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PubMed2005

Pharmacological profile of 4-(2',4'-difluorobiphenyl-4-yl)-2-methylbutyric acid (deoxoflobufen).

4-(2',4'- Difluorobiphenyl-4-yl)-2-methylbutyric acid (deoxoflobufen, VUFB 19053, CAS 847475-35-8) has been developed as a new omega-biphenyl-alkanoic acid and studied in comparison with the racemic form of 4-(2',4'-difluorobiphenyl-4-yl)-2-methyl-4-oxobutanoic acid (flobufen, CAS 112344-52-2). The compounds were tested in a series of models including acute inflammation induced by carrageenan, adjuvant arthritis, in vitro inhibition of the leuktotriene B4 (LTB4) production, reaction of the graft versus the host (GVHR), production of specific antibodies against ovalbumin, peritoneal exudate formation induced by thioglycollate and phagocytosis of thioglycollate-stimulated mouse peritoneal macrophages. Deoxoflobufen exhibited strong anti-inflammatory, antiarthritic and immunomodulatory effects in most of the performed tests. Anti-inflammatory and antiarthritic effects are fully comparable with those of flobufen, however, the compound is less toxic and has apparently stronger immunomodulating effects.

Animals↗
PubMed1995

Formation of second messenger diradylglycerol in murine peritoneal macrophages is altered after in vivo (n-3) polyunsaturated fatty acid supplementation.

The consequences of macrophage membrane incorporation of (n-3) polyunsaturated fatty acids (PUFA) on diradylglycerol (DG) formation and phospholipase-mediated signal transduction in vivo remain largely unknown. Three-to four-week-old C57BL/6 mice were randomly assigned to diets in which the 10% lipid component of the purified diet was either corn oil ethyl ester (control) or (n-3) ethyl ester [(n-3) PUFA-enriched]. After 4 wk, thioglycollate-elicited peritoneal macrophages were harvested and assayed for (1) total DG mass, (2) DG molecular species fraction analyses by argentation TLC and (3) separation of phospholipid classes and analyses of their molecular species fractions. We found that basal DG mass and the increase in DG mass after stimulation with platelet-activating factor or phorbol myristate acetate were similar in cells from control and (n-3) PUFA-enriched diet groups, whereas ionomycin-stimulated DG formation was less in the cells from the (n-3) PUFA-enriched diet group. Analyses of DG molecular species fractions showed that the proportions of species with five and six double bonds were markedly greater in the (n-3) PUFA-enriched diet group macrophages compared with those of the control diet group. The molecular species fractions of all phospholipid classes including phosphatidylinositol showed substantial incorporation of (n-3) PUFA. These results demonstrate that dietary enrichment with (n-3) PUFA induces marked changes in DG metabolism in murine peritoneal macrophages. These changes may contribute to the mechanisms of antiinflammatory, antithrombotic and antineoplastic actions associated with dietary (n-3) PUFA supplementation.

Animals↗
PubMed2000

Effects of blockers of carbohydrate and lipid metabolism on expression of mRNA of some hypothalamic neuropeptides.

The effects of single injections of 2-deoxyglucose or 2-mercaptoacetate on the expression of mRNA of neuropeptide Y, pro-opiomelanocortin, and melanin-concentrating hormone in rat hypothalamus were studied by in situ hybridization in order to elucidate the role of these neuropeptides in the mechanisms of alimentary behavior caused by decreased levels of available fatty acids and glucose. The levels of neuropeptide Y mRNA in arcuate nuclei neurons are significantly increased under conditions of glucose deficiency, while the synthesis of melanin-concentrating hormone in the lateral hypothalamic neurons is increased in fatty acid deficiency. These data indicate that glyco- and lipodeprivation are different metabolic signals activating various neuropeptide systems responsible for alimentary behavior.

Animals↗
PubMed2001

N-methyltryptophan oxidase from Escherichia coli: reaction kinetics with N-methyl amino acid and carbinolamine substrates.

