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1.
T. Hamada 《Cellular and molecular life sciences : CMLS》1994,50(Z1):49-53
Several vanadium compounds were tested for their ability to induce in vitro hemolysis of vitamin E-deficient hamster erythrocytes. Free vanadyl caused hemolysis in Hepes buffer but not in Tris or phosphate buffer, while hemolysis was inhibited by catalase, chelators such as deferoxamine mesylate and EDTA, and hydroxyl radical scavengers such as ethanol andd-mannitol. Although metavanadate itself could not induce hemolysis, metavanadate with NAD(P)H caused hemolysis in Hepes buffer only, and superoxide dismutase prevented it. Hydrogen peroxide, hydroxyl radical and Hepes radical were involved in vanadyl-induced hemolysis; superoxide anion was further involved in metavanadate plus NAD(P)H-induced hemolysis. Vitamin E prevented hemolysis under both conditions. 相似文献
2.
Summary Erythrocytes of vitamin E-deficient kids and chicks were hemolyzed at concentrations of Tween 20 above 1%. In vivo or in vitro uptake of vitamin E by the erythrocytes, or the addition of dithiothreitol or 2-mercaptoethanol, prevented the hemolysis with Tween 20. 相似文献
3.
Summary The effective Tween 20 concentration at which 70% hemolysis was achieved in vitro correlated with the plasma vitamin E content of chicks (r=0.85). Addition of catalase, MnCl2, CoCl2 or dithiothreitol in vitro showed significant protection against the hemolysis induced by Tween 20 in vitamin E-deficient chick and kid erythrocytes. 相似文献
4.
Summary Exrtensive in vitro hemolysis of erythrocytes, induced in vitamie E-deficient rats by 0.001% Tween 20 with ascorbic acid and azide, or in goats by 2.5% Tween 20, could be counteracted by either the inclusion of vitamin E in the cells or by the in vitro addition of 0.25–0.4 mM dithiothreitol. 相似文献