ABSTRACT
The present study aimed to characterize the chlorogenic acid (ChlA) capacity to reverse the toxic effects induced by ochratoxin A (OTA) in a subacute toxicity test in rats. Male Wistar rats were fed orally by gavage for 28 days with OTA (0.4mg/kg bw/day), ChlA (5mg/kg bw/day) or the combination OTA (0.4mg/kg bw/day)+ChlA (5mg/kg bw/day). No deaths, no decrease in feed intake or body weight in any experimental group were recorded. The negative control group and the animals treated with ChlA alone showed no changes in any parameters evaluated. In OTA-treated group significant changes such as decrease in urine volume, proteinuria, occult blood, increase in serum creatinine values; decrease in absolute and relative kidney weight and characteristics histopathological lesions that indicated kidney damage were observed. However, limited effect on oxidative stress parameters were detected in kidneys of OTA-treated group. Animals treated with the combination OTA+ChlA were showed as negative control group in the evaluation of several parameters of toxicity. In conclusion, ChlA, at given concentration, improved biochemical parameters altered in urine and serum and pathological damages in kidneys induced by OTA exposure, showing a good protective activity, but not by an apparent antioxidant mechanism.
Subject(s)
Carcinogens/toxicity , Hydroxybenzoates/pharmacology , Ochratoxins/toxicity , Protective Agents/pharmacology , Animals , Kidney/drug effects , Male , Oxidative Stress/drug effects , Rats , Rats, Wistar , Toxicity Tests, ChronicABSTRACT
The aqueous fraction of the ethanolic extract (AFL) of Cissampelos sympodialis Eichl (Menispermaceae), popularly known as milona, has been shown to have both immunosuppressive and anti-inflammatory effects. In the present study we investigated the modulation of macrophage antimicrobicidal activity by in vitro treatment with the extract from C. sympodialis. Normal and thioglycolate-elicited mouse peritoneal macrophages were infected in vitro with the protozoan Trypanosoma cruzi DM28c clone. We observed that the AFL (used at doses ranging from 13 to 100 microg/ml) increased T. cruzi growth and induced a 75% reduction in nitric oxide production. This inhibition could be mediated by the stimulation of macrophage interleukin-10 (IL-10) secretion since the in vitro treatment with the AFL stimulated IL-10 production by T. cruzi-infected macrophages. These results suggest that the anti-inflammatory effect of the AFL from C. sympodialis could be, at least in part, mediated by the inhibition of macrophage functions and that the inhibition of macrophage microbicidal activity induced by the C. sympodialis extract may be mediated by the decrease in macrophage function mediated by interleukin-10 production.
Subject(s)
Anti-Inflammatory Agents/pharmacology , Cissampelos/chemistry , Interleukin-10/biosynthesis , Macrophages, Peritoneal/drug effects , Plant Extracts/pharmacology , Trypanosoma cruzi/drug effects , Animals , Cells, Cultured , Female , Macrophage Activation/drug effects , Macrophages, Peritoneal/parasitology , Macrophages, Peritoneal/physiology , Male , Mice , Mice, Inbred BALB C , Nitric Oxide/biosynthesis , Plant Leaves , Trypanosoma cruzi/growth & developmentABSTRACT
The aqueous fraction of the ethanolic extract (AFL) of Cissampelos sympodialis Eichl (Menispermaceae), popularly known as milona, has been shown to have both immunosuppressive and anti-inflammatory effects. In the present study we investigated the modulation of macrophage antimicrobicidal activity by in vitro treatment with the extract from C. sympodialis. Normal and thioglycolate-elicited mouse peritoneal macrophages were infected in vitro with the protozoan Trypanosoma cruzi DM28c clone. We observed that the AFL (used at doses ranging from 13 to 100 æg/ml) increased T. cruzi growth and induced a 75 percent reduction in nitric oxide production. This inhibition could be mediated by the stimulation of macrophage interleukin-10 (IL-10) secretion since the in vitro treatment with the AFL stimulated IL-10 production by T. cruzi-infected macrophages. These results suggest that the anti-inflammatory effect of the AFL from C. sympodialis could be, at least in part, mediated by the inhibition of macrophage functions and that the inhibition of macrophage microbicidal activity induced by the C. sympodialis extract may be mediated by the decrease in macrophage function mediated by interleukin-10 production
Subject(s)
Animals , Male , Female , Mice , Anti-Inflammatory Agents , Cissampelos/chemistry , Interleukin-10 , Macrophages, Peritoneal , Plant Extracts , Trypanosoma cruzi , Cells, Cultured , Macrophage Activation , Macrophages, Peritoneal , Mice, Inbred BALB C , Nitric Oxide , Plant Leaves , Trypanosoma cruziABSTRACT
After apoptosis, phagocytes prevent inflammation and tissue damage by the uptake and removal of dead cells. In addition, apoptotic cells evoke an anti-inflammatory response through macrophages. We have previously shown that there is intense lymphocyte apoptosis in an experimental model of Chagas' disease, a debilitating cardiac illness caused by the protozoan Trypanosoma cruzi. Here we show that the interaction of apoptotic, but not necrotic T lymphocytes with macrophages infected with T. cruzi fuels parasite growth in a manner dependent on prostaglandins, transforming growth factor-beta (TGF-beta) and polyamine biosynthesis. We show that the vitronectin receptor is critical, in both apoptotic-cell cytoadherence and the induction of prostaglandin E2/TGF-beta release and ornithine decarboxylase activity in macrophages. A single injection of apoptotic cells in infected mice increases parasitaemia, whereas treatment with cyclooxygenase inhibitors almost completely ablates it in vivo. These results suggest that continual lymphocyte apoptosis and phagocytosis of apoptotic cells by macrophages have a role in parasite persistence in the host, and that cyclooxygenase inhibitors have potential therapeutic application in the control of parasite replication and spread in Chagas' disease.
