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Biomedical subjects

V C Morris

Publications and source records attributed to V C Morris.

At least 37 records · Page 2Linked to original sources
PubMed1986

Nutritional availability to rats of selenium in four seafoods: crab (Callinectes sapidus), oyster (Crassostrea virginica), shrimp (Penaeus duorarum) and Baltic herring (Clupea harengus).

1. The present study was conducted to determine the biological availability to rats of the selenium in four high-Se seafoods: crab (Callinectes sapidus), oyster (Crassostrea virginica), shrimp (Penaeus duorarum) and Baltic herring (Clupea harengus). 2. Weanling male rats were fed on a Se-deficient Torula yeast diet for 4 weeks followed by either continued depletion or repletion for 4 weeks with 0.05, 0.1 or 0.2 microgram Se as selenite/g, or 0.1 or 0.2 microgram Se as freeze-dried cooked test food/g. Plasma and liver Se levels or glutathione peroxidase (EC 1.11.1.9; GSH-Px) activities were used as indicators of body Se status. 3. Except for oysters, the biological availability of Se in all these seafoods was close to that of selenite (selenite 100%) when the criterion used was either plasma Se level or plasma GSH-Px activity. 4. By the criterion of increased liver Se level of restored hepatic GSH-Px activity, only herring-Se had a biological availability comparable to that of selenite-Se under all conditions tested, whereas crab-Se and oyster-Se were distinctly inferior in this regard. 5. Increasing the amount of crab-Se, oyster-Se or shrimp-Se supplied in the diet from 0.1 to 0.2 microgram/g changed the apparent availability (%) of Se for hepatic GSH-Px restoration from 38 to 78, 22 to 53 and 57 to 90 respectively. 6. The present study demonstrates that the availability of Se in certain foods is a function of the criterion chosen, the level of Se supplied in the diet, and possibly other unknown interacting dietary factors.

Animal Nutritional Physiological Phenomena↗
PubMed1986

Effect of selenium deficiency on the chronic toxicity of adriamycin in rats.

The effect of selenium deficiency on the chronic toxicity of adriamycin was examined in rats fed diets adequate in vitamin E. Selenium-deficient and selenium-supplemented diets were fed to rats for 10 wk, after which groups of 10 rats fed each diet were given weekly intravenous injections of adriamycin in saline at doses of 0, 0.5 or 1.0 mg/kg body weight for 12 wk. All rats were killed at 24 wk. Even though the cardiac glutathione peroxidase activity in the selenium-deficient group was less than 1% of that of the selenium-supplemented group, the severity of the adriamycin-induced cardiomyopathy was similar in both groups. However, the selenium-deficient rats were more sensitive to the growth-inhibiting effect of the higher dose of adriamycin than the selenium-supplemented rats. Moreover, the lower dose of adriamycin caused a mild nephropathy in 70% of the deficient rats but affected only 10% of the supplemented rats. Selenium status may have to be considered when adriamycin is used as a chemotherapeutic agent.

Animals↗
PubMed1984

Dietary selenium levels needed to maintain balance in North American adults consuming self-selected diets.

Dietary selenium intake and selenium balance were measured during 4 1-wk metabolic periods over the course of 12 months in 27 free-living adult volunteers consuming self-selected diets. Men consumed more selenium in their diets than women (90 +/- 4 versus 74 +/- 3 micrograms/day), but plasma selenium levels were similar for both sexes (136 +/- 4 versus 133 +/- 4 ng/ml, respectively). Neither dietary selenium intake nor plasma selenium levels varied seasonally. Regression of selenium balance versus intake indicated that adult men needed 80 micrograms SE/day to stay in balance, whereas women needed only 57 micrograms SE/day. When balance and intake were adjusted for body weight, the sex difference disappeared, and both men and women needed about 1 microgram of dietary selenium per kg of body weight per day to maintain balance. The levels of dietary selenium reported here as necessary to maintain balance in North American adults are considerably higher than those previously reported as needed for balance in adult women from New Zealand, a country where low selenium status is common. Our results indicate that the levels of dietary selenium needed to achieve balance are a function of lean body mass and historical selenium intake.

Adult↗
PubMed1983

Platelet glutathione peroxidase activity as an index of selenium status in rats.

