Lichen Metabolites. 1. Inhibitory Action Against Leukotriene B4 Biosynthesis by a Non-Redox Mechanism

• Published in: Journal of natural products (Washington, D.C.) D.C.), 1999-06, Vol.62 (6), p.817-820
• Main Authors: Kumar KC, Sunil, Müller, Klaus
• Format: Article
• Language: English
• Subjects: (+)-protolichesterinic acid; (+)-usnic acid; Animals; atranorin; Bepridil - analogs & derivatives; biochemical pathways; Biological and medical sciences; biosynthesis; Biphenyl Compounds; Cattle; chemical constituents of plants; chemical structure; Deoxyribose - chemistry; diffractaic acid; ethyl haematommate; Free Radicals; General pharmacology; gyrophoric acid; In Vitro Techniques; inhibition; leukocytes; Leukocytes - drug effects; Leukocytes - metabolism; Leukotriene B4 - biosynthesis; leukotrienes; lichens; Lichens - chemistry; Lichens - metabolism; Lipid Peroxidation; Medical sciences; medicinal properties; metabolites; methyl beta-orcinolcarboxylate; Oxidation-Reduction; Parmelia; parmelia nepalensis; parmelia tinctorum; Pharmacognosy. Homeopathy. Health food; Pharmacology. Drug treatments; Phospholipids - chemistry; Picrates; redox reactions; spectral analysis
• ISSN: 0163-3864; 1520-6025
• DOI: 10.1021/np9803777

Of several lichen metabolites isolated from Parmelia nepalensis and Parmelia tinctorum, the didepsides atranorin (4) and diffractaic acid (5), as well as (+)-protolichesterinic acid (7), inhibited LTB4 biosynthesis in polymorphonuclear leukocytes. Ethyl hematommate (3) and (+)-usnic acid (1) were only weak inhibitors, while methyl β-orcinolcarboxylate (2) and gyrophoric acid (6) were inactive at concentrations up to 60 μM. Redox properties of the compounds were evaluated in terms of inhibition of nonenzymatic lipid peroxidation in model membranes, reactivity against the stable free radical 2,2-diphenyl-1-picrylhydrazyl, and deoxyribose degradation as a measure of hydroxyl-radical generation. The results revealed that lichen metabolites neither acted as antioxidants against the peroxidation process in model membranes nor did they scavenge or produce free radicals, suggesting that the inhibitory effects on LTB4 biosynthesis was due to specific enzyme interaction rather than a nonspecific redox mechanism.