The enzymic deacetylation of 4-acetamidobenzoic acid by rat tissues and the effect of manganese ions.
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Acetamides↗
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Results for “THIOGLYCOLLIC ACID”
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Extract of gum resins of Boswellia serrata L. inhibits lipopolysaccharide induced nitric oxide production in rat macrophages along with hypolipidemic property.
Boswellia serrata, Linn F (Burseraceae) is commonly used in Indian system of medicine (Ayurvedic) as an anti-inflammatory, analgesic, anti-arthritic and anti-proliferative agent. This study was planned to investigate the water-soluble fraction of the oleoresin gum of Boswellia serrata (BS extract) on lipopolysaccharide (LPS) induced nitric oxide (NO) production by macrophages under in vivo and in vitro conditions. In the previous condition, rats were fed on atherogenic diet (2.5% cholesterol, 1% cholic acid, 15.7 % saturated fat) along with the BS extract for 90 days. Blood was collected for lipid profile and toxicological safety parameters. Peritoneal macrophages were isolated and cultured to see the LPS induced NO production. Under in vivo experiment, BS extract significantly reduced serum total cholesterol (38-48 %), increased serum high-density lipoprotein- cholesterol (HDL-cholesterol, 22-30%). Under in vitro experiments with thioglycolate activated macrophages, it inhibited LPS induced (NO) production with IC 50 value at 662 ng /ml. Further, this fraction, in the dose of 15 mg/100 g body wt for 90 days, did not show any increase in serum glutamate-pyruvate transaminase (SGPT) and blood urea, in normal control animals. However, it significantly reversed the raised SGPT and blood urea in the atherogenic diet-fed animals. Transverse section of liver and kidney also supported its protective effect. Thus it may be concluded that water extract of Boswellia serrata possesses strong hypocholesterolemic property along with increase in serum HDL. It inhibits the LPS induced NO production by the activated rat peritoneal macrophages and show hepato-protective and reno-protective property.
Animals↗
Effect of tumour growth on the macrophage response to the antitumour agent 5,6-dimethylxanthenone-4-acetic acid.
Peritoneal macrophages from C3H/HeN mice bearing subcutaneous M-16/C or Spon-2 mammary carcinomas had enhanced tumouricidal activity over control macrophages from non-tumour bearers in response to 5,6-dimethylxanthenone-4-acetic acid (5,6-MeXAA), a novel antitumour agent which has been scheduled for clinical evaluation. The effect of a palpable M-16/C tumour growing in C3H/HeN mice was similar to that of Bacillus Calmette-Guerin (BCG) infection, with macrophages being fully activated and tumouricidal without any further stimulus being required in culture. Macrophages from Spon-2 tumour bearing mice behaved like "primed" thioglycollate-elicited macrophages and produced a tumouricidal response to 5,6-MeXXA which was significantly higher than that obtained from resident peritoneal macrophages from non-tumour bearing mice. Resident and thioglycollate-elicited macrophages from C3H/HeJ mice were hyporesponsive not only to lipopolysaccharide (LPS), but to 5,6-MeXAA as well. Hyporesponsiveness was abrogated by BCG infection or by the presence of the M-16/C tumour, but not by the presence of the Spon-2 tumour. In response to LPS at low concentrations, or to 5,6-MeXAA at all concentrations, tumouricidal activity from macrophages from Spon-2-bearing C3H/HeJ mice was severely depressed compared with activity from their C3H/HeN counterparts. However, 5,6-MeXAA induced similar levels of haemorrhagic necrosis of tumours implanted in either C3H/HeJ or C3H/HeN hosts. LPS-induced haemorrhagic necrosis was significantly lower in C3H/HeJ than in C3H/HeN hosts. The results show that the presence of subcutaneous tumours modulates the activity of peritoneal macrophages in mice.
Animals↗
Biosynthesis of membrane factor B by mouse peritoneal macrophages.
The biosynthesis of many of the complement proteins by cells of the monocyte-macrophage series has been established. Studies on these cells using radiolabelled amino acids demonstrated synthesis of precursor proteins (pro-complement), and the native complement protein similar in size to that found in the plasma. However, synthesis of membrane complement proteins has not been demonstrated, although it has been suggested by previous studies using indirect techniques. In particular, there is evidence for the membrane-associated factor B in human lymphocytes. We report here that resident and thioglycollate-stimulated mouse peritoneal macrophages synthesized, in short-term primary cultures membrane factor B of molecular weight (MW) 95,000 and secreted factor B (MW 90,000) as single chain polypeptides. We also found a large single chain polypeptide with an approximate molecular weight of 195,000, which may be the putative factor B precursor.