Glutathione peroxidase activity in platelets increased stepwise in selenium-depleted rats that were repleted with graded levels of dietary sodium selenite. In a 3-phase depletion/repletion/depletion feeding study, glutathione peroxidase activity was similar in platelets and liver, which apparently contains the largest labile pool of selenium in the body. The activity of glutathione S-transferase (selenium-independent glutathione peroxidase) in platelets was low and was not affected by selenium deficiency, even though hepatic transferase was markedly elevated in selenium-deficient rats. Vitamin E deficiency did not affect activities of glutathione peroxidase or glutathione S-transferase in platelets or liver. Determination of glutathione peroxidase activity in platelets apparently is a promising technique for assessing selenium status and, possibly, for measuring selenium bioavailability.

Animals↗
PubMed1983

The gap between basic sciences and clinical pharmacy practice: is it epistemological?

In this article, it is argued that the perceived gap between basic scientists and clinical practitioners originates in the epistemological persuasions of each group, that is, in their view of genuine knowledge and the process by which knowledge is obtained. The broad implications of this disparity for the education of practicing pharmacists are discussed. The Instrumentalist epistemology, adopted, in part, by clinical pharmacy faculty, is proposed as a framework to guide undergraduate, graduate, and continuing pharmacy education. To improve the "fit" between underlying epistemology and clinical instruction, specific changes in curricular content, organization, and delivery parameters is essential to therapy.

Education, Pharmacy↗
PubMed1981

Selenium balance in young men during selenium depletion and repletion.

Selenium balance was determined in six young men fed for 45 days a formula depletion diet (33 to 36 micrograms Se/day) then fed for 25 days a repletion of diet (depletion diet plus 200 micrograms Se/day as high-Se wheat or wheat plus tuna fish). After 12 days of adaptation, Se balance during depletion was rather constant at -21 micrograms/day and Se losses in urine and feces were 54 micrograms/day. During repletion, Se balance was +64 micrograms/day for the first 12 days and +25 micrograms/day thereafter and the subjects regained all the Se lost during depletion. If the gastrointestinal absorption of the food Se in North Americans and New Zealanders is similar (80%), young North American men need a dietary Se intake of about 70 micrograms/day to replace losses and maintain body stores.

Adult↗
PubMed1981

Nutritional availability to rats of selenium in tuna, beef kidney, and wheat.

Weanling male rats were fed a selenium (Se)-deficient 40% Torula yeast diet for 4 weeks and were then continued on depletion for another 4 weeks or were repleted with 0.1, 0.2, or 0.3 ppm Se as sodium selenite or 0.2 ppm Se as tuna, beef kidney, or high-Se wheat. There were no significant differences in young red blood cell Se, unfractionated red blood cell Se, or liver Se levels in groups fed diets containing 0.2 ppm Se. Glutathione peroxidase (GSH-Px) activity in young red blood cells was lower in the three groups fed food Se than in the group fed selenite (0.2 ppm Se). Young red blood cell GSH-Px was significantly lower in rats fed tuna than in rats fed wheat. Unfractionated red blood cell GSH-Px was lower in rats fed tuna than in rats fed selenite, but did not differ significantly among groups fed food Se sources. Liver GSH-Px was significantly lower in rats fed tuna than in rats fed kidney, wheat, or selenite. Availability of Se was only 54-58% as great from tuna as from selenite for induction of GSH-Px in liver and in red blood cell populations. Therefore, low availability of Se from fish may have to be considered when assessing Se status of human beings from dietary intake.

Animals↗
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↗
PubMed1975

Lead poisoning in vitamin E-deficient rats.

Weanling male rats were fed either a vitamin E-deficient Torula yeast diet or the same diet supplemented with 100 ppm vitamin E for a period of 3 months. One group of animals fed each diet received 250 ppm lead in the drinking water, whereas another group of animals fed each diet received no lead in the water. Vitamin E deficiency per se had little or no effect on hematocrit value, reticulocyte count, spleen weight, or erythrocyte mechanical fragility in rats not poisoned with lead. On the other hand, the decreased hematocrit, increased reticulocyte count, and splenic enlargement due to lead poisoning were much more pronounced in vitamin E-deficient rats than in rats supplemented with vitamin E. The resistance to mechanical trauma of red blood cells from vitamin E-deficient lead-poisoned rats was much less than that of red cells from vitamin E-adequate lead-poisoned rats. Dietary vitamin E status had no significant influence on the increased mechanical fragility of erythrocytes from nonpoisoned rats caused by exposure to lead in vitro. These results suggest that vitamin E deficiency enhances the susceptibility of animals to the in vivo hemolytic effect of lead poisoning.

Animals↗