The decreased hepatic drug metabolism (predominately first phase) is one of the essential\nreasons for numerous side effects and for increased drug toxicity during influenza virus infection (IVI).\nThe present study aims to investigate some mechanisms of the preventive effect of a standardized\npolyphenol complex from the medicinal plant Geranium sanguineum L. (PPhC) (10 mg/kg nasally).\nAverified experimental model of IVIA/Aichi/2/68 (H3N2) (4.5 lg LD50) in male ICR (Institute of Cancer\nResearch, USA) mice was used. Changes in hepatic monooxygenase activities as well as nicotinamide\nadenine dinucleotide phosphate (NADPH)-cytochrome C reductase activity and cytochtome P450\ncontent were studied on days 2, 6, 9, 21 of the infection together with thiobarbituric acid reactive\nsubstances in the liver supernatant. Our data clearly demonstrates that IVI affects all components of\nthe electronic chain of cytochrome P-450. N-demethylases and hydroxylases as well as the activity\nof cytochrome C reductase and cytochtome P-450 content were decreased in the course of the virus\ninfection. This implies that free radicals play an important role not only in the pathogenesis of IVI,\nbut also in the modulation of the hepatic monooxygenase activity. This is also consistent with the\nestablished polyphenol complex PPhC from the medicinal plant Geranium sanguineum L. preventive\neffect against increased thiobarbituric acid reactive substances (TBARS)-levels. PPhC restored most\nof the monooxygenase activities that were inhibited in IVI animals, even over the control levels,\nprobably via multiple mechanisms that may entail antioxidant activity and selective antiviral and\nprotein-binding effects. In contrast to infected animals, in healthy mice, PPhC showed moderate\nreversible inhibitory effect on hepatic monooxygenase activities.
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