N-Methyltryptophan oxidase (MTOX), a flavoenzyme from Escherichia coli, catalyzes the oxidative demethylation of N-methyl-L-tryptophan (k(cat) = 4600 min(-1)). Other secondary amino acids (e.g., sarcosine) are oxidized at a slower rate. We have identified carbinolamines as a new class of alternate substrate. MTOX oxidation of the carbinolamine formed with L-tryptophan and formaldehyde yields N-formyl-L-tryptophan in a relatively slow reaction that does not compete with turnover of MTOX with N-methyl-L-tryptophan. Double reciprocal plots with N-methyl-L-tryptophan as the varied substrate are nearly parallel, but the slopes show a small, systematic variation depending on the oxygen concentration. N-Benzylglycine, a dead-end competitive inhibitor with respect to N-methyl-L-tryptophan, acts as a noncompetitive inhibitor with respect to oxygen. The results are consistent with a modified ping pong mechanism where oxygen binds to the reduced enzyme prior to dissociation of the imino acid product. MTOX is converted to a 2-electron reduced form upon anaerobic reaction with N-methyl-L-tryptophan, sarcosine, or the carbinolamine formed with L-tryptophan and formaldehyde. No evidence for a detectable intermediate was obtained by monitoring the spectral course of the latter two reactions. MTOX reduction with thioglycolate does, however, proceed via a readily detectable anionic, flavin radical intermediate. The reductive half-reaction with sarcosine at 4 degrees C exhibits saturation kinetics (k(lim) = 6.8 min(-1), K = 39 mM) and other features consistent with a mechanism in which a nearly irreversible reduction step (E(ox).S --> E(red).P) (k(lim)) is preceded by a rapidly attained equilibrium (K) between free E and the E.S complex. The 21 degrees C temperature difference can reasonably account for the 3.6-fold lower value obtained for k(lim) as compared with turnover at 25 degrees C (k(cat) = 24.5 min(-1)), suggesting that sarcosine is oxidized at a kinetically significant rate under anaerobic conditions and the reductive half-reaction is rate-limiting during turnover. These conclusions are, however, difficult to reconcile with steady-state kinetic patterns obtained with sarcosine that are consistent with a rapid equilibrium ordered mechanism with oxygen as the first substrate. The basis for the apparent stability of the MTOX.oxygen complex (K(d) = 72 microM) is unknown.

Amines↗
PubMed1997

Molecular characterization of a germination-specific muramidase from Clostridium perfringens S40 spores and nucleotide sequence of the corresponding gene.

The exudate of fully germinated spores of Clostridium perfringens S40 in 0.15 M KCI-50 mM potassium phosphate (pH 7.0) was found to contain another spore-lytic enzyme in addition to the germination-specific amidase previously characterized (S. Miyata, R. Moriyama, N. Miyahara, and S. Makino, Microbiology 141:2643-2650, 1995). The lytic enzyme was purified to homogeneity by anion-exchange chromatography and shown to be a muramidase which requires divalent cations (Ca2+, Mg2+, or Mn2+) for its activity. The enzyme was inactivated by sulfhydryl reagents, and sodium thioglycolate reversed the inactivation by Hg2+. The muramidase hydrolyzed isolated spore cortical fragments from a variety of wild-type organisms but had minimal activity on decoated spores and isolated cell walls. However, the enzyme was not capable of digesting isolated cortical fragments from spores of Bacillus subtilis ADD1, which lacks muramic acid delta-lactam in its cortical peptidoglycan. This indicates that the enzyme recognizes the delta-lactam residue peculiar to spore peptidoglycan, suggesting an involvement of the enzyme in spore germination. Immunochemical studies indicated that the muramidase in its mature form is localized on the exterior of the cortex layer in the dormant spore. A gene encoding the muramidase, sleM, was cloned into Escherichia coli, and the nucleotide sequence was determined. The gene encoded a protein of 321 amino acids with a deduced molecular weight of 36,358. The deduced amino acid sequence of the sleM gene indicated that the enzyme is produced in a mature form. It was suggested that the muramidase belongs to a separate group within the lysozyme family typified by the fungus Chalaropsis lysozyme. A possible mechanism for cortex degradation in C. perfringens S40 spores is discussed.

Amino Acid Sequence↗
PubMed1985

Vaccinia virus proteins on the plasma membrane of infected cells. III. Infection of peritoneal macrophages.

