMtL, respectively. The scheme also contained a stadium of reversible reduction of laccase active centre with the mediator explaining the different saturation rate of triiodide production. The fitting kinetic data revealed that the reversibility of the reaction increased for laccases containing lower redox potential of copper type I.

Ascomycota↗