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PubMed2006

Non-PKC DAG/phorbol-ester receptor(s) inhibit complement receptor-3 and nPKC inhibit scavenger receptor-AI/II-mediated myelin phagocytosis but cPKC, PI3k, and PLCgamma activate myelin phagocytosis by both.

Complement-receptor-3 (CR3/MAC-1), scavenger-receptor-AI/II (SRAI/II), and Fcgamma-receptor (FcgammaR) can mediate myelin phagocytosis in macrophages and microglia. Paradoxically, after injury to CNS axons these receptors are expressed but myelin is not phagocytosed, suggesting that phagocytosis is subject to regulation between efficient and inefficient states. In the present work, we focus on CR3/MAC-1 and SRAI/II-mediated myelin phagocytosis. Phagocytosis by CR3/MAC-1 and SRAI/II was inhibited by cPKC inhibitor Go-6976, general-PKC inhibitors Ro-318220 and calphostin-C, and BAPTA/AM, which chelates intracellular Ca2+ required for cPKC activation. Signaling/activation by cPKC are thus suggested. PMA, which mimics diacylglycerol (DAG) as an activator of cPKC, novel-PKC (nPKC), and non-PKC DAG-driven molecule(s), produced a dose-dependent dual effect on phagocytosis by CR3/MAC-1 and SRAI/II, i.e., augmentation at low concentrations and inhibition at high concentrations. Inhibition of phagocytosis by CR3/MAC-1 was enhanced by combining inhibiting concentrations of PMA with PKC inhibitors Go-6976 or Ro-318220, suggesting inhibition by PMA/DAG-driven non-PKC molecule(s). In contrast, inhibition of phagocytosis by SRAI/II was enhanced by combining inhibiting concentrations of PMA with cPKC inhibitor Go-6976 but not with general-PKC inhibitor Ro-318220, suggesting inhibition by nPKC. Phagocytosis by CR3/MAC-1 and SRAI/II was further inhibited by PI3K inhibitors wortmannin and LY-294002 and PLCgamma inhibitor U-73122. Altogether, our observations suggest that CR3/MAC-1 and SRAI/II-mediated myelin phagocytosis share activation by PI3K, PLCgamma and cPKC. The two differ, however, in that non-PKC DAG-driven molecule(s) inhibit CR3/MAC-1-mediated phagocytosis, whereas nPKC inhibit SRAI/II-mediated phagocytosis. Each of these signaling steps may be targeted for regulating CR3/MAC-1 and/or SRAI/II-mediated phagocytosis between efficient and inefficient states.

Animals↗

PubMed1985

Technetium thiodiglycollic acid (99mTc-TDG). A new radiopharmaceutical with the potential for the assessment of renal function.

A mixture of hydrophilic complexes is formed on the reduction (employing tin metal as a reductant) of sodium pertechnetate 99mTc in the presence of the ligand thiodiglycollic acid (TDG). When administered to rats, the mixture demonstrated a renal clearance rate marginally greater than Glomerular filtration rate (GFR). HPLC analysis indicated the formation of two technetium complexes of TDG. After isolation of the complexes and their administration to rats, one (complex 1) showed renal clearance similar to that of 99mTc Diethylenetriamine pentaacetic acid (DTPA), while the other (complex 2) demonstrated renal clearance similar to that of 125I o-iodo hippuric acid. On heating the mixture of complexes, the proportion of the faster-clearing 99mTc TDG complex increased to 92% of the total activity, and the biodistribution of the material following heat rearrangement was equivalent to that of isolated complex 2.

Animals↗

PubMed1991

Approaches to some biochemical mechanisms of action of tuftsin and analogues.

Tuftsin, T-K-P-R, is a phagocytosis-stimulating peptide described as a natural immunostimulant. Four analogues of this peptide were synthesized. These compounds were assayed for their ability to compete with [3H]tuftsin for its specific receptor from thioglycollate-elicited mouse peritoneal macrophages. They were also tested for their ability to change level in intracellular cGMP and to stimulate phagocytosis through the nitroblue tetrazolium reduction measurement. Surprisingly, all the analogues were poor competitors of [3H]tuftsin binding but possess potent tuftsin-like activities.

Amino Acid Sequence↗

PubMed1990

Clinical and microbiologic characteristics of pediococci.

