Browsing by Author "Schlachter, Manfred"

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    Reduced cavitation-induced cellular damage by the antioxidative effect of vitamin E
    (1994) Suhr, Dierk; Brümmer, Franz; Irmer, Ulrich; Schlachter, Manfred; Hülser, Dieter F.
    Fragmentation of human urinary and biliary stones by shock waves in extracorporeal lithotripsy is accompanied by tissue damage. Both the fragmentation as well as the side effects are often attributed to cavitation. The hazardous potential of cavitation is not only of a physical nature but also of a chemical nature, because of the generation of free radicals, e.g. ·OH, ·H and ·O2. After the application of shock waves, we have demonstrated cavitation-generated free radicals in cell-free solutions and also in the surviving and intact suspended MGH-U1 cells by hydroethidine measurements. Under electron microscopical inspection, the same cells exhibited perinuclear cisternae, damaged mitochondria and numerous intracellular vacuoles. The contribution of free radicals to cell damage was investigated by reducing the vitamin E level in rats by a tocopherol free diet and by incubating L1210 cells in a tocopherol enriched medium. After 250 shock waves, ex vivo erythrocytes revealed a 75% increase in total cell disruption over cells from non-depleted rats. The in vitro experiments with L1210 cells exhibited a moderate protection by the addition of this scavenger of free radicals.
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    Shock waves and free radicals : cell protection by vitamin E in vitro and ex vivo
    (1993) Suhr, Dierk; Brümmer, Franz; Irmer, Ulrich; Schlachter, Manfred; Hülser, Dieter F.
    The application of extracorporeal generated shock waves in medicine for the fragmentation of human kidney and gall stones proved to be a very successful technique. Shock wave lithotripsy, however, is not free of tissue damaging side effects. One major mechanism for the fragmentation of stones as well as for the side effects is cavitation, ie. the formation and movement of bubbles in liquids exposed to tensile forces. Collapse of cavitation bubbIes is accompanied by local "hot spots" of several 1,000 K, thus generating free radicals. We investigated the contribution of these free radicals to cellular injury by varying the cellular amount of a well known scavenger of free radicals, α-tocopherol.