Primary macrophage cultures were prepared from the peritoneal exudate cell population harvested from mice challenged intraperitoneally with saline, thioglycollate, or vaccinia virus. Vaccinia virus was adsorbed and penetrated into primary macrophages and L-cells with similar kinetics. As evidenced by the expression of some "early" virus-specified proteins, partial uncoating and activation of the virion-associated DNA-dependent RNA polymerase occurred in the infected macrophages. Subsequently, the viral replication cycle in macrophages was aborted; with time after infection, viral DNA and virion proteins initially associated with infected cells could be detected in an acid-soluble form in the medium harvested from infected macrophage cultures. The results suggest that at the time that the final stages of virus uncoating should have occurred, intracellular subviral particles were, instead, degraded in the infected, primary macrophages. Viral DNA synthesis could not be measured in vaccinia virus-infected macrophages, no "late" virus functions were expressed, and progeny virions were not assembled. As measured by the binding of antiviral-antibody-125I-protein A complexes to the surface of vaccinia virus-infected cells, the expression of virus-specified antigens on the surfaces of infected macrophages was significantly reduced and never exceeded that measured at 2 hr after infection on the surfaces of infected L-cells. The expression of virus-specified polypeptides with mol mass of 48-50, 45-46, 36-37, and 25 kDa on the plasma membranes of vaccinia virus-infected, thioglycollate-elicited macrophages, rendered the infected macrophages susceptible to lysis by vaccinia virus-specific cytotoxic T-cells.

Adsorption↗
PubMed1992

Characterization of immunosuppressive functions of murine peritoneal macrophages induced with various agents.

Murine peritoneal macrophages (M phi s), induced with stimuli such as thioglycollate, zymosan A, OK-432, bacille Calmette-Guérin (BCG), or live Mycobacterium intracellulare, showed varying levels of inhibitory activity against the concanavalin A (Con A) blastogenic response of splenic T cells. All test M phi s significantly inhibited the interleukin 2 (IL-2)-producing ability of T cells but this inhibition was not enough to explain the observed reduction in T cell Con A mitogenesis. In contrast, they markedly inhibited IL-2-reactive T cell generation, and the inhibition was sufficient to cause the reduction in T cell mitogenesis. A general relationship was observed between immunosuppressive activity of a given M phi and its active oxygen-producing ability (measured in terms of chemiluminescence) in response to phorbol myristate acetate triggering (r = .84, P less than .005). However, the suppressor activity of test M phi s was not reduced by superoxide dismutase and catalase, indicating that active oxygen radicals themselves did not mediate the expression of the immunosuppressive activity of these M phi s. On the other ahnd, indomethacin (an inhibitor of prostaglandin synthesis) caused a partial reduction in their immunosuppressive activity. The suppressor activity of M phi s induced with intraperitoneal injection of recombinant interferon gamma (IFN-gamma) was markedly reduced in the presence of myoglobin, a scavenger for nitric oxide radical (NO.). Tumor necrosis factor alpha (TNF alpha) failed to affect Con A mitogenesis of splenic T cells, even in combination with IFN-gamma. On the other hand, unsaturated long-chain fatty acids including oleic, linoleic, linolenic, and arachidonic acids markedly reduced the T cell function. These findings suggest some important roles of prostaglandins, NO., and long-chain unsaturated fatty acids as mediators of the expression of immunosuppressive function of the peritoneal M phi s.

Animals↗
PubMed1982

Effects of 2-mercaptoacetate in isolated liver mitochondria in vitro. Competitive inhibition of 3-hydroxybutyrate dehydrogenase and depression of the beta-oxidation pathway.

The effects of 2-mercaptoacetate on the respiration rates induced by different substrates were studied in vitro in isolated liver mitochondria. With palmitoyl-L-carnitine or 2-oxoglutarate as the substrate, the ADP-stimulated respiration (State 3) was dose-dependently inhibited by 2-mercaptoacetate. with glutamate or succinate as the substrate. State-3 respiration was only slightly inhibited by 2-mercaptoacetate. In contrast, the oxidation rate of 3-hydroxybutyrate was competitively inhibited by 2-mercaptoacetate in both isolated mitochondria and submitochondrial particles. In uncoupled mitochondria and in mitochondria in which ATP- and GTP-dependent acyl-CoA biosynthesis was inhibited, the inhibitory effect of 2-mercaptoacetate on palmitoyl-L-carnitine oxidation was abolished; under the same conditions, however, inhibition of 3-hydroxybutyrate oxidation by 2-mercaptoacetate still persisted. These results led to the following conclusions: 2-mercaptoacetate itself enters the mitochondrial matrix, inhibits fatty acid oxidation through a mechanism requiring an energy-dependent activation of 2-mercaptoacetate and itself inhibits 3-hydroxybutyrate oxidation through a competitive inhibition of the membrane-bound 3-hydroxybutyrate dehydrogenase. This study also strongly suggests that the compound responsible for the inhibition of fatty acid oxidation is 2-mercaptoacetyl-CoA.

