Abstract

We compared the protective abilities of Mangifera indica L. stem bark extract (Vimang® ) 50–250 mgkg−1, mangiferin 50 mgkg−1, vitamin C 100mgkg−1 , vitamin E 100 mgkg−1and β -carotene 50mgkg−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 H2O2levels 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 β -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 H2O2production 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.

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