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Biomedical subjects

E O Uthus

Publications and source records attributed to E O Uthus.

At least 19 recordsLinked to original sources

Use of bioimpedance spectroscopy to estimate body water distribution in rats fed high dietary sulfur amino acids.

The effect of dietary sulfur amino acids on bioelectric properties was studied in rats by using bioimpedance spectroscopy. Weanling rats were assigned to one of 12 groups in a factorially arranged experiment with dietary variables of supplemental sulfur amino acid (none, 10 g DL-methionine/kg or 10 g DL-homocystine/kg), pyridoxine hydrochloride (0 or 7.5 mg/kg) and nickel (0 or 1 mg/kg). After 9 wk of feeding, 20-h urine specimens were collected from food-deprived rats for measurements of creatinine, and then bioimpedance was measured with multifrequency (Hydra ECF/ICF 4200) and single-frequency (RJL Systems model 101) analyzers. Urinary creatinine excretion was measured by intracellular water (ICW), total body solid and urinary volume (R2 = 0.675). Extracellular water (ECW) did not add significantly to the model. Rats fed methionine had significantly lower total body water, ICW and ECW than rats fed no supplemental sulfur amino acid. Rats fed homocystine had significantly lower ECW and a significantly higher ratio of ICW to ECW. Rats fed methionine or homocystine had significantly lower capacitance corrected for body length and ICW than those fed no supplemental sulfur amino acids. These results suggest that dietary homocystine changes the distribution of body water and that sulfur amino acids can affect membrane porosity and/or membrane thickness.

Amino Acids, Sulfur↗

Dietary selenium and arsenic affect DNA methylation in vitro in Caco-2 cells and in vivo in rat liver and colon.

Selenium is an essential trace element for human health, and it has received considerable attention for its possible role as an anticarcinogenic agent. The purpose of the present study was to determine whether changes in the amount and the chemical form of selenium would affect DNA methylation and whether this effect would be modified by arsenic. Caco-2 cells, a human colon cancer cell line, were exposed to 0, 1 or 2 micromol supplemental selenite/L and 0, 1 or 2 micromol supplemental arsenite/L for 7 d. DNA isolated from Caco-2 cells not treated with selenite was significantly (P: < 0. 0001) hypomethylated compared with that from cells treated with 1 or 2 micromol selenite/L. DNA isolated from Caco-2 cells not treated with arsenite was significantly (P: < 0.0001) hypomethylated compared with DNA isolated from cells treated with 1 or 2 micromol arsenite/L. In addition, methylation of the p53 promoter region of Caco-2 cells decreased when cells were cultured in the absence of selenite and in the absence of arsenite. Sixty weanling male Fischer 344 rats were fed a torula yeast-based diet supplemented with 0, 0.1 or 2 mg selenium/kg diet as either selenite or selenomethionine in the presence or absence of 5 mg arsenic/kg diet as arsenite for 6 wk. Similar to the results with Caco-2 cells, rats fed selenium-deficient diets had significantly (P: < 0.0001) hypomethylated liver and colon DNA compared with rats fed 0.1 or 2.0 microg selenium/g diets as either selenite or selenomethionine. Thus, alterations in DNA methylation may be a potential mechanism, whereby deficient dietary selenium increases liver and colon tumorigenesis.

Animals↗

Fuzzy sets and fuzzy decision making in nutrition.

OBJECTIVE: This paper demonstrates that a nutrient intake can be described in a differentiated way and can be evaluated by employing fuzzy decision making. It also examines whether fuzzy decision making can simplify nutrition education by small individual improvements in food selection behaviour. RESULTS: The recommendations for nutrient intakes are presented as fuzzy sets, so that the intake of each nutrient can be evaluated by an objective fuzzy value. The evaluation of the harmonic minimum allows, for the first time, that the fuzzy value of an individual nutrient can be stated as a total value. On the basis of individual nutrition assessment, fuzzy logic in connection with fuzzy decision making, allows optimization of meals considering individual food preferences. This makes it possible in nutrition counselling to improve the nutrient intake markedly with relative small changes in food choice. CONCLUSION: Fuzzy decision making can simplify and optimize nutrition education.

Adult↗

Suppression of plasma estradiol and progesterone concentrations by buthionine sulfoximine in female rats.

Glutathione (GSH) is an important factor involved in the resistance of tumor cells to anticancer agents. Buthionine sulfoximine (BSO), a specific inhibitor of GSH synthesis, effectively decreases cellular GSH concentrations both in vitro and in vivo. Depletion of GSH by BSO sensitizes a variety of cancer cells to chemotherapeutic agents. Therefore, BSO has been on clinical trial as an anticancer adjuvant. For this purpose, it is important to understand the effect of BSO treatment not only on the sensitivity of tumor cells to anticancer agents, but also on the metabolism and function of normal tissues. The present study was undertaken to determine the effect of BSO treatment on GSH concentrations in the blood, liver, and ovary, and changes in concentrations of ovarian hormones and other important components in plasma. Female Sprague-Dawley rats, 90 days of age, were treated with 2.0 mmol/kg BSO in saline by intraperitoneal injection, twice daily for 7 days. This treatment depressed GSH concentrations in the blood, liver and ovary by 95, 75, and 85%, respectively. Several blood components were measured. These included red blood cells, hemoglobin, ceruloplasmin, hematocrit, mean corpuscular volume and hemoglobin concentration, alkaline phosphatase, urea nitrogen, creatine and creatinine, glucose, cholesterol, triglycerides, triiodothyronine (T3), thyroxine (T4), and hormones including estradiol, progesterone, and prolactin. BSO treatment