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      Influence of metal ions on flavonoid protection against asbestos-induced cell injury.

      Archives of Biochemistry and Biophysics
      Adsorption, Animals, Asbestos, adverse effects, chemistry, Catechin, metabolism, Cell Survival, drug effects, Copper, pharmacology, Dose-Response Relationship, Drug, Flavonoids, Flavonols, Hemolysis, Inflammation, Ions, Iron, L-Lactate Dehydrogenase, Lipid Peroxidation, Liver, Macrophages, Microsomes, Liver, NADP, Quercetin, analogs & derivatives, Rats, Rats, Wistar, Reactive Oxygen Species, Rutin, Spectrophotometry, Tetrazolium Salts, Zinc

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          Abstract

          Influence of metal ions (Fe2+, Fe3+, Cu2+, Zn2+) on the protective effect of rutin, dihydroquercetin, and green tea epicatechins against in vitro asbestos-induced cell injury was studied. Metals have been found to increase the capacity of rutin and dihydroquercetin to protect peritoneal macrophages against chrysotile asbestos-induced injury. The data presented here show that this effect is due to the formation of flavonoid metal complexes, which turned out to be more effective radical scavengers than uncomplexed flavonoids. At the same time epicatechins and their metal complexes have similar antiradical properties and protective capacities against the asbestos induced injury of macrophages. Metal complexes of all flavonoids were found to be considerably more potent than parent flavonoids in protecting red blood cells against asbestos-induced injury. It was also found that the metal complexes of all flavonoids were absorbed by chrysotile asbestos fibers considerably better than uncomplexed compounds and probably for this reason flavonoid metal complexes have better protective properties against asbestos induced hemolysis. Thus, the results of the present study show that flavonoid metal complexes may be effective therapy for the inflammatory response associated with the inhalation of asbestos fiber. The advantage of their application could be the strong increase in ROS scavenging by flavonoids and finally a better cell protection under the conditions of cellular oxidative stress.

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