salicylates and 1-1-diphenyl-2-picrylhydrazyl

The aim of this study was to investigate the chemical composition of acetone extracts of the lichens Toninia candida and Usnea barbata and in vitro antioxidant, antimicrobial, and anticancer activities of these extracts together with some of their major metabolites. The chemical composition of T. candida and U. barbata extracts was determined using HPLC-UV analysis. The major phenolic compounds in these extracts were norstictic acid (T. candida) and usnic acid (U. barbata). Antioxidant activity was evaluated by free radical scavenging, superoxide anion radical scavenging, reducing power and determination of total phenolic compounds. Results of the study proved that norstictic acid had the largest antioxidant activity. The total content of phenols in the extracts was determined as the pyrocatechol equivalent. The antimicrobial activity was estimated by determination of the minimal inhibitory concentration using the broth microdilution method. The most active was usnic acid with minimum inhibitory concentration values ranging from 0.0008 to 0.5 mg/mL. Anticancer activity was tested against FemX (human melanoma) and LS174 (human colon carcinoma) cell lines using the microculture tetrazolium test. Usnic acid was found to have the strongest anticancer activity towards both cell lines with IC(50) values of 12.72 and 15.66 μg/mL.

Topics: Anti-Infective Agents; Antioxidants; Ascomycota; Bacteria; Benzofurans; Biphenyl Compounds; Cell Cycle; Cell Line, Tumor; Cell Survival; Fungi; Humans; Inhibitory Concentration 50; Lactones; Lichens; Microbial Sensitivity Tests; Molecular Structure; Phenols; Picrates; Salicylates; Usnea

Antioxidant activity of several classes of lichen metabolites were assessed in the in vitro superoxide radical (SOR), nitric oxide radical and 2,2-diphenyl-1-picrylhydrazil radical scavenging assays. The despsides sekikaic acid and lecanoric acid showed promising antioxidant activity in SOR assay with IC₅₀ values of 82.0 ± 0.3 µmol and 91.5 ± 2.1 µmol, respectively, while the depsidone lobaric acid exhibited an IC₅₀ value of 97.9 ± 1.6 µmol, all relative to the standard, propyl gallate (IC₅₀ = 106.0 ± 1.7 µmol). One of the most abundant mononuclear phenolic compounds, methyl-β-orcinol carboxylate was found to be a potent NO scavenger (IC₅₀ = 84.7 ± 0.1 µmol), compared to the standard rutin (IC₅₀ = 86.8 ± 1.9 µmol).

Topics: Antioxidants; Biphenyl Compounds; Chemical Fractionation; Complex Mixtures; Depsides; Enzyme-Linked Immunosorbent Assay; Free Radical Scavengers; In Vitro Techniques; Inhibitory Concentration 50; Lactones; Lichens; Molecular Structure; Nitric Oxide; Picrates; Salicylates; Species Specificity; Superoxides

The effects of paracetamol and sodium salicylate on the susceptibility of LDL to oxidative modification were studied. LDL was subjected to Cu(2+)-, azo compound-, or peripheral blood mononuclear cell-initiated oxidation in the absence and presence of paracetamol and salicylate. Paracetamol (100 mumol/L; 25 micrograms LDL/mL) reduced the rate of formation of conjugated dienes and the amount of conjugated dienes formed during Cu(2+)-induced oxidation by 67% and 58%, respectively. Paracetamol (400 mumol/L; 100 micrograms LDL/mL) reduced the generation of lipid peroxides during Cu(2+)-induced oxidation by 43% (P < .05), the relative electrophoretic mobility in agarose gels by 16% (P < .05), and the amount of oxidized LDL taken up by J774 macrophages by 22% (P < .05). Paracetamol (100 mumol/L; 100 micrograms LDL/mL) reduced the 2,2'-azobis-(2-amidinopropane hydrochloride)-initiated lipid peroxidation by 70% (P < .05) and the relative electrophoretic mobility by 34% (P < .05). Paracetamol (100 mumol/L; 100 micrograms LDL/mL) reduced the amount of lipid peroxides generated in LDL during mononuclear cell-mediated oxidation by 69% (P < .01) and the relative electrophoretic mobility by 38% (P < .01). In comparison, 10 mumol/L alpha-tocopherol reduced the amount of lipid peroxides formed during cellular LDL oxidation and the relative electrophoretic mobility by 52% and 65%, respectively (P < .05). In the absence of paracetamol, SOD and catalase inhibited the modification of LDL (P < .05), suggesting that superoxide anions and hydrogen peroxide might be involved in the cell-mediated modification pathway. In the presence of paracetamol, SOD showed no additional inhibitory effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acetaminophen; Amidines; Bepridil; Biphenyl Compounds; Catalase; Copper; Free Radical Scavengers; Humans; Kinetics; Leukocytes, Mononuclear; Lipid Peroxidation; Lipoproteins, LDL; Picrates; Salicylates; Salicylic Acid; Superoxide Dismutase