Animals↗
Adjuvant activity of purified peptidoglycan of Listeria monocytogenes in mice and guinea pigs.
The immunological properties of peptidoglycan (L-PG) purified from the cell wall skeleton (L-CWS) of Listeria monocytogenes strain EGD were investigated and compared with the properties of L-CWS. L-PG consisted of alanine, glutamic acid, alpha, epsilon-diaminopimelic acid, muramic acid, and glucosamine. L-PG showed potent adjuvant activities for circulating antibody formation and development of delayed-type hypersensitivity to bacterial alpha-amylase in vivo and for the primary immune response to sheep erythrocytes in vitro, as well as L-CWS. Both L-PG and L-CWS enhanced the generation of cell-mediated cytotoxicity in allogeneic mice and activated thioglycolate-elicited peritoneal macrophages and macrophage cell line RAW 264 to kill tumor target cells in vitro. We also found that L-PG acted on normal spleen cells as a mitogen. Both L-PG and L-CWS had tumor (Meth A)-suppressive and -regressive activities in syngeneic mice. Our results suggest that the L-PG moiety retains the adjuvant and antitumor activities of L-CWS.
Adjuvants, Immunologic↗
Feeding response to mercaptoacetate in Osborne-Mendel and S5B/PL rats.
The purpose of this experiment was to determine if Osborne-Mendel (OM) rats, which are susceptible to dietary-induced obesity, and S5B/PL (S5B) rats, which are resistant to dietary-induced obesity, differ in their feeding responses to mercaptoacetate (MA), which blocks fatty acid oxidation, or 2-deoxy-D-glucose (2DG), which blocks glucose utilization. 2DG (100 mg/kg or 200 mg/kg) increased food intake in both strains of rats on a high-fat diet (56% energy from fat). Mercaptoacetate (600 mumol/kg) increased food intake in OM but not S5B rats on a high-fat diet. When maintained on a low-fat diet (10% energy from fat), MA (400 mumol/kg or 600 mumol/kg) stimulated food intake in OM rats, whereas S5B rats increased food intake only after the highest dose of MA (600 mumol/kg). MA stimulated carbohydrate and protein intake in OM rats maintained on a macronutrient selection diet, whereas S5B rats maintained on this diet did not significantly increase intake of any macronutrient after MA. These results demonstrate that OM and S5B rats have a similar food intake response to 2DG but a dissimilar response to MA. The variable response to MA in these strains may be due to a difference in peripheral or central signaling systems related to fatty acid oxidation or a difference in metabolic environments between the strains, which in turn affects the feeding response to MA. These studies suggest that a difference in control of fatty acid oxidation may account for the difference in susceptibility to obesity when eating a high-fat diet.
Animals↗
Hydrogen production from glucose by anaerobes.
Various anaerobes were cultivated in media containing glucose. When 100 mL of thioglycollate medium containing 2.0% (w/v) glucose was used, Clostridium butyricum ATCC 859, NBRC 3315, and NBRC 13949 evolved 227-243 mL of biogas containing about 180 mL of hydrogen in 1 day. Although some strains had some resistance against oxygen, C. butyricum ATCC 859 and 860 did not have it. C. butyricum NBRC 3315 and Enterobacter aerogenes NBRC 13534 produced hydrogen in the presence of glucose or pyruvic acid, and E. aerogenes NBRC 13534 produced hydrogen by not only glucose and pyruvic acid but also dextrin, sucrose, maltose, galactose, fructose, mannose, and mannitol. When a medium containing 0.5% (w/v) yeast extract and 2.0% (w/v) glucose was used, E. aerogenes NBRC 13534 evolved more biogas and hydrogen than C. butyricum NBRC 3315 in the absence of reducing agent.
Bacteria, Anaerobic↗
Suppression of in vitro cytotoxic response by macrophages due to induced arginase.
