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SILICA HYDRIDE EXHIBITS DIRECT ANTIOXIDANT CAPACITY AND HEPATOPROTECTIVE EFFECT ON CARBON TETRACHLORIDE TOXICITY IN VIVO
Author(s) -
MendietaWejebe Jessica Elena,
RosalesHernández Martha Cecilia,
CorreaBasurto José,
TrujilloFerrara José
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.718.1
Subject(s) - chemistry , carbon tetrachloride , tbars , glutathione , antioxidant , in vivo , thiobarbituric acid , pharmacology , biochemistry , hepatoprotection , toxicity , lipid peroxidation , enzyme , organic chemistry , medicine , microbiology and biotechnology , biology
Silica hydride (SiH − ), a derivative of the silsesquioxane family, has been evaluated as an antioxidant in vitro due to its interesting biochemical properties, but there is still no evidence that this compound shows the same effect in vivo. For this reason, this work evaluated the antioxidant capacity and hepatoprotective effect of SiH − in a model of liver injury induced by carbon tetrachloride (CCl 4 ) in rats. Previous assays had demonstrated that when the animals were treated with the tested compound followed by the administration of CCl 4 , the hepatic reduced glutathione (GSH) returned to its normal levels and the content of thiobarbituric acid reactive species (TBARS) diminished in relation to the control samples. The results of this study corroborated those results. Therefore, the mechanism by which SiH − exerts these effects in vivo is by the reduction of oxidized glutathione (GSSG) and oxidized nicotinamide adenine dinucleotide phosphate (NADP + ), as well as by the inactivation of free radicals (FR). In addition, it was observed a decrease in the catalytic activity of P450, suggesting that SiH − is able to inhibit this enzyme too. This result is important because it has been demonstrated that several antioxidants act by this mechanism, which lead to a diminishing of the metabolic bioactivation of CCl 4 and, in consequence, of its hepatotoxic effects.