Abstract
Since most of the O2 utilized by mammals takes place in mitochondria, the organelle would be particularly subject to free radical-induced changes. Attempts to decrease the rate of production of these changes with antioxidants may be thwarted because of the highly selective permeability of the inner membrane and/or adverse effects of antioxidants on mitochondrial function (Darley-Usmar et al. 1987; Horrum et al. 1987; Szabados et al. 1989). Recently, formation of oxygen free radicals was reported to be involved in the development of reperfusion injury (Gauduel and Duvelleroy 1984; Powell and Tortolani 1992). One of the sources of oxygen free radicals is suggested to be the mitochondrial electron transport system (Gonzalez-Flecha et al. 1993; Powell and Tortolani 1992). Acteoside is a phenyl-propanoid glycoside widely distributed in plants, especially in tonic drugs (Birkofer et al. 1968; Miyase et al. 1982; Kobayashi et al. 1984; Imakura et al. 1985; Takeda et al. 1985). We present the anti-peroxidative effects of acteoside on the lipid peroxidation in isolated rat liver mitochondria.
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Pan, N., Hori, H. (1994). The Interaction of Acteoside with Mitochondrial Lipid Peroxidation as an Ischemia/Reperfusion Injury Model. In: Hogan, M.C., Mathieu-Costello, O., Poole, D.C., Wagner, P.D. (eds) Oxygen Transport to Tissue XVI. Advances in Experimental Medicine and Biology, vol 361. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1875-4_51
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DOI: https://doi.org/10.1007/978-1-4615-1875-4_51
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