Arginine was found to be completely depleted from cell-free supernates of mixed leukocyte cultures suppressed by the addition of excess macrophages. Partial reversal of macrophage-mediated suppression was accomplished by daily addition of a cocktail containing arginine and nonamino acid nutrients. Complete reversal of the suppression was accomplished by the addition of arginine and glucose to the medium and the nonadherent cells after their separation from the adherent macrophages. A marked increase in the enzyme arginase was found in macrophages that had been cultured 24 h in vitro in Eagle's minimum essential medium plus 10% fetal calf serum, in peritoneal cells activated by prior injection of thioglycollate, and in one spleen activated by a graft vs. host reaction.
Animals↗
Cyclic AMP and the regulation of prostaglandin production by macrophages.
The ionophore A23187 (6.7 microM) increased the rates of formation of prostaglandins and cyclic AMP in suspensions of thioglycollate-elicited rat peritoneal macrophages. Both effects were inhibited by the calmodulin blocker trifluoperazine (50 microM) and the calcium channel blocker verapamil (500 microM). Inhibitors of phospholipase A2 and cyclo-oxygenase also blocked both actions of A23187. The stimulated prostaglandin formation was markedly reduced when the cells were preincubated with 8-bromo-cyclic AMP (1mM), dibutyryl cyclic AMP (1mM) or cholera toxin (500ng/ml). Addition of exogenous arachidonic acid (30 microM) alleviated this inhibition. We propose that the effect of A23187 on macrophages includes a 'self-limiting' mechanism whereby newly-synthesized prostaglandins can inhibit, via cyclic AMP, a step(s) prior to the transformation of arachidonic acid and thus modulate their own production.
8-Bromo Cyclic Adenosine Monophosphate↗
Biosynthesis of porphyrins in Rhodopseudomonas palustris--VI. The effect of metals, thiols and other reagents on the activity of uroporphyrinogen decarboxylase.
The effect of several metals and reagents on the decarboxylation rate of uroporphyrinogen I by using a 16-fold purified preparation of Uroporphyrinogen Decarboxylase from Rhodopseudomonas palustris, was studied. 1 mM Hg2+ and Cu2+ were strong inhibitors, 1 mM Zn2+ and Fe2+ under certain conditions and 1 mM Fe3+ and Cr3+ also inactivated the enzyme, but Pb2+, Cd2+ and Al3+ did not. Metals inhibition was reversed by 1 mM GSH or CySH. 0.1 mM DTNB and PCMB, 1 mM pyridoxal phosphate and 100 mM chloral hydrate, as well as 1 mM 2-methoxy-5-nitrotropone and 0.2 mM diethylpyrocarbonate inhibited Uroporphyrinogen Decarboxylase; while GSH, CySH, N-ethylmaleimide, sodium thioglycolate, 1,4-dithioerythritol, EDTA and O-phenantroline did not modify activity. Data obtained would indicate that one cysteine, one or two histidine residues and probably a lysine group are required for enzyme activity.
Carboxy-Lyases↗
Therapeutic potential of a novel synthetic selectin blocker, OJ-R9188, in allergic dermatitis.
1. We investigated the ability of a newly synthesized sugar derivative, OJ-R9188, [N-(2-tetradecylhexadecanoyl)-O-(L-alpha-fucofuranosyl)-D-seryl]-L-glutamic acid 1-methylamide 5-L-arginine salt, to block binding of selectins to their ligands in vitro and inhibit the infiltration of leukocytes in vivo. 2. OJ-R9188 prevented the binding of human E-, P- and L-selectin-IgG fusion proteins to immobilized sialyl Lewis(x) (sLe(x))-pentasaccharide glycolipid, with IC(50) values of 4.3, 1.3, and 1.2 microM, respectively. 3. In a mouse model of thioglycollate-induced peritonitis, OJ-R9188 at 10 mg kg(-1), i.v. inhibited neutrophil accumulation in the peritoneal cavity. In the IgE-mediated skin reaction, OJ-R9188 at 3 and 10 mg kg(-1), i.v. significantly inhibited extravasation of neutrophils and eosinophils into the inflammatory sites and at 10 mg kg(-1), i.v. also inhibited infiltration caused by picryl chloride-induced delayed-type hypersensitivity in mice. These results suggest that OJ-R9188 may be a useful selectin blocker, with activity against human and mouse E-, P- and L-selectins in vitro and in vivo, and that blocking selectin-sLe(x) binding is a promising strategy for the treatment of allergic skin diseases.
Animals↗
Uptake and deacylation of bacterial lipopolysaccharides by macrophages from normal and endotoxin-hyporesponsive mice.
