[Alloxan cytotoxicity: a new aspect of the problem]

The effect of alloxan on human intact erythrocytes (in the suspension and whole blood) was studied using an original potentiometric apparatus permitting continuous registration of the flow rate of reducing equivalents ('RE) through a plasmatic membrane. Acceleration of RE flow from erythrocytes due to the activation of hexosomonophosphate shunt (HMPS) was established. This effect was inhibited by P-chlormercury benzoate proving the involvement of the SH-groups of erythrocyte membrane proteins in the interaction of alloxan with erythrocytes. Oxygen consumption after adding alloxan was recorded by polarography that indicated the "start" of the alloxan----dialuric acid (A in equilibrium with DA) cycle. Enhanced RE production in erythrocytes may be caused by H2O2 and free radicals forming in this cycle. It was shown that HMPS activation i.e. transition to a more intense stationary regimen was maintained for a period exceeding the calculated period of alloxan "halt--life". This residual effect of alloxan "depleted" erythrocyte protective mechanisms that was expressed in a decrease in maximum capacity of HMPS of rat whole blood after receiving by the animals a diabetogenic dose of alloxan (150 mg/kg body mass). Thus a specific cumulation of the effect of alloxan expressed in the transition of the RE generation system to a more intense stationary regimen, was revealed. In investigating the mechanism of alloxan cytotoxicity one should take into account this peculiarity of alloxan along with the factor of affinity and conditions for initiation of the A in equilibrium with DA cycle.