Over a 43-month period, 23 separate isolates of nonenterococcal alpha- and nonhemolytic streptococci were reported by our clinical microbiology laboratory to be resistant to vancomycin. This constituted 0.32% of nonenterococcal alpha- and nonhemolytic streptococci reported and 4.4% of such streptococci upon which susceptibility testing was performed. Of 13 isolates which were available for further study, all were highly resistant to vancomycin (MIC greater than or equal to 1,024 micrograms/ml), but none were actually streptococci. Three were clearly gram-positive rods by Gram stain and were found to be homofermentative lactobacilli. Two strains with elongated gram-positive cocci from colonies on agar showed small gram-positive rods when grown in thioglycolate broth and were physiologically identified as Lactobacillus confusus. Two isolates with lenticular gram-positive cocci appeared to be Leuconostoc mesenteroides subsp. mesenteroides. Six gram-positive isolates with round cells from growth on agar and from broth were arranged in tetrads in broth and closely resembled Pediococcus acidilactici. Twelve additional strains of pediococci that were not of human origin were also found to be highly resistant to vancomycin. These findings confirm published reports of clinical isolation of organisms resembling pediococci and suggest that clinically isolated, vancomycin-resistant bacteria which superficially resemble streptococci are probably other lactic acid bacteria.

Drug Resistance, Microbial↗

PubMed2006

Re-identification of the halotolerant, biosurfactant-producing Bacillus licheniformis strain JF-2 as Bacillus mojavensis strain JF-2.

Bacillus strain JF-2 (ATCC 39307) is a halotolerant, biosurfactant-producing bacterium that was initially described as a member of the species Bacillus licheniformis based on a limited set of phenotypic characteristics. Here, genetic and phenotypic analyses were employed to determine the relationship of Bacillus strain JF-2 to other Bacillus strains. The restriction patterns with AluI and analysis of gyrA and 16S rRNA gene sequences grouped Bacillus strain JF-2 with B. mojavensis(T) and not with B. licheniformis(T). DNA-DNA similarity showed JF-2 was 75% similar to B. mojavensis(T) and only 11% similar to B. licheniformis(T). Both strain JF-2 and B. mojavensis(T) required DNA for anaerobic growth, but B. licheniformis(T) did not. B. mojavensis(T) and strain JF-2 did not grow anaerobically in thioglycollate medium or aerobically with propionate while B. licheniformis(T) grew under these conditions. DNA-DNA similarity, gene sequence data and phenotypic characteristics all support the assignment of JF-2 as a member of the species B. mojavensis.

Anaerobiosis↗

PubMedDate not supplied

Synthesis and some biological properties of new derivatives of 1-S-phenylthioglycolonitrile.

A series of new S-phenylthioglycolic acid derivatives was synthetized via common transformations of alkylated S-phenyl-thioglycolonitrile. The compounds were submitted to pharmacological screening. N,N-Diethylaminoethyl ester of 1-S-phenylcyclopentane carboxylic acid was submitted to detailed studies and showed high local anesthetic properties.

Anesthetics, Local↗

PubMed1983

Ingestion of yeast forms of Sporothrix schenckii by mouse peritoneal macrophages.

The ingestion by thioglycolate-elicited mouse peritoneal macrophages of yeast forms of two strains of Sporothrix schenckii was studied. Yeast forms opsonized with concanavalin A (ConA) were extensively phagocytized, and the phagocytic indexes depended on the concentration of ConA and apparently on the number of lectin receptors at the yeast surface as well. Neuraminidase treatment of S. schenckii increased the ingestion of unopsonized yeasts 7.7-fold. The addition of monosaccharides and derivatives partially inhibited phagocytosis. Mannose, rhamnose, and galactose, which are major constituents of S. schenckii surface antigens, reduced the phagocytic indexes by 40 to 50%. Glucosamine, N-acetylglucosamine, and N-acetylneuraminic acid were equally effective as inhibitors of phagocytosis. A mixture of five neutral sugars and glucosamine inhibited phagocytosis by 73%. The inhibitory effect of simple sugars could be amplified by using neuraminidase-treated yeast cells. Pentoses and glucose were inactive or slightly inhibitory. A purified rhamnomannan inhibited phagocytosis of the homologous strain, whereas partially purified peptidopolysaccharides were toxic to peritoneal macrophages. A partially purified galactomannan from S. schenckii was inhibitory (62% inhibition), and a peptidopolysaccharide fraction in which the O-linked carbohydrate chains had been removed neither was toxic to macrophages nor inhibited phagocytosis. Pretreatment of macrophages with simple sugars under conditions inhibiting ingestion or binding of S. schenckii did not affect phagocytosis of latex particles or sensitized sheep erythrocytes. The presence of receptors at the peritoneal macrophages which bind S. schenckii cell surface components is suggested.