Macrophages are thought to play a central role in the responses of animals to gram-negative bacterial lipopolysaccharides (LPS). Since nothing is known about the metabolism of LPS by these cells, we studied the uptake and deacylation of radiolabeled LPS by thioglycolate-elicited peritoneal macrophages from normal (C3H/HeN) and LPS-hyporesponsive (C3H/HeJ) mice. Macrophages from both kinds of mice took up and deacylated LPS that were added to the culture medium. Opsonization of the LPS with anti-LPS immunoglobulin G antibodies greatly increased LPS uptake; the opsonized LPS also underwent deacylation at rates that were directly related to the amount of cell-associated LPS. An analysis of the fatty acid composition of the cell-associated LPS indicated that the cells have one or more acyloxyacyl hydrolases that remove the non-hydroxylated fatty acids that are normally substituted to the hydroxyl groups of (glucosamine-linked) 3-hydroxytetradecanoate residues in lipid A; we also found evidence for deacylation of 3-hydroxytetradecanoate from the glucosamine backbone. LPS deacylation by macrophages from C3H/HeN and C3H/HeJ mice was qualitatively and quantitatively similar. Nonopsonized LPS are able to stimulate LPS-responsive cells; in these studies we established that animal cells can deacylate nonopsonized LPS, thus raising the possibility that LPS metabolism may play a role in modulating cellular stimulation.
Animals↗
Discordance between macrophage arachidonate metabolic phenotype and the expression of cytosolic phospholipase A2 and cyclooxygenase.
Macrophages (M phi s) exhibit variations in their ability to release and metabolize arachidonate (AA) depending on their state of activation, differentiation, and tissue origin. In order to understand these variations on a molecular level, we determined whether differences in AA release and metabolism by murine peritoneal M phi s could be explained in terms of cytosolic phospholipase A2 (cPLA2) and cyclooxygenase (COX) expression. Resident M phi s exhibited greater COX capacity (conversion of exogenous AA to PGE2) but lower phospholipase (PLase) activity (release of endogenous AA) than elicited M phi s. Activation of resident M phi s in vivo with endotoxin increased both their PLase activity and COX capacity. Despite the observed differences in PLase activity, peritoneal M phi s under all conditions expressed similar amounts of cPLA2 mRNA and protein. All M phi s exhibited COX-1 mRNA and protein (i.e., the constitutive isoform of COX), although elicited M phi s exhibited increased mRNA for COX-1 but decreased levels of protein, relative to resident M phi s. Elicited (but not resident) cells also exhibited COX-2 mRNA but not COX-2 protein (i.e., the inducible form of COX). Despite the increased COX capacity of resident cells with in vivo activation, their expression of COX-2 mRNA and protein was equivalent to that of unactivated cells, becoming apparent only after cell adherence in vitro. In sum, there is no simple relationship between the ability of M phi s to release and metabolize AA, and the expression of cPLA2 or COX isoforms. Moreover, adherence appears to be important for the expression of COX-2 by M phi s.
Analysis of Variance↗
Nutrition of five Bacteroides strains.
Quinto, Grace (University of Kentucky College of Medicine, Lexington). Nutrition of five Bacteroides strains. J. Bacteriol. 84:559-562. 1962.-Some of the nutritional requirements of five gram-negative anaerobic bacilli, including Ristella perfoetens, Zuberella clostridiformis, and three Bacteroides strains freshly isolated from clinical exudates, were investigated. A fluid maintenance medium was developed in which the three freshly isolated strains, C-4, C-7, and C-2795, grew maximally in 12 to 24 hr. The maintenance medium contained 2.0% Trypticase and Proteose Peptone, 0.5% glucose, and 0.1% sodium thioglycolate; it was adjusted to pH 7.2 and supplemented with 0.1 mug of hemin/ml. Strains C-4, C-7, and C-2795 were cultivated through 14 serial cultures in fluid maintenance medium containing 0.1 mug of hemin/ml. The most satisfactory inoculum was a 1:100 or 1:1,000 dilution of a 24-hr seed culture. All the strains except Z. clostridiformis grew serially in a defined medium. R. perfoetens required pantothenic acid, nicotinic acid, and the following amino acids: histidine, tryptophan, tyrosine, valine, phenylalanine, cystine, and probably arginine, glutamic acid, methionine, glycine, isoleucine, leucine, and lysine. The C-4, C-7, and C-2795 strains required the hemin supplement in defined medium, but not vitamins, purines, or pyrimidines.
