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Biomedical subjects

R R Bell

Publications and source records attributed to R R Bell.

At least 37 records · Page 2Linked to original sources

Composition and protein quality of honeybee-collected pollen of Eucalyptus marginata and Eucalyptus calophylla.

The composition and protein quality of the two most important Western Australian export-quality pollens were investigated. Crude pollen protein content was 20.6% and 27.9% for Jarrah (Eucalyptus marginata) and Marri (Eucalyptus calophylla), respectively. Lysine was the limiting amino acid relative to the FAO protein scoring pattern (Food and Agriculture Organization of the United Nations), and the amino acid scores were 0.73 and 0.66 for Jarrah and Marri pollen, respectively. Apparent biological value (BV) was 61.7 for Jarrah pollen, 66.9 for Marri pollen and 71.4 for the casein controls. Adjusted protein efficiency ratio (PER) values were 2.5, 1.2 and 1.1 for casein and Jarrah and Marri pollens, respectively. Apparent net protein utilization (NPU) was significantly reduced for both pollens (32.8 for Jarrah and 39.5 for Marri) compared to casein (63.6). The low apparent NPU values result from the relatively low digestibility of pollens. Apparent digestibility was 52 and 59% for Jarrah and Marri pollen compared to 89% for casein. Although both Jarrah and Marri pollen are relatively high in protein and have favorable amino acid patterns, their relatively low digestibility will be a limiting factor in their usefulness as a food for humans and monogastric animals. The proximate analysis and mineral content of the pollens are also presented.

Amino Acids↗

Effect of protein-induced calciuria on calcium metabolism and bone status in adult rats.

45Ca-labeled adult male rats were fed diets high in protein to determine long-term effects on calcium metabolism and bone status. Factors influencing renal excretion of calcium were examined for their involvement in protein-induced hypercalciuria. Control rats were fed a 6% casein diet. Test diets contained 6% casein plus 24% protein as lactalbumin, beef, casein, soy, egg white or gelatin. All diets were equal in Mg, P, and Ca. Collections made during the 20-week feeding regimen indicated a transient but marked calciuria (greater than or equal to 200% of control) occurring at or prior to days 56-59 by rats fed the lactalbumin, egg white, gelatin (P less than or equal to 0.001) and 30% casein (P less than or equal 0.01) diets. Soy and beef diets were not calciuric. At days 56-59, rats fed lactalbumin, 30% casein, soy and egg white exhibited significantly depressed urinary specific activity of calcium (P less than or equal to 0.001), and all rats fed test diets produced higher fecal endogenous calcium, suggesting an increased absorption. No compositional differences indicative of bone resorption were present in the femur or mandibles of any rat fed test protein, dismissing bone as the source of calciuria. End-products of protein metabolism known to chelate calcium or compete with its renal reabsorption were significantly correlated with urinary calcium; these included sulfate, oxalate and sodium.

Animals↗

Glutathione peroxidase activity in iron-deficient rats.

The response of glutathione peroxidase (GSH-Px) to dietary iron deficiency was studied in red blood cells and liver from male Sprague-Dawley rats. A casein-based purified diet containing 0.02 ppm Se and 7 ppm Fe was used as the basal diet. Rats were given the basal diet supplemented with either 0.5 ppm Se or 30 ppm Fe or both for 10 weeks. Food consumption in iron-deficient rats was 79% of controls. Iron deficiency caused a significant decrease of GSH-Px and catalase activities in red blood cells (RBC) expressed per cell. However, enzyme activities expressed per gram of hemoglobin or per milligram or protein increased. These data suggest that GSH-Px is present in adequate quantities in iron-deficient red blood cells to protect cell membranes and hemoglobin as long as the rats receive adequate Se. Hepatic catalase was not altered by iron or Se deficiency. Liver Se GSH-Px activity/g tissue decreased to 75% of control activity during iron deficiency. Non Se GSH-Px activity increased during Se or iron deficiencies and may compensate to a limited extent for decreased Se GSH-Px activity. In contrast to earlier reports, RBC GSH-Px activity was not altered by iron deficiency except for possible indirect effects related to changes in red blood cell size or food intake.

Animals↗

Response of glutathione peroxidase and catalase to excess dietary iron in rats.

