Antioxidant, antimicrobial and anticancer activity of the lichens Cladonia furcata, Lecanora atra and Lecanora muralis

<p>Abstract</p> <p>Background</p> <p>The aim of this study is to investigate in vitro antioxidant, antimicrobial and anticancer activity of the acetone extracts of the lichens <it>Cladonia furcata, Lecanora atra </it>and <it>Lecanora muralis</it>.</p> <p>Methods</p> <p>Antioxidant activity was evaluated by five separate methods: free radical scavenging, superoxide anion radical scavenging, reducing power, determination of total phenolic compounds and determination of total flavonoid content. The antimicrobial activity was estimated by determination of the minimal inhibitory concentration by the broth microdilution method against six species of bacteria and ten species of fungi. Anticancer activity was tested against FemX (human melanoma) and LS174 (human colon carcinoma) cell lines using MTT method.</p> <p>Results</p> <p>Of the lichens tested, <it>Lecanora atra </it>had largest free radical scavenging activity (94.7% inhibition), which was greater than the standard antioxidants. Moreover, the tested extracts had effective reducing power and superoxide anion radical scavenging. The strong relationships between total phenolic and flavonoid contents and the antioxidant effect of tested extracts were observed. Extract of <it>Cladonia furcata </it>was the most active antimicrobial agent with minimum inhibitory concentration values ranging from 0.78 to 25 mg/mL. All extracts were found to be strong anticancer activity toward both cell lines with IC₅₀values ranging from 8.51 to 40.22 μg/mL.</p> <p>Conclusions</p> <p>The present study shows that tested lichen extracts demonstrated a strong antioxidant, antimicrobial and anticancer effects. That suggest that lichens may be used as as possible natural antioxidant, antimicrobial and anticancer agents to control various human, animal and plant diseases.</p

'-Azobispyridine (abpy), (mu-abpy)[Cd(HsaI)(2)(abpy)](2)

mu-2,2'-Azobispyridinebis[2,2'-azobispyridinesalicylato(O)-salicylato(O,O') cadmium(II), (mu-abpY)[Cd(HsaI)(2)(abpy)](2) (I) was synthesized and characterized by IR and UV/Vis spectroscopy, thermal analysis, and X-ray diffraction techniques. Two abpy ligands and two salicylato ligands coordinate to the Cd2+ ion in a monocapped trigonal-prismatic arrangement. The capping atom is the N3 atom. One of the two abpy ligands behaves as a "s-frame" bridging ligand and adopts a s-cis/E/s-cis conformation, whereas the other one adopts as a s-cis/E/s-trans conformation. One of the two salicylato ligands acts as a monodentate ligand, which coordinates with the carboxylate oxygen atom, whereas the other one adopts bidentate coordination through two carboxylate oxygen atoms. The hydroxy groups of salicylato ligands, which coordinate in a monodentate fashion, are disordered over two positions, with occupancies of 0.52 for group A and 0.48 for group B. The decomposition reaction takes place in the temperature range 20-1000 degrees C under nitrogen. Thermal decomposition of the title complex proceeds in two stages

bis[(R)-(-)-hydroxymethylpropylimine o-vanillinato]copper(II)

The novel complexes bis(o-vanillinato)-triethylenglycoldiiminecopper(II) (1) and bis[(R)-(-)-hydroxymethylpropylimine o-vanillinato]copper(II) (2) have been synthesized and characterized by elemental analysis, magnetic susceptibility, spectral methods (UV-Vis and FT-IR), simultaneous TG, DTA techniques and X-ray diffraction. The crystal structure of (1) determined that the Cu atom is coordinated by two imine N atoms and two phenol O atoms from the Schiff base ligand in a slightly distorted square-planar coordination. The o-vanillinato ligands moieties of the molecule are in a trans configuration and the dihedral angle between the aromatic ring planes is 43.97(14)degrees. Compound (2) crystallizes in the triclinic space group P (1) over bar with unit-cell parameters a = 8.054(7), b = 8.684(7), c = 10.258(8) angstrom, alpha = 79.452(6)degrees, beta = 70.454(6)degrees, gamma = 65.427(6)degrees and Z = 1. The crystal structure of (2) has indicated that the complex is slightly distorted square planar and is chelated by the two imine N atoms and two phenol O atoms from the Schiff base ligand. The o-vanillinato ligands moieties of (2) are in a trans configuration and the torsion angle between the aromatic ring planes is 60.5(3)degrees. The crystal packing involves both hydrogen-bonding and C-H center dot center dot center dot pi interactions. Thermal analyses showed that the title compounds decompose in two stages over the temperature range 20-1000 degrees C in a static air atmosphere. (C) 2009 Elsevier Ltd. All rights reserved

Gastroprotective and antioxidant effects of montelukast on indomethacin-induced gastric ulcer in rats