Amino Acids↗
Regulation of plasminogen binding to neutrophils.
Plasminogen plays an integral role in the inflammatory response, and this participation is likely to depend on its interaction with cell surfaces. It has previously been reported that isolation of human neutrophils from blood leads to a spontaneous increase in their plasminogen-binding capacity, and the basis for this up-regulation has been explored as a model for mechanisms for modulation of plasminogen receptor expression. Freshly isolated human peripheral blood neutrophils exhibited relatively low plasminogen binding, but when cultured for 20 hours, they increased this capacity dramatically, up to 50-fold. This increase was abolished by soybean trypsin inhibitor and was susceptible to carboxypeptidase B treatment, implicating proteolysis and exposure of carboxy-terminal lysines in the enhanced interaction. In support of this hypothesis, treatment of neutrophils with elastase, cathepsin G, or plasmin increased their plasminogen binding, and specific inhibitors of elastase and cathepsin G suppressed the up-regulation that occurred during neutrophil culture. When neutrophils were stimulated with phorbol ester, their plasminogen binding increased rapidly, but this increase was insensitive to the protease inhibitors. These results indicate that plasminogen binding to neutrophils can be up-regulated by 2 distinct pathways. A major pathway with the propensity to markedly up-regulate plasminogen binding depends upon the proteolytic remodeling of the cell surface. In response to thioglycollate, neutrophils recruited into the peritoneum of mice were shown to bind more plasminogen than those in peripheral blood, suggesting that modulation of plasminogen binding by these or other pathways may also occur in vivo.
Amino Acid Chloromethyl Ketones↗
Antimicrobial activity of the leprostatic drug 3-(p-chloranilino)-10(p-chlorphenyl)-2,10-dihydro-2-(isopropylimino)-phenazine (G 30 320). I. Studies in vitro.
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Amino Acids↗
Suppression of fibroblast proliferation by activated macrophages: involvement of H2O2 and a non-prostaglandin E product of the cyclooxygenase pathway.
Macrophages are considered promoters of fibroblast proliferation; however, suppression by activated macrophages may outweigh this effect. Activated murine peritoneal macrophages obtained by in vivo exposure to C. parvum or by in vitro LPS-activation of thioglycollate-induced macrophages, were tested for their effect on normal syngeneic dermal fibroblasts. C. parvum-activated macrophages, but not resident peritoneal macrophages suppressed fibroblast proliferation. Similarly, macrophages activated in vitro by LPS, but not those unexposed to LPS, suppressed fibroblast proliferation. Catalase partially protected fibroblasts from suppression by either activated macrophage population, suggesting involvement of H2O2 in the suppression. The effect of cyclooxygenase inhibitors on the suppression was also tested. Indomethacin, acetylsalicyclic acid, or eicosatetraynoic acid, all partially protected the fibroblasts from macrophage-mediated suppression. Prostaglandins E2, E1, and F2 alpha, added exogenously at concentrations as high as 10(-6) M, failed to suppress the proliferation of the fibroblasts. These findings suggest that a non-prostaglandin product of the cyclooxygenase pathway is involved in macrophage-mediated suppression of fibroblast proliferation.
Animals↗
Transformation of thiodiglycol by resting cells of Alcaligenes xylosoxydans PGH10.
A new strain of Alcaligenes xylosoxydans able to aerobically cometabolize thiodiglycol, the primary hydrolysis product of sulfur mustard, was isolated and tested in a laboratory scale stirred tank reactor. The strain, named PGH10, cannot use TDG as sole carbon and energy source for growth, but resting cells previously grown on either rich broth or defined mineral media efficiently metabolize this compound through [(2-hydroxyethyl)thio]acetic acid and thiodiacetic acid as intermediates. Degradation of TDG by PGH10 is shown to take place at late exponential and stationary phase but is not triggered by carbon exhaustion. Cultures pregrown to saturation for 48 h in the absence of TDG can be stored and used for degradation of TDG, reducing significantly the time required to achieve the reduction of the compound concentration to undetectable levels. Degradation can take place in buffered media with no carbon source added, although best results were obtained in mineral media supplemented with citrate or fructose. Oxidation to [(2-hydroxyethyl)thio]acetic acid and thiodiacetic acid was proposed to be catalyzed by a butanol-dehydrogenase activity. Inhibition of TDG transformation in the presence of several alcohols is also shown.
Alcaligenes↗