Glutathione peroxidase (GSH-Px) and catalase activities were evaluated during intake of excess dietary iron. Male Sprague-Dawley rats were randomized into seven dietary treatments. The treatments included three levels of dietary iron (35, 305, and 1255 ppm) plus deficiencies of Se or Se and vitamin E at the two high iron levels. Lipid peroxidation in liver and GSH-Px and catalase activities in erythrocytes and liver were measured. Lipid peroxidation was elevated in all high iron groups compared to controls. Total GSH-Px in erythrocytes and liver remained constant or decreased in animals receiving high iron, but non Se GSH-Px increased significantly in liver from rats fed high iron (305 ppm: 155% and 1255 ppm: 131%) and increased additionally in Se and vitamin E deficient groups. No differences in RBC catalase activity were observed. Liver catalase activity increased at least 72% during deficiencies of Se and vitamin E. In summary, GSH-Px did not respond to increased oxidative stress associated with elevated dietary iron except for the non Se GSH-Px which accounts for a relatively small amount of total activity in liver. Catalase increased in liver only when GSH-Px and vitamin E are limiting.

Animals↗

Influence of adult age on the skeletal response to phosphate and estrogen in rats.

Sixteen-month-old ("aged") female rats were less susceptible than 6-month-old ("mature") females to parathyroid hormone (PTH)-mediated bone resorption induced by excess dietary phosphate. Ovariectomy enhanced 45Ca loss from the bones of mature rats but not of aged rats. In mature ovariectomized (OX) females, estradiol initially suppressed phosphate-induced bone resorption but its effectiveness decreased with continued administration. Diethylstilbestrol (DES) administered continuously or on a 3-weeks-on, 1-week-off schedule in the diet suppressed the increase in 45Ca loss in OX mature females fed a high (1.2%) P diet. In contrast, DES had no consistent effect on 45Ca loss by the aged animals. Urinary cyclic adenosine monophosphate (cAMP) was increased to a similar extent in both groups by feeding excess phosphate, indicating that the reduced effect of phosphate on 45Ca loss in the aged females was due to decreased bone response to PTH. Ovariectomies produced an increase in cAMP excretion which was suppressed by DES administration. DES also suppressed the increase in urinary cAMP induced by dietary phosphate, signifying that the decrease in bone resorption produced by estrogen is associated with an inhibition either of PTH synthesis or function.

Aging↗

A controlled evaluation of albendazole against natural infections with Fasciola hepatica and Fascioloides magna in cattle.

Albendazole administered to cattle at doses of 45, 35, 25, and 15 mg/kg of body weight reduced the number of viable Fasciola hepatica adults by 99.8%, 97.6%, 97.6%, and 95.7%, F hepatica immatures by 100%, 98.6%, 98.6% and 91.9% and Fascioloides magna by 96.5%, 99.1%, 94.0%, and 94.0%, respectively. Statistical evaluation by one-way analysis of variance, showed significant (P less than 0.05) differences in burdens of each fluke species between treated and untreated cattle, but differences in efficacy between any two of the four drug doses were not significant. Signs of toxicosis were not observed between the time of drug administration and slaughter 7 to 10 days later.

Animals↗

Evaluation of fenbendazole as an anthelmintic for gastrointestinal nematodes of cattle.

Calves naturally infected with Ostertagia, Haemonchus, Trichostrongylus, and Cooperia were used in a controlled experiment to determine the anthelmintic efficacy of fenbendazole, methyl-5-(phenylthio)-2-benzimidazolecarbamate, and to compare this with the efficacy of levamisole. The calves were placed in dry lots for approximately 3 weeks, ensuring that immature Ostertagia larvae were in arrested development before the calves were treated. In calves given doses of 8 mg of levamisole/kg of body weight and 5 and 7.5 mg of fenbendazole/kg, reductions of adult Ostertagia were 95%, 99%, and 99% respectively. Reductions of developing Ostertagia L4 were 29%, 99%, and 100%; of arrested Ostertagia L4--5%, 24%, and 72%; of adult Haemonchus--97%, 100%, and 100%; of adult Trichostrongylus--97%, 99%, and 100%, and of adult Cooperia--100%, 100%, and 100%--as compared with data in untreated controls.

Animals↗

Evaluation of less than recommended dosages of levamisole phosphate for the treatment of gastrointestinal nematodes of cattle.

