Effect of Oxidants, Hydrazines, and Aminoquinolines on the Filterability of Erythrocytes from Vitamin E-deficient Lead-poisoned Rats

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Abstract
Weanling male rats were fed, for 3 months, either a vitamin E-deficient Torula yeast diet or the same diet supplemented with 100 ppm vitamin E. Of rats fed each diet, one group received 250 ppm lead in the drinking water, whereas another group received no lead. Incubation in vitro with dialuric acid, hydrogen peroxide, or methylhydrazine had little effect on the filterability of suspensions of erythrocytes from vitamin E-supplemented rats, poisoned with lead or not. However, such chemical stress markedly reduced the filterability of red cells from vitamin E-deficient non-poisoned rats and the reduction was accentuated by lead poisoning. The aminoquinolines chloroquine and especially primaquine decreased the filterability of erythrocytes from both vitamin E-supplemented and E-deficient non-poisoned rats. The decrease in filterability of erythrocytes from vitamin E-deficient rats caused by either aminoquinoline was accentuated by concurrent lead poisoning. Under conditions which decreased filterability of erythrocytes from vitamin E-deficient lead-poisoned rats, hydrogen peroxide caused a great increase in red cell lipid peroxidation and smaller declines in glutathione and hemoglobin. On the other hand, hydrazines had little effect on red cell lipid peroxidation, but caused marked decreases in glutathione and hemoglobin levels and great increases in methemoglobin and sulfhemoglobin. Primaquine had no significant effect on any of these biochemical parameters but caused profound cell membrane invaginations in erythrocytes from both vitamin E-supplemented and E-deficient non-poisoned rats. These results show that a variety of mechanisms account for the decreased erythrocyte filterability caused by different chemical stresses and that the response to such stress can be greatly influenced by vitamin E status and/or lead exposure.