Modifications on Antioxidant Capacity and Lipid Peroxidation in Mice under Fraxetin Treatment

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  • Sagrario Martín-Aragón
    Department of Pharmacology, Faculty of Pharmacy, Complutense University , 28040 Madrid,
  • Juana M Benedí
    Department of Pharmacology, Faculty of Pharmacy, Complutense University , 28040 Madrid,
  • Angel M Villar
    Department of Pharmacology, Faculty of Pharmacy, Complutense University , 28040 Madrid,

書誌事項

公開日
1997-01-01
権利情報
  • https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model
DOI
  • 10.1111/j.2042-7158.1997.tb06751.x
公開者
Oxford University Press (OUP)

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<jats:title>Abstract</jats:title> <jats:p>Fraxetin belongs to an extensive group of natural phenolic antioxidants. We have investigated the modifications in endogenous antioxidant capacity; superoxide dismutase (SOD), catalase (CAT), total and selenium-dependent glutathione peroxidases (GPx) and glutathione reductase (GR) and stress index; glutathione disulphide (GSSG)/reduced glutathione (GSH) ratio and thiobarbituric acid-reactive substances (TBARs) in liver and brain supernatants of C57BL/6J male 12-month-old mice under fraxetin treatment for 30 days.</jats:p> <jats:p>Liver SOD and GPx (total and Se-dependent) activities were not significantly affected by fraxetin, whereas they were increased in the brain compared with control animals. GR activity increased significantly only in the liver of treated mice. Fraxetin treatment-related decreases were shown for GSSG/GSH ratio and rate of accumulation of TBARs (not significant in TBARs) in both tissues.</jats:p> <jats:p>We concluded that the net effect of fraxetin treatment on endogenous antioxidant capacity suggests that this compound might provide an important resistance to, or protection against, free-radical-mediated events which contribute to degenerative diseases of ageing.</jats:p>

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