Animals↗

PubMed1988

Lipoprotein metabolism by macrophages from atherosclerosis-susceptible White Carneau and resistant Show Racer pigeons.

The presence of specific receptors for the metabolism of acetylated low density lipoprotein (AcLDL) and beta-migrating very low density lipoprotein (beta-VLDL) was demonstrated in thioglycolate-elicited peritoneal macrophages from both atherosclerosis-susceptible White Carneau (WC) and resistant Show Racer (SR) pigeons. Macrophages from both breeds metabolized AcLDL through a single class of receptors that were similar, but not identical, to the scavenger receptors described in mammalian macrophages. Both pigeon and mammalian AcLDL bound to this receptor. At 37 degrees C, AcLDL was internalized and degraded in the lysosomes, and cholesterol esterification and cholesteryl ester accumulation were stimulated. As in mammalian macrophages, AcLDL receptor activity was not down-regulated by cholesterol loading. In contrast, AcLDL binding was poorly competed for by fucoidin or polyinosinic acid, and the magnitude of cholesteryl ester accumulation was only about one-half of that seen with mouse peritoneal macrophages. Pigeon beta-VLDL bound to both a high and a low affinity site on pigeon macrophages. Binding to the high affinity site was calcium-dependent, pronase-sensitive, and down-regulated by cholesterol loading. Cholesterol esterification and cholesteryl ester accumulation with beta-VLDL were stimulated to an equal or greater extent than with AcLDL. Unlike mammalian macrophages, the pigeon beta-VLDL receptor did not require apolipoprotein E, as evidenced by the lack of apoE in pigeon lipoproteins and by the failure of rabbit beta-VLDL, containing apoE, to compete for binding. Pigeon LDL, but not mammalian LDL, was recognized by the pigeon beta-VLDL receptor, suggesting that like the mammalian beta-VLDL receptor, the pigeon beta-VLDL receptor may be a form of an LDL receptor. This was an unexpected finding since pigeon fibroblasts and smooth muscle cells in culture do not express LDL receptors. Thus, pigeon macrophages have receptors for the uptake of abnormal lipoproteins that could play a role in the development of macrophage-derived foam cells that are prevalent in the early stages of atherosclerosis in this species. No quantitative or qualitative differences in these receptors, however, were identified that could account for the differences in atherosclerosis susceptibility between the WC and SR breeds.

Animals↗

PubMed1994

Methionine enkephalin metabolism by murine macrophage ectopeptidase(s).

Ectopeptidases which hydrolyze opioid and other neuropeptides have been identified in brain, kidney and intestine. In this study, identification of the enzymes metabolizing the opioid peptide methionine enkephalin (YGGFM) in murine macrophages was undertaken. Incubation of methionine enkephalin with intact murine peritoneal macrophages results in five products identified as Y, F, FM, GFM and GGFM by amino acid analysis and peptide microsequencing after fractionation by HPLC. The spectrum of metabolites results from at least two distinct aminopeptidase activities. The enzyme hydrolyzing YGGFM to GGFM is identified as the membrane-anchored aminopeptidase N (ApN; EC 3.4.11.2) based on its substrate specificity and inhibitor profile. A distinct bestatin and amastatin sensitive aminopeptidase catalyzes hydrolysis of GGFM to GFM. The macrophage ApN protein has a larger mass and is antigenically distinct from murine kidney ApN, which is suggested to result from glycosylation differences rather than expression of a distinct protein. The ApN catalytic activity and mRNA levels are increased in thioglycollate-elicited as compared to resident peritoneal macrophages. RT-PCR analysis identified a 0.7 kb fragment of the ApN coding sequence which was identical in mouse kidney and thioglycollate-elicited peritoneal macrophages and which has 89% identity with the corresponding rat kidney ApN cDNA sequence.

Aminopeptidases↗

PubMed1978

Differences in metabolism of vinylidene chloride between mice and rats.

The present finding that mice metabolize a greater proportion of an oral dose (50 mg/kg) of vinylidence chloride. (1,1 - dichloroethylene, DCE) than rats implies (a) that the efficiency of DCE metabolism follows the known activity of cytochrome P-450 in the organs of these animals, and (b) that, in accordance with the LD(50) values, the real exposure (expressed as the amount of DCE metabolized) is relatively higher for orally dosed mice than rats, and (c) that DCE carcinogenicity would appear to be more likely in mice than rats.Mice metabolize DCE simiarly to rats (Jones and Hathway, 1977) but there are some differences. Thus, qualitatively, treated mice (but not rats) excrete a small amount of N-acetyl-S-(2carboxymethyl)cysteine. Quantitatively, (i) the relative proportions of the N-acetyl-S-(2-cysteinyl acetyl derivative that are formed in mice and rats parallel the activity of liver glutathione-S-epoxide transferase in these rodents, and (ii) there are marked differences in the proportions of DCE metabolites belonging to the chloroacetic acid branch of the metabolic pathway. Furthermore, the previously assumed β-thionase hydrolysis of thiodiglycollic acid (Jones and Hathway, 1977) is now established in vivo, and the possible biogenesis of the N-acetyl-S-cysteinyl acetyl derivative is verified by another tracer study. The conclusion is drawn that the DCE metabolites, 1,1-dichloroethylene oxide and chloroacetyl chloride, may be important to murine DCE carcinogenicity.

