The hemolytic activity of some trialkyltin and triphenyltin compounds

Abstract

Triphenyltin chloride caused the rapid hemolysis of dog, hog, rabbit, or rat blood; however, human blood was resistant to hemolysis by triphenyltin chloride. Trialkytin compounds with alkyl groups having 3–6 carbon atoms were hemolytic to both human and rat blood. Tri- n-butyltin derivatives in which the fourth group or atom bonded to tin was acetate, methoxide, hydroxide, oxygen, bromide or chloride were all hemolytic; however, bis(triphenyltin) sulfide was not hemolytic. Butyltins having 1, 2 or 4 carbon-tin bonds, trimethyltin chloride and triethyltin bromide all exhibited low hemolytic activity. It was demonstrated that the rate of hemolysis of human blood by tri- n-butyltin chloride was reduced when the solutes of the medium were predominantly nonelectrolytes and that potassium leaked from the cells faster than hemoglobin during tri- n-butyltin induced hemolysis. A nitrogen atmosphere or the addition of low concentrations of dl-α-tocopherol also reduced the rate of hemolysis of human blood in the presence of tri- n-butyltin chloride. Human plasma, but not human serum albumin, was partially effective in protecting washed, human red cells from tri- n-butyltin induced hemolysis. Sodium sulfide and several sulfhydryl compounds, in concentrations about equal to that of the organotin, protected human and rat blood from the hemolytic activity of tri- n-butyltin chloride, tricyclohexyltin hydroxide, or triphenyltin chloride. It was concluded that the most hemolytic organotins were the trialkyltins with alkyl groups having 3–6 carbon atoms and that some sulfhydryl compounds can react chemically with the organotins to reduce hemolytic activity.