| Abstract [eng] |
ABSTRACT Flavonoids are widely distributed in edible plants, and considered to be dietary antioxidants. Flavonoids can protect cell from „oxidative stress“, but the same flavonoids compound could behave in two ways as an both antioxidant and prooxidant, depending on the concentration used and free radical source. Among the flavonoids, quercetin is one of the most widely studied flavonoid and has biological, pharmocological, and medicinal properties. Besides the chemopreventive effects, other biological functions of quercetin are believed to improve antioxidant defence systems in living organizms. The aim of this work was to analize the effects of flavonoids (quercetin, myricetin and morin) in Hep 22a cells. Materials and methods: 1. Cell culture cytotoxicity studies; Flavonoids and the other components were obtained from Sigma, and used as received. 2. Study with fluorescence microscope 3. Statistical analysis Results and discusion: Hep 22a cell line is a mouse hepatoma cell line, which posseses the unlimited proliferation and migration features. Quercetin concentration for 50 % death of Hep 22a cells (cL50) was 160 µM, myricetin concentration was 60 µM, and morin concentration was 190 µM,. The citotoxity of flavonoids in Hep 22a cells was partly inhibited by catalase, by the antioxidant N,N‘-diphenyl-p-phenylene diamine DPPD, desferrioxamine and by dicumarol and an inhibitor of DT-diaphorase thus showing its prooxidant character. Inhibitors of cytochromes P-450, α-naphthoflavone and izoniazide, decreased the cytotoxicity of flavonoids, whereas 3,5-dinitrocatechol, an inhibitor of catechol-o-methyltransferase (COMT), increased it. Next, we examined the effects of the antioxidant on cytotoxicity and apoptosis induction. Quercetis is a dietary anticancer chemical that is capable of inducing apoptosis in tumor cells. We also investigated the effects of quercetin and myricetin on apoptosis of Hep 22a cells. Quercetin and myricetin induced apoptosis in 30 % of cells. The antioxidant N,N‘-diphenyl-p-phenylene diamine DPPD, desferrioxamine and the inhibitor of NQ01 dicumarol, protect against apoptosis with all compounds investigated, but only to a different extent. This shows that for all compounds investigated, there exists a common apoptosis and cytotoxity mechanism, namely an oxidative stress. |