Animals↗

PubMed1994

Formation of amide bonds without a condensation agent and implications for origin of life.

Amide bonds are of central importance for biochemistry; in the guise of peptide bonds, they form the backbone of proteins. The formation of amide bonds without the assistance of enzymes poses a major challenge for theories of the origin of life. Enzyme-free formation of amide bonds between amino acids has been demonstrated in the presence of condensing agents such as cyanamide. Here we report the formation of amide bonds in aqueous solution in the absence of any condensing agent. We find that the formation of pyrite (FeS2) from FeS and H2S can provide the driving force for reductive acetylation of amino acids with mercaptoacetic acid (HSCH2COOH). The redox energy of pyrite formation permits the activation of the carboxylic acid group, which is converted to a species that reacts readily with amines. This process provides support for the chemo-autotrophic theory for the origin of life, in which pyrite formation supplies the energy source for the first autocatalytic reproduction cycle.

Acetylation↗

PubMed1981

Antigen-induced proliferation of murine T-lymphocytes in vitro. II. The effect of different macrophage populations on the antigen-induced proliferative response.

Various macrophage-containing preparations were tested for their ability to increase the antigen-specific proliferative response of murine T-lymphocytes. The preparations examined included: peritoneal exudate cells (PEC) from mice injected with mineral oil or thioglycolate; fresh bone-marrow cells; bone marrow cells grown in culture for up to 11 days; normal spleen cells, and spleen cells from mice injected with mineral oil. The best proliferative response was obtained when the lymphocytes were supplemented with 30% spleen cells from mice injected with mineral oil. When spleen cells from mineral oil injected mice are compared with those of spleen cells from normal mice, it is evident that mineral oil given i.p. activates the spleen macrophages. Although the number and percentage of macrophages in the spleen does not increase following mineral oil injection, the activities of some of their enzymes (acid phosphatase and beta-glucuronidase) increase while others do not change (Cathepsin D and lysozyme). Furthermore, the Fc-dependent phagocytic activity of spleen macrophages and their spreading on plastic culture dishes is increased after mineral oil treatment. We conclude that the activation of spleen macrophages caused by an i.p. injection of mineral oil also induces the changes in their antigen-presenting apparatus. Consequently, macrophages from spleens of mineral oil-injected mice are most suitable cell preparations for antigen presentation to T-lymphocytes.

Animals↗

PubMed2002

The effect of 1,2,4-thiotriazolyl 5-mercaptoacetic acid new derivatives on lipid peroxidation in the heart from adult and old rats during stress.

The effect of 3-(4-pyridyl)-1,2,4-thiotriazolyl 5-mercaptoacetic acid kalium salt (Rumosol) and 3-(4-pyridyl)-1,2,4-thiotriazolyl 5-mercaptoacetic acid morpholinium salt (drug 2) on the concentration of Schiff base in myocardium of adult (10-12 months) and old (22-25 months) Wistar rats during immobilized stress were investigated. Here we show that the accumulation of Schiff base in the heart from both age groups was inhibited after injection of derivatives of 1,2,4-thiotriazolyl 5-mercaptoacetic acid prior to immobilization. Drug 2 possessed a two-fold higher pronounced capacity against Rumosol to inhibit the accumulation of Schiff base in the heart during stress. In myocardium from old rats, drug 2 decreased more effectively the stress-induced stimulation of lipid peroxidation as compared to dimethyl sulfoxide.

Acetates↗

PubMed1965

A STUDY OF SOME THIOL ESTER HYDROLYSES AS MODELS FOR THE DEACYLATION STEP OF PAPAIN-CATALYSED HYDROLYSES.