3-Hydroxybutyric Acid↗
PubMedDate not supplied

Thiodiacetic acid--a metabolite of Ethylene oxide.

Urine samples of premature babies contain high amounts of thiodiacetic acid (TDA). Since these pre-term infants are exposed to an increased oxygen atmosphere in the incubator, we supposed that these high levels of thiodiacetic acid might be produced from ethylene, generated in the course of lipid peroxidation processes. Considering that conversion of ethylene to ethylene oxide (EO) is well known in biology we investigated whether ethylene oxide is metabolised to thiodiacetic acid or not. Therefore Sprague-Dawley rats and NMRI mice were exposed to ethylene oxide for six hours. Urine specimens were collected after exposure and the amount of thiodiacetic acid was determined by gas chromatography/mass spectrometry. The quantity of excreted TDA increased enormously compared to control samples. So thiodiacetic acid seems to be a metabolite of ethylene oxide in vivo.

Animals↗
PubMed1991

Lack of gastric adverse effects of erdosteine in rats and men.

Erdosteine is a thiol derivative endowed with mucolytic, mucomodulator and free radical scavenging properties. Studies were performed in rats and men with the aim to assess its safety on gastric mucous barrier. Two experiments were performed in rats by comparing the effects of erdosteine, homocysteine thiolactone (HTL), carbocysteine, tiopronin and placebo on a) macroscopic appearance of G. I. ulcer, total HCl, pH and volume of gastric juice 4 and 6 hours after, respectively, pylorus ligation in Shay rats and drug oral treatment, and on b) macroscopic appearance of G. I. ulcer in fasting rats for 50 hours, during which the animals received 4 oral doses of each compound. In both conditions erdosteine was completely inactive in the dose-range of 500-1000 mg/kg p.o. while HTL, carbocysteine and tiopronin were ulcerogenic already at the dose of 500 mg/kg p.o. Accordingly, 15 human beings, undergoing gastroscopy, well tolerated erdosteine at the oral dose of 300 mg TID for 9-13 days. In this open study the patients neither revealed worsening of their pre-existing gastric complains, nor indicated new subjective symptoms, nor manifested macroscopic and histological alterations concerning the parietal tonus, the status of epithelial mucosa and of gastric content (including: volume, total acidity and total, bound and free sialic acid).

Administration, Oral↗
PubMed2002

Molecular cloning and characterization of a novel mouse macrophage C-type lectin, mMGL2, which has a distinct carbohydrate specificity from mMGL1.

A novel mouse macrophage galactose-type C-type lectin 2 (mMGL2) was identified by BLAST analysis of expressed sequence tags. The sequence of mMGL2 is highly homologous to the mMGL, which should now be called mMGL1. The open reading frame of mMGL2 contains a sequence corresponding to a type II transmembrane protein with 332 amino acids having a single extracellular C-type lectin domain. The 3'-untranslated region included long terminal repeats of mouse early transposon. The Mgl2 gene was cloned from a 129/SvJ mouse genomic library and sequenced. The gene spans 7,136 base pairs and consists of 10 exons, which is similar to the genomic organization of mMGL1. The reverse transcriptase-PCR analysis indicates that mMGL2 is expressed in cell lines and normal mouse tissues in a macrophage-restricted manner, also very similar to that of mMGL1. The mMGL2 mRNA was also detected in mMGL1-positive cells, which were sorted from thioglycollate-induced peritoneal cells with a mMGL1-specific monoclonal antibody, LOM-8.7. The soluble recombinant proteins of mMGL2 exhibited carbohydrate specificity for alpha- and beta-GalNAc-conjugated soluble polyacrylamides, whereas mMGL1 preferentially bound Lewis X-conjugated soluble polyacrylamides in solid phase assays. These two lectins may function cooperatively as recognition and endocytic molecules on macrophages and related cells.

3' Untranslated Regions↗
PubMed1999

Plant polyphenols inhibit benzoyl peroxide-induced superoxide anion radical production and diacylglyceride formation in murine peritoneal macrophages.