Montelukast, a selective reversible cysteinyl leukotriene D4-receptor (LTD4 receptor) antagonist, is used in the treatment of asthma. We have investigated alterations in the glutathione (GSH) and activity levels of antioxidative enzymes [superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), and glutathione reductase (GR)] and myeloperoxidase (MPO), as markers of the ulceration process following oral administration of montelukast, lansoprazole, famotidine, and ranitidine, respectively, in rats with indomethacin-induced ulcers. In the present study, we found that 1) montelukast, lansoprazole, famotidine, and ranitidine all reduced the development of indomethacin-induced gastric damage, with this reduction occurring at a greater magnitude for montelukast, famotidine, and lansoprazole than for ranitidine; 2) montelukast and ranitidine both alleviated increases in the activity levels of CAT and GST enzymes resulting from gastric injury; 3) montelukast and ranitidine both ameliorated depressions in the GSH and activity levels of SOD and GR enzymes caused by indomethacin administration; and 4) all doses of montelukast, lansoprazole, and ranitidine decreased amplification of MPO activity resulting from induced gastric injuries. These results suggest that the gastroprotective effects of montelukast on indomethacin-induced ulcerations can be attributed to its ameliorating effect on oxidative damage and MPO activity. ©2007 The Japanese Pharmacological Society

Gastroprotective and antioxidant effects of amiodarone on lndomethacin-induced gastric ulcers in rats

WOS: 000251242300011PubMed: 18087811Reactive oxygen species (ROS) have been implicated in the etiology-of indomethacin-induced gastric mucosal damage. This study investigated amiodarone's protective effects against oxidative gastric mucosal damage induced by indomethacin. Amiodarone is a widely used antiarrhythmic agent. We have investigated alterations in the glutathione level, and the activities of antioxidative enzymes [superoxide dismutase, catalase, glutathione s-transferase glutathione reductase and myeloperoxidase], as markers for ulceration process following oral administration of amiodarone and ranitidine in rats with indomethacin-induced ulcers. In the present study we found that 1) amiodarone, lansoprazole and ranitidine reduced the development of indomethacin-induced gastric damages, at a greater magnitude for amiodarone and lansoprazole than for ranitidine; 2) arniodarone and ranitidine alleviated increases in the activities of catalase and glutathione s-transferase enzymes resulting from ulcers; 3) arniodarone and ranitidine ameliorated depressions in the glutathione level and the activities of superoxide dismutase and glutathione reductase enzymes caused by indomethacin administration; and 4) all doses of amiodarone amplified the myeloperoxidase activity resulting from indomethacin-induced gastric ulcers. The results indicate that the gastroprotective activity of arniodarone, which may be linked to its intrinsic antioxidant properties, cannot be attributed to its effect on myeloperoxidase activity

Amiodarone has anti-inflammatory and anti-oxidative properties: An experimental study in rats with carrageenan-induced paw edema

Amiodarone is a widely used anti-arrhythmic agent. We have investigated alterations in the glutathione (GSH) level and the activities of anti-oxidative enzymes (superoxide dismutase, catalase, glutathione s-transferase and glutathione reductase) and myeloperoxidase, as marker of acute inflammation, following oral administration of amiodarone and diclofenac in rats with carrageenan-induced paw edema. In the present study, we found that 1) Amiodarone reduced the development of carrageenan-induced paw edema, to a greater degree than diclofenac; 2) Amiodarone and diclofenac alleviated increases in the activities of catalase and glutathione s-transferase enzymes resulting from edema; 3) Amiodarone and diclofenac ameliorated depressions in the GSH level and the activities of superoxide dismutase and glutathione reductase enzymes caused by carrageenan injection; and 4) All doses of amiodarone and diclofenac caused an amplification in myeloperoxidase activity resulting from induced paw edema. These results suggest that the anti-inflammatory effect of amiodarone on carrageenan-induced acute inflammation can be attributed to its ameliorating effect on the oxidative damage. © 2007 Elsevier B.V. All rights reserved

Gastroprotective and antioxidant effects of amiodarone on indomethacin-induced gastric ulcers in rats

Reactive oxygen species (ROS) have been implicated in the etiology of indomethacin-induced gastric mucosal damage. This study investigated amiodarone's protective effects against oxidative gastric mucosal damage induced by indomethacin. Amiodarone is a widely used antiarrhythmic agent. We have investigated alterations in the glutathione level, and the activities of antioxidative enzymes [superoxide dismutase, catalase, glutathione s-transferase glutathione reductase and myeloperoxidase], as markers for ulceration process following oral administration of amiodarone and ranitidine in rats with indomethacin-induced ulcers. In the present study we found that 1) amiodarone, lansoprazole and ranitidine reduced the development of indomethacin-induced gastric damages, at a greater magnitude for amiodarone and lansoprazole than for ranitidine; 2) amiodarone and ranitidine alleviated increases in the activities of catalase and glutathione s-transferase enzymes resulting from ulcers; 3) amiodarone and ranitidine ameliorated depressions in the glutathione level and the activities of superoxide dismutase and glutathione reductase enzymes caused by indomethacin administration; and 4) all doses of amiodarone amplified the myeloperoxidase activity resulting from indomethacin-induced gastric ulcers. The results indicate that the gastroprotective activity of amiodarone, which may be linked to its intrinsic antioxidant properties, cannot be attributed to its effect on myeloperoxidase activity