Filterability of erythrocytes from vitamin E-deficient lead-poisoned rats.
The time required for red blood cells (RBC) from vitamin E-deficient lead-poisoned (-E + Pb) rats to pass through polycarbonate filters after incubation in vitro was much greater than that of RBC from vitamin E-supplemented non-poisoned rats. Vitamin E deficiency per se (i.e., in non-poisoned rats) often increased filtration times, but in all such experiments the RBC from -E + Pb groups had even longer filtration times. Administration of lead to rats supplemented with vitamin E had little effect on the filtration rate of RBC. N,N'-diphenyl-p-phenylenediamine (DPPD) prevented the increased filtration times characteristic of RBC from -E + Pb rats, but replacement of the lard in the vitamin E-deficient basal diet by more highly polyunsaturated fats did not exacerbate the increased filtration times of RBC from -E + Pb rats. The increased filtration time of RBC from -E + Pb rats appeared to be related to the extent of RBC lipid peroxidation. Decreasing the pH of the RBC incubation medium from 7.4 to 6.6, an acidity typical of the spleen, markedly increased the filtration times of RBC from -E + Pb rats. Addition of lead in vitro increased filtration times of RBC from both vitamin E-deficient and supplemented non-poisoned rats, but filtration times tended to be longer in the deficient group. These results suggest that vitamin E deficiency and lead toxicity act synergistically to alter the deformability of the RBC thereby rendering it vulnerable to sequestration in the spleen.
Filterability of erythrocytes from vitamin E-deficient lead-poisoned rats. The time required for red blood cells (RBC) from vitamin E-deficient lead-poisoned (-E + Pb) rats to pass through polycarbonate filters after incubation in vitro was much greater than that of RBC from vitamin E-supplemented non-poisoned rats. Vitamin E deficiency per se (i.e., in non-poisoned rats) often increased filtration times, but in all such experiments the RBC from -E + Pb groups had even longer filtration times. Administration of lead to rats supplemented with vitamin E had little effect on the filtration rate of RBC. N,N'-diphenyl-p-phenylenediamine (DPPD) prevented the increased filtration times characteristic of RBC from -E + Pb rats, but replacement of the lard in the vitamin E-deficient basal diet by more highly polyunsaturated fats did not exacerbate the increased filtration times of RBC from -E + Pb rats. The increased filtration time of RBC from -E + Pb rats appeared to be related to the extent of RBC lipid peroxidation. Decreasing the pH of the RBC incubation medium from 7.4 to 6.6, an acidity typical of the spleen, markedly increased the filtration times of RBC from -E + Pb rats. Addition of lead in vitro increased filtration times of RBC from both vitamin E-deficient and supplemented non-poisoned rats, but filtration times tended to be longer in the deficient group. These results suggest that vitamin E deficiency and lead toxicity act synergistically to alter the deformability of the RBC thereby rendering it vulnerable to sequestration in the spleen.