Naturally occurring plant polyphenols, which include ellagic acid (EA), tannic acid (TA), caffeic acid (CA), and ferulic acid (FA), were tested for their superoxide anion radical (SOR)-scavenging activities. SOR were produced by interaction of the tumor promoter benzoyl peroxide (BPO) with murine peritoneal macrophages in vitro. The levels of SOR were assessed microscopically by counting the number of formazan-positive cells per 250 cells produced by the reduction of nitro blue tetrazolium. BPO at a concentration of 15 micrograms/1.85 x 10(6) cells/0.5 ml induced maximum formation of SOR in resident and thioglycollate-elicited cells. All the tested polyphenols were able to inhibit the formation of SOR induced by the tumor promoter to a variable degree. Inhibition of BPO-induced SOR formation by polyphenols was in the following order: FA > TA > CA > EA. BPO stimulated the accumulation of diacylglycerol (DAG) in resident and elicited macrophages with concurrent release of choline equivalents from macrophages. Polyphenols inhibited DAG accumulation, which paralleled the inhibition of choline equivalent release. FA was observed to be the most effective and EA the least effective inhibitor of SOR formation, DAG accumulation, and release of choline equivalents. It is likely that inhibition of SOR formation might be due to some interference in the cellular lipid metabolism and phospholipid equivalent deacylation and choline release.

Animals↗
PubMed1982

Control of macrophage Ia expression in neonatal mice--role of a splenic suppressor cell.

The control of macrophage expression of I region-associated antigens (Ia) in neonatal mice was studied by comparing responses of neonatal and adult mice to immune vs nonimmune stimuli. Adults generated peritoneal exudates rich in Ia-bearing macrophages in response to i.p. injection of live Listeria monocytogenes, Listeria-immune T cells, and heat-killed Listeria, or a soluble mediator termed macrophage Ia-recruiting factor (MIRF). Neonates failed to respond to these stimuli. In contrast, both neonates and adults generated Ia-negative peritoneal exudates when stimulated with thioglycollate. A neonatal spleen cell that blocked the response of adults both to immune T cells and heat-killed Listeria and to MIRF was identified and characterized. Some of the suppressor cells appeared to be early precursors of the phagocytic lineage that develop into mature monocyte-macrophages. Suppression was apparently mediated by metabolites of arachidonic acid since indomethacin and aspirin in vivo blocked the effect. Similar suppressor activity was found in adult bone marrow and in adult resident peritoneal exudate cells. Thus, the phagocytic line autoregulates its surface expression of Ia in both neonatal and adult mice. This mechanism becomes particularly pointed during early development and could contribute to the lack of immunity during ontogeny.

Animals↗
PubMed1996

Macrophages have cell surface IL-10 that regulates macrophage bactericidal activity.

IL-10, which is secreted by multiple cell types, has regulatory effects on macrophages, including decreasing their ability to kill some microorganisms. The experiments presented here test the hypothesis that endogenous IL-10 inhibits the ability of macrophages to kill the facultative intracellular bacterium, Listeria monocytogenes. We show that the nonbactericidal macrophage hybrid, H36.12j (12j), can kill Listeria after incubation for 3 days with anti-IL-10 mAb. IL-10 was not detected in 12j macrophage supernatants by ELISA. However, flow cytometric analysis revealed high levels of IL-10 on the 12j cell surface. This indicates that macrophages that fail to secrete IL-10 may express IL-10 on the cell surface, and this IL-10 appears to suppress listericidal activity. Surface IL-10 is not unique to the 12j macrophage hybrid and may correlate with the absence of bactericidal activity in other macrophages. For instance, nonlistericidal resident and thioglycolate-elicited peritoneal exudate cells have 24 to 72% IL-10-positive macrophages. In contrast listericidal proteose peptone-elicited peritoneal exudate cells contained < 5% IL-10-positive macrophages. Whether this IL-10 is an integral membrane protein or is bound to IL-10 receptors is not yet known. However, the IL-10 does not elute with acid as other passively bound molecules do, nor does exogenous IL-10 bind to macrophages. In either case, since anti-IL-10 induces nonbactericidal macrophages to become bactericidal, the surface IL-10 is biologically active, and it appears to regulate macrophage bactericidal activity.

Animals↗