The anthelmintic activity of 3 dosages of injectable levamisole phosphate was evaluated in 84- to 145-kg calves from a herd of cattle with a history of heavy gastrointestinal nematode infections. Trichostrongylid egg counts in the calves varied from 450 to 700/g of feces. The anthelmintic was administered subcutaneously to 3 groups of 10 calves each, at the rate of 8 mg/kg of body weight (current manufacturer's recommendation), 6 mg/kg, and 4 mg/kg. A 4th group of 10 calves was utilized as untreated control calves. At necropsy, comparison of worm burdens between treated and untreated calves indicated apparent reductions (at 8 mg/kg, 6 mg/kg, and 4 mg/kg, respectively) for the various nematodes to be: Haemonchus placei adults-99.9, 100, and 98.3%; H placei L4-91.0, 94.0, 98.0%; O ostertagia late L4-93.8, 86.7, and 96.3%; Trichostrongylus axei adults-99.1, 100, and 100%; Cooperia spp adults-99.8, 99.5, and 99.5%; and Oesophagostomum radiatum adults-100, 100, and 100%. Statistical evaluation, by one-way analysis of variance, of the mean number of each species recovered showed significant (P less than 0.05) differences in the worm burdens between treated and untreated calves, but differences in efficacy between any 2 of the 3 drug dosages were not significant.

Animals↗

Physiological responses of human adults to foods containing phosphate additives.

An experiment was conducted to assess the physiological effects of a diet rich in foods cotaining phosphate additives. During a 4-week control period, eight adults were fed a balanced diet free of phosphate additives providing approximately 95 g protein 0.7 g Ca and 1.0 g P per day. During a subsequent 4-week period, food items containing phosphate additives were substituted for counterpart items devoid of added phosphates. This diet contained 0.7 g Ca and 2.1 g P per day. The introduction of foods containing phosphate additives was associated with intestinal distress, soft stools or mild diarrhea. These symptoms subsided in six subjects but occurred intermittently throughout the experimental period in the other two subjects. The high-phosphorus diet induced increases in serum phosphorus and urinary phosphorus and decreases in serum calcium and urinary calcium. Hydroxyproline excretion in the urine was increased and cyclic AMP excretion was elevated in six of the eight subjects. These changes are analogous to those seen in experimental animals fed high-phosphorus diets which were shown to be due to enhanced parathyroid activity (secondary hyperparathyroidism). The use of phosphate food additives is discussed with respect to their possible stimulating effect on adult bone resorption.

Adult↗

Influence of dietary peroxides, selenium and vitamin E on glutathione peroxidase of the gastrointestinal tract.

The influence of dietary peroxides, vitamin E and selenium on glutathione peroxidase (GSH-Px) activity in the gastrointestinal tract of the rat was investigated. Feeding 7% oxidized stripped corn oid (peroxide value 1,000) in a diet adequate in selenium and vitamin E increased the specific activity of GSH-Px in the stomach mucosa. Feeding oxidized oil produced an increase in the wet weight of the intestinal mucosa which was associated with a decrease in the specific activity of the enzyme. Total GSH-Px activity in the intestinal mucosa was unchanged or moderately increased. These changes were unaffected by the presence of vitamin E in the diet. Dietary peroxides had no effect on GSH-Px activity in the plasma or in the perirenal and paraepididymal adipose tissues. Subacute vitamin E deficiency had no consistent effect on the activity of the enzyme in several tissues examined. In rats fed a Se deficient diet glutathione peroxidase activity decreased markedly in most tissues but only slightly in the intestinal mucosa. The moderate decrease in the intestine may be explained by the accessibility of residual dietary Se to the mucosal cells. The role of Se in the detoxification of peroxides in foods and the response of gastrointestinal GSH-Px to dietary peroxides are discussed.

Adipose Tissue↗

Glutathione peroxidase activity and glutathione concentration in genetically dystrophic mice.

The present studies were conducted to determine whether inherited muscular dystrophy in the 129/ReJ-dy mouse was associated with differences in specific activity, substrate availability, or apparent Km of glutathione peroxidase. The results indicate that glutathione peroxidase is elevated in skeletal muscle of mice with genetic muscular dystrophy when the activity is expressed on a protein basis. This elevation precedes the development of severe paralysis since muscles from the fore legs showed increased enzyme activity as early as the more severely affected hind legs. There was no difference in glutathione peroxidase activity in tissues other than skeletal muscle. GSH concentration was elevated in muscle and normal in other tissues of dystrophic mice, showing that adequate substrate was available to the enzyme. The apparent Km for cumene hydroperoxide was also similar for muscle of normal and dystrophic mice. This report provides further evidence that mice with dystrophia muscularis have a functional glutathione peroxidase system in all tissues including skeletal muscle, and that a defect in this in vivo protective system is apparently not a contributing factor in the pathology of the disease.

Aging↗