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V C Morris

Publications and source records attributed to V C Morris.

At least 19 recordsLinked to original sources
PubMed1991

Effect of aging and diet on proton NMR spectra of rat urine.

500 MHz 1H NMR studies of rat urine are used to assess metabolic changes resulting from aging (0.5-20 months) and changes in diet (casein versus chow). Aging rats fed chow diets decrease their excretion of citrate and 2-oxoglutarate, while the output of taurine and creatinine increases. Only young rats (1 month or less postweaning) excrete significant amounts of betaine and trimethylamine-N-oxide. Rats fed casein diets for 1 month postweaning do not excrete 2-oxoglutarate and excrete lower levels of hippurate, succinate, and citrate compared to rats fed chow diets. They also excrete N-methylnicotinamide. These high resolution proton NMR studies provide metabolic profiles which are not readily available by other techniques.

Aging↗
PubMed1990

Plasmodium yoelii: comparative antimalarial activities of dietary fish oils and fish oil concentrates in vitamin E-deficient mice.

Feeding vitamin E-deficient diets containing either fish oils such as menhaden, salmon, or anchovy oil or fish oil concentrates based on n-3 ethyl esters or free fatty acids protected mice against Plasmodium yoelii as indicated by decreased parasitemia and improved survival. The fish oil concentrates depressed plasma tocopherol levels more strongly in vitamin E-supplemented mice than the menhaden oil. The free fatty acid concentrate appeared to suppress parasitemia in vitamin E-deficient mice better than the menhaden oil, although ultimate survival was similar in both groups. Dietary manipulation of host antioxidant status offers promise as a possible means of malaria control.

Animals↗
PubMed1989

Qinghaosu, dietary vitamin E, selenium, and cod-liver oil: effect on the susceptibility of mice to the malarial parasite Plasmodium yoelii.

Young female mice were fed torula-yeast-based diets deficient in vitamin E or selenium or supplemented with cod-liver oil to determine the effect of host antioxidant status on the therapeutic efficacy of the Chinese traditional antimalarial drug qinghaosu (QHS), a sesquiterpene endoperoxide. Vitamin E deficiency enhanced the antimalarial action of QHS against Plasmodium yoelii, both in terms of decreased parasitemia and improved survival but Se deficiency did not. A vitamin E-deficient diet containing 5% cod-liver oil had such strong antimalarial activity in itself that no additional therapeutic benefit of QHS could be demonstrated. Hematocrit values in parasitized mice treated with QHS or fed the cod-liver-oil-supplemented, vitamin E-deficient diet were normal. Nutritional manipulation of host antioxidant status may provide a promising prophylactic and/or therapeutic tool for the control of malaria.

Animals↗
PubMed1987

Relative nutritional availability to rats of selenium in Finnish spring wheat (Triticum aestivum L.) fertilized or sprayed with sodium selenate and in an American winter bread wheat naturally high in Se.

A Finnish national programme to fertilize crops with sodium selenate led us to compare the nutritional availability to rats of selenium in two Finnish spring wheats (Triticum aestivum L.), either fertilized or sprayed with sodium selenate, with that in an American winter bread wheat naturally high in Se. Weanling male rats were given a Se-deficient Torula yeast diet for 4 weeks followed by either continued depletion or repletion for 4 weeks with graded levels of Se as sodium selenite (standard) or wheat (test food). Plasma and liver Se levels and plasma and liver glutathione peroxidase (EC 1.11.1.9; GSH-Px) activities were used as criteria of body Se status. The availability of Se under these conditions was calculated with the point-slope technique at two dietary levels of Se (Expt 1) and with the slope-ratio method (Expt 2). In the point-slope assay, the level of dietary Se fed had a considerable effect on the apparent availability values obtained which made interpretation of the results difficult. In the slope-ratio assay, no difference in the availability of Se from the various wheats was observed when plasma or liver Se levels were used as the response criteria. The Se in the fertilized wheat was somewhat more available than that in the sprayed wheat when plasma or liver GSH-Px activities were the response criteria. Overall, availability values (%) derived by averaging all four response criteria were 86, 77 and 73 for the fertilized and sprayed Finnish wheats and the American wheat respectively (sodium selenite 100). These results show that wheat is a relatively available source of Se to rats regardless of whether its Se content is naturally high or is increased by fertilization or spraying.

Animals↗
PubMed1987

Dietary selenium intake and selenium concentrations of plasma, erythrocytes, and breast milk in pregnant and postpartum lactating and nonlactating women.

The selenium status of a group of 23 lactating and 13 nonlactating women was assessed from 37-wk gestation through 6-mo postpartum. The mean overall dietary Se intake of both groups of women was 80 +/- 37 micrograms/d. Plasma and erythrocyte Se levels were lower in the lactating than in the nonlactating mothers both before and after parturition. Breast-milk Se concentrations fell from 20 micrograms/L (0.25 mumol/L) at 1-mo postpartum to 15 micrograms/L (0.19 mumol/L) at 3- and 6-mo postpartum. A weak (r = 0.38) but statistically significant (p less than 0.025) relationship was observed between maternal plasma Se level and breast-milk Se concentration. The dietary Se intake of these lactating North American women appears sufficient to maintain satisfactory Se nutriture in their breast-fed infants during the first 6 mo of lactation.

Adult↗
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↗
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↗