Abstract
Acute influenza virus infection causes accumulation of reactive oxygen species (ROS) in target organs, initiating the processes of free radical lipid peroxidation (LPO) (Peterhanse 1997, Buffinton et al. 1992, Chetverikova et al. 1996). Rimantadine (Rim), (α-methyl-l-adamantil-methylamin hydrochlorid), a universal inhibitor of type A virus, is widely used in chemotherapeutic treatment and prevention of influenza. Rim interacts with the M-2 protein of the virus, inhibits its replication and blocks the formation of some replicative components of the influenza virus (Belshe et al. 1988, Zhiravetskii 1986). At present, it is not clear how Rim can affect the processes of LPO and drug metabolizing enzyme systems (DMES) during experimental influenza virus infection.
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Tantcheva, L., Pavlova, E., Savov, V., Galabov, A., Mileva, M., Braykova, A. (2001). Free Radical Lipid Peroxidation and Monooxygenase Activity in Experimental Influenza Virus Infection after Treatment with Rimantadine. In: Dansette, P.M., et al. Biological Reactive Intermediates VI. Advances in Experimental Medicine and Biology, vol 500. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0667-6_30
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DOI: https://doi.org/10.1007/978-1-4615-0667-6_30
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