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Abstract
Background
In a previous report, we have characterized the antiperoxidative properties of alpha-mangostin in different toxic models tested in nerve tissue preparations.
Objectives
Here, the modulatory effects of this xanthone on the glutathione system (reduced glutathione (GSH) levels, glutathione peroxidase (GPx), and glutathione S-transferase (GST) activities) were tested in synaptosomal P2 fractions isolated from rat brains in order to provide further information on key mechanisms exerted by this antioxidant in the nervous system.
Methods
Synaptosomes were exposed to increasing concentrations of the xanthone, and also challenged to the toxic actions of a free radical generator, ferrous sulfate (FeSO4). For comparative purposes, the mitochondrial toxin 3-nitropropionic acid (3-NP) was also explored.
Results
Alpha-mangostin significantly decreased the levels of GSH, and increased GPx activity.
Discussion
This finding was interpreted as a modulatory action of the GSH system in preparation to exert antioxidant responses. Although FeSO4 exhibited similar effects, these were interpreted as a compensatory response to the toxic actions of the pro-oxidant. We came to this conclusion based on our previous report where alpha-mangostin produced antiperoxidative effects and FeSO4 produced oxidative damage to lipids. GST activity remained unaffected by both the antioxidant and the pro-oxidant. Our results suggest that alpha-mangostin is able to modulate GPx activity as a potential antioxidant strategy, thereby transiently consuming GSH levels.
Acknowledgement
This work was supported in part by PAPIIT IN201910.