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DOI 10.1007/bf00117823

Медицинская библиотека · Cell biology and toxicology · 1987

Organotin-induced hemolysis, shape transformation and intramembranous aggregates in human erythrocytes.

Gray B H, Porvaznik M, Flemming C, Lee L H

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Аннотация

Organotin compounds examined in this study exhibited a relative order of potency for induction of in vitro hemolysis in human erythrocytes as follows: tri-n-butyltin greater than tri-n-propyltin greater than tetra-n-butyltin greater than triphenyltin chloride greater than tri-n-ethyltin bromide greater than dibutyltin dichloride greater than stannous chloride greater than tri-n-methyltin chloride = butyltin chloride dihydroxide. All of the organotin compounds induced erythrocyte shape transformation from the normal discocyte to an echinocyte and, in addition, triphenyltin chloride, tetra-n-butyltin and tri-n-ethyltin bromide also elicited stomatocyte formation at higher concentrations. Select organotin compounds also formed tin-containing aggregates within the plasma membrane. The relative order of effectiveness for organotin induction of intramembranous aggregates was tri-n-butyltin greater than tri-n-propyltin greater than tetra-n-butyltin greater than tri-n-ethyltin bromide, which was based upon the lowest concentration at which they were observed. These results support the previously suggested theory that organotins are membrane effectors because of their comparatively high hydrophobic, lipid partitioning properties. The relatively lipophilic compound, triphenyltin chloride, appeared to be anomalous because it did not readily promote hemolysis or induce the formation of intramembranous aggregates in human erythrocytes. A log-linear statistical model demonstrated an association of hemolysis with both tri-n-butyltin aggregate formation and shape transformation. Select organotin compounds should be useful probes in membrane studies because of their numerous effects.

Для цитирования: Gray B H, Porvaznik M, Flemming C, Lee L H. Organotin-induced hemolysis, shape transformation and intramembranous aggregates in human erythrocytes.. Cell biology and toxicology. 1987. DOI: 10.1007/bf00117823.

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