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R J Ferretti

Publications and source records attributed to R J Ferretti.

5 recordsLinked to original sources
PubMed1977

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.

Anemia, Hemolytic↗
PubMed1977

Osmotic and peroxidative fragilities of erythrocytes from vitamin E-deficient lead-poisoned rats.

Weanling male rats were fed either a vitamin E-deficient Torula yeast diet fortified with selenium or the same diet supplemented with 100 ppm vitamin E. One group of rats fed each diet received plain distilled water, whereas another group received 250 ppm lead as lead acetate in the drinking water. After a 3 month feeding period, erythrocyte osmotic and peroxidative fragilities were determined in an osmotic test recorder. Dietary vitamin E had little or no effect on the osmotic fragility of red cells. Lead in the drinking water, however, decreased the osmotic fragility of red cells from deficient rats. Lead poisoning also markedly decreased the elevated peroxidative fragility characteristic of erythrocytes from vitamin E-deficient rats. This effect of lead in reducing the peroxidative fragility of red cells from deficient rats could be seen at levels as low as 25 ppm lead in the drinking water. Lead added in vitro decreased the peroxidative fragility of red cells from vitamin E-deficient non-poisoned rats, whereas neither mercury nor cadmium had such an effect. Lead may decrease the osmotic and peroxidative fragility of erythrocytes from vitamin E-deficient rats by "tanning" the red cell membrane. These results suggest that the peroxidative fagility test as carried out with an osmotic test recorder may not be a valid indicator of the vitamin E status of animals exposed to lead.

Anemia, Hemolytic↗
PubMed1977

Comparative effects of selenium and vitamin E in lead-poisoned rats.

Weanling male rats were fed a Torula yeast diet supplemented with selenium, vitamin E, or both for 3 months. Of rats fed each diet, one group received 250 ppm lead in the drinking water and another group did not. In rats not poisoned with lead, neither vitamin E nor selenium deficiency affected spleen weight, hematocrit value, or erythrocyte mechanical fragility. Vitamin E deficiency increased the splenomegaly, anemia, and mechanical fragility of red cells of lead-poisoned rats, whereas selenium deficiency did not. Addition of 0.5 ppm selenium to the vitamin E-supplemented diet increased slightly the splenomegaly and anemia in lead-poisoned rats. Excess levels of selenium (2.5 and 5 ppm) in the vitamin E-deficient diet had little or no effect on spleen size or hematocrit of rats not receiving lead, but partially prevented the splenomegaly and anemia of red cells from either non-poisoned or lead-oisoned vitamin E-deficient rats, but not as effectively as vitamin E. These results show that vitamin E status of rats is more important that selenium status in determining response to toxic levels of lead. Excess dietary selenium did protect partially against lead poisoning in vitamin E-deficient rats, but the levels of selenium used were toxic in themselves.

Anemia, Hemolytic↗