Subject(s)
Apoptosis , Macrophages/parasitology , T-Lymphocytes/physiology , Trypanosoma cruzi/growth & development , Amino Acid Chloromethyl Ketones/pharmacology , Animals , Cells, Cultured , Chagas Disease/immunology , Chagas Disease/parasitology , Cysteine Proteinase Inhibitors/pharmacology , Dinoprostone/biosynthesis , Dinoprostone/physiology , Male , Mice , Mice, Inbred BALB C , Necrosis , Phagocytosis/physiology , Putrescine/biosynthesis , Putrescine/physiology , Receptors, Vitronectin/metabolism , T-Lymphocytes/drug effects , T-Lymphocytes/pathology , Transforming Growth Factor beta/physiologyABSTRACT
The effects of glycoinositolphospholipid (GIPL), from the pathogenic protozoan Trypanosoma cruzi, and its isolated glycan and lipid (dihydroceramide) components, were investigated in J774 cells and primary macrophages. Isolated GIPL ceramide, but not intact GIPL or its glycan, induced intense fluid phase endocytosis when added exogenously. In the presence of the cytokine IFN-gamma, GIPL ceramide induced marked apoptosis in J774 cells and macrophages, independent of nitric oxide secretion. When cells were preincubated with the GIPL-derived glycan chain, addition of intact GIPL induced macrophage apoptosis in the presence of IFN-gamma. Synthetic C2-dihydroceramide also induced apoptosis in the presence of IFN-gamma. Induction of apoptosis in T. cruzi-infected macrophages by GIPL ceramide plus IFN-gamma led to increased parasite release compared with IFN-gamma treatment alone. Viable parasites released comprised both infective trypomastigote and spheromastigote forms. These results identify a novel pathway by which T. cruzi glycosylphosphatidylinositol family molecules affect host macrophages, with implications for the infectious process.
Subject(s)
Apoptosis/drug effects , Gene Expression Regulation/drug effects , Glycolipids/pharmacology , Interferon-gamma/physiology , Macrophages, Peritoneal/parasitology , Phospholipids/pharmacology , Trypanosoma cruzi/chemistry , Animals , Ceramides/pharmacology , Drug Synergism , Endocytosis/drug effects , Female , Interferon-gamma/pharmacology , Lipopolysaccharides/pharmacology , Macrophages, Peritoneal/drug effects , Macrophages, Peritoneal/pathology , Mice , Mice, Inbred BALB C , Nitric Oxide/biosynthesis , Nitric Oxide Synthase/antagonists & inhibitors , Nitric Oxide Synthase/metabolism , Nitric Oxide Synthase Type II , Polysaccharides/pharmacology , Trypanosoma cruzi/immunology , Trypanosoma cruzi/pathogenicity , Tumor Cells, Cultured , Virulence , omega-N-Methylarginine/pharmacologyABSTRACT
An expansion of the utilisation of o-phthalaldehyde in sulphuric acid medium as spray reagent was carried out when tryptophan and some tryptophan-derived indole alkylamines such as tryptamine, serotonin, bufotenine, dehydrobufotenine and bufotenidine were examined by thin-layer chromatography. Rf-values and limits of detection ranging from 20 (serotonin) to 100 (dehydrobufotenine) ng per spot were found. Application of this reagent for the detection of some of these compounds was carried out, using either methanolic extracts or column chromatographic fractions of the skin secretion of the toads Bufo ictericus and Odontophrynus cultripes.
ABSTRACT
A simple method is described which can be used for the determination of certain sulphur compounds found in industrial ethanol obtained from fermentation of molasses. The method is based on the turbidimetric determination of sulphate after the sample has been treated with dilute hydrogen peroxide solution, by precipitation of the sulphate with barium chloride under appropriate conditions. Several samples of fermentation ethanol have been analysed by this method and the sulphur contents found compared with the total acidity.