The action of the phenolic compounds acetaminophen, salicylate, and 5-aminosalicylate (5-ASA) as inhibitors of lipid peroxidation was studied under conditions suitable for establishing their antioxidant potencies. These phenolic compounds react differently with diphenylpicrylhydrazyl (DPPH) and protect differently sarcoplasmic reticulum membranes against lipid peroxidation induced by Fe2+/ascorbate, as evaluated by the formation of thiobarbituric acid-reactive substances (TBARS) and by the loss of the polyunsaturated fatty acyl chains. 5-Aminosalicylate reacts promptly with DPPH, suggesting a potent radical scavenger activity and was found to be the most active in inhibiting Fe2+/ascorbate-induced lipid peroxidation. These compounds also exhibit peroxyl radical scavenging activity generated by the water-soluble 2,2'-azobis-(2-amidinopropane hydrochloride) azoinitiator of peroxyl radicals, as evidenced by the inhibition of cis-parinaric acid fluorescence decay or oxygen consumption. 5-ASA rapidly scavenges peroxyl radicals in the aqueous phase, producing a concentration-dependent inhibition period similar to Trolox or cysteine, suggesting an antioxidant activity of chain-breaking type. By comparison, the reactivities of acetaminophen and salicylate are significantly weaker, acting essentially as oxidation retardants. Although closely related in structure, the antioxidant efficiencies of the three phenolic compounds are significantly different. The higher antioxidant activity of 5-ASA is putatively related with the p-amine relative to the hydroxyl group, potentially increasing the stability of the phenoxyl radical. Such a stabilization is not possible with salicylate and is decreased in acetaminophen by an electron withdrawing effect of the p-acetyl.

Topics: Acetaminophen; Aminosalicylic Acids; Animals; Bepridil; Biphenyl Compounds; Dose-Response Relationship, Drug; Fatty Acids; Fatty Acids, Unsaturated; Ferrozine; Free Radical Scavengers; Free Radicals; Iron; Lipid Peroxidation; Mesalamine; Oxidation-Reduction; Oxygen Consumption; Peroxides; Picrates; Rabbits; Salicylates; Salicylic Acid; Sarcoplasmic Reticulum; Thiobarbituric Acid Reactive Substances

Using a novel spectrophotometric assay to detect free radical scavengers, the effects of sulfasalazine, a compound frequently administered in the treatment of chronic inflammatory bowel disease, and its main metabolites, 5-aminosalicylic acid (5-ASA), sulfapyridine, and N-acetyl-5-ASA, were compared with biological antioxidants (nordihydroguaiaretic acid (NDGA), alpha-tocopherol, and ascorbic acid) and antiinflammatory salicylates (acetylsalicylic acid and sodium salicylate). The results show that 5-ASA, but neither sulfasalazine and its other metabolites, nor the salicylates, shares with the biological antioxidants the property of being a potent scavenger of free radicals. Since 5-ASA is formed in millimolar concentrations in the colon of sulfasalazine-treated patients this mode of action may explain the beneficial effect of sulfasalazine in inflammatory bowel disease. Locally formed 5-ASA may break the free radical chain reaction initiated and maintained by activated phagocytes, thus arresting the perpetuating tissue destruction. This mechanism may indicate a general potential for radical scavengers in chronic inflammation.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Biphenyl Compounds; Free Radicals; Hydrazines; Oxidation-Reduction; Picrates; Salicylates; Spectrophotometry; Sulfasalazine