title: Protective effects of Mangifera indica L. extract, mangiferin and selected antioxidants against TPA-induced biomolecules oxidation and peritoneal macrophage activation in mice.
abstract: We compared the protective abilities of Mangifera indica L. stem bark extract (Vimang) 50-250 mgkg(-1), mangiferin 50 mgkg(-1), vitamin C 100 mgkg(-1), vitamin E 100 mgkg(-1)and beta -carotene 50 mgkg(-1)against the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced oxidative damage in serum, liver, brain as well as in the hyper-production of reactive oxygen species (ROS) by peritoneal macrophages. The treatment of mice with Vimang, vitamin E and mangiferin reduced the TPA-induced production of ROS by the peritoneal macrophages by 70, 17 and 44%, respectively. Similarly, the H(2)O(2)levels were reduced by 55-73, 37 and 40%, respectively, when compared to the control group. The TPA-induced sulfhydryl group loss in liver homogenates was attenuated by all the tested antioxidants. Vimang, mangiferin, vitamin C plus E and beta -carotene decreased TPA-induced DNA fragmentation by 46-52, 35, 42 and 17%, respectively, in hepatic tissues, and by 29-34, 22, 41 and 17%, in brain tissues. Similar results were observed in respect to lipid peroxidation in serum, in hepatic mitochondria and microsomes, and in brain homogenate supernatants. Vimang exhibited a dose-dependent inhibition of TPA-induced biomolecule oxidation and of H(2)O(2)production by peritoneal macrophages. Even if Vimang, as well as other antioxidants, provided significant protection against TPA-induced oxidative damage, the former lead to better protection when compared with the other antioxidants at the used doses. Furthermore, the results indicated that Vimang is bioavailable for some vital target organs, including liver and brain tissues, peritoneal exudate cells and serum. Therefore, we conclude that Vimang could be useful to prevent the production of ROS and the oxidative tissue damages in vivo.
authors.affiliation: Centre for Research and Biological Evaluation, Pharmacy Institute, Havana University, P.O. 10 400, Havana, Cuba. gregorio@infomed.sld.cu
authors.forename: G M
authors.initials: GM
authors.lastname: Sánchez
authors.forename: L
authors.initials: L
authors.lastname: Re
authors.forename: A
authors.initials: A
authors.lastname: Giuliani
authors.forename: A J
authors.initials: AJ
authors.lastname: Núñez-Sellés
authors.forename: G P
authors.initials: GP
authors.lastname: Davison
authors.forename: O S
authors.initials: OS
authors.lastname: León-Fernández
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D053938:DNA Fragmentation / Q000187:drug effects; D005979:Glutathione Peroxidase / Q000097:blood; D015227:Lipid Peroxidation / Q000187:drug effects; D008262:Macrophage Activation / Q000187:drug effects*; D017737:Macrophages, Peritoneal / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D010084:Oxidation-Reduction; D010946:Plants, Medicinal; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000097:blood; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*; D014966:Xanthenes / Q000494:pharmacology*; D044004:Xanthones
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species; D014966:Xanthenes; D044004:Xanthones; C013592:mangiferin; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D013755:Tetradecanoylphorbol Acetate