1. The self-catalysed hydrolyses of the thiol esters, S-hippurylthioglycollic acid and S-ethyl monothiolsuccinate, have been shown to be slower than the deacylation step for the papain-catalysed hydrolysis of hippuric esters, by a factor approx. 10(5). This difference in rate constants largely reflects a difference in activation energy, which together with other evidence drawn from the literature make it unlikely that a carboxylate ion could be the nucleophile responsible for the deacylation of acyl-papain. 2. The imidazole-catalysed hydrolysis of S-hippurylthioglycollic acid and ethyl thiolacetate have activation energies similar to that for the deacylation step in papain-catalysed hydrolyses. This, together with other evidence drawn from the literature, suggests that the imidazole of a histidine residue is the nucleophile responsible for the deacylation of acyl-papain.

Acylation↗

PubMed1981

2-Mercaptoacetate administration depresses the beta-oxidation pathway through an inhibition of long-chain acyl-CoA dehydrogenase activity.

To elucidate the mechanisms through which 2-mercaptoacetate administration inhibits fatty acid oxidation in the liver, the respiration rates induced by different substrates were studied polarographically in rat hepatic mitochondria isolated 3 h after 2-mercaptoacetate administration. Palmitoyl-L-carnitine oxidation was almost completely inhibited in either the absence or presence of malonate. Octanoate oxidation was also inhibited, and the intramitochondrial acyl-CoA content was markedly increased. The oxidation rate of pyruvate and 2-oxoglutarate on the one hand and of 3-hydroxybutyrate, succinate and glutamate on the other was either normal or only slightly decreased. In the presence of 2,4-dinitrophenol, the extent of the inhibition of palmitoyl-L-carnitine oxidation was unchanged. All these results are consistent with the hypothesis that the 2-mercaptoacetate inhibition of fatty acid oxidation is due to an inhibition of the beta-oxidation pathway itself. Finally, the mitochondrial defect responsible for this inhibition was shown to be an inhibition of palmitoyl-CoA dehydrogenase activity (EC 1.3.99.3).

Acyl-CoA Dehydrogenase, Long-Chain↗

PubMed1993

Neuropeptide Y in the arcuate nucleus is modulated by alterations in glucose utilization.

This study examined the response of hypothalamic neuropeptide Y (NPY) to specific metabolic challenges. After intraperitoneal administration of 2-deoxy-D-glucose, which blocks glucose utilization, NPY levels measured via radioimmunoassay were significantly potentiated in the arcuate (ARC) and suprachiasmatic nuclei of the rat hypothalamus. The antimetabolite mercaptoacetate, in contrast, which blocks fatty acid oxidation, produced no significant change and actually tended to reduce NPY levels in the ARC. It is concluded that glucose utilization, in particular, may constitute an important signal, either direct or indirect, in the modulation of NPY production in the hypothalamus.

Animals↗

PubMed2000

Effect of 2-mercaptoacetate and 2-deoxy-D-glucose administration on the expression of NPY, AGRP, POMC, MCH and hypocretin/orexin in the rat hypothalamus.

Using in situ hybridization, the mRNA levels encoding neuropeptide Y (NPY), agouti gene-related protein (AGRP), proopiomelanocortin (POMC), melanin-concentrating hormone (MCH) and hypocretin/orexin (HC/ORX) were investigated in the rat arcuate nucleus (Arc) and lateral hypothalamic area (LHA) 2 h after a single dose of the glucose antimetabolite 2-deoxy-D-glucose (2-DG; 600 mg/kg) or of the fatty acid oxidation inhibitor mercaptoacetate (MA; 600 mumol/kg). Two hours after 2-DG or MA injection food intake was significantly increased. NPY and AGRP mRNA levels in the Arc were increased by 2-DG but not affected by MA, and MCH mRNA levels in the LHA were increased by both antimetabolites. These results suggest that Arc neurons expressing NPY and AGRP are regulated by changes in glucose, but not fatty acid availability, whereas both factors affect MCH neurons in the LHA.

Agouti-Related Protein↗

PubMed1993

Relationship among bile tolerance, bile salt deconjugation, and assimilation of cholesterol by Lactobacillus acidophilus.

The relationships among growth in the presence of bile, deconjugation of sodium taurocholate, and assimilation of cholesterol by 19 cultures of Lactobacillus acidophilus were examined. Cultures of L. acidophilus were grown at 37 degrees C in lactobacilli MRS broth supplemented with sodium thioglycollate, sodium taurocholate, and cholesterol (cholesterol phosphatidyl choline micelles). Deconjugation activity was maximum in the late exponential phase of growth, which also coincided with maximum assimilation of cholesterol. Considerable variation existed among cultures in their ability to grow in the presence of bile, to deconjugate sodium taurocholate, and to assimilate cholesterol. However, statistical analyses revealed no significant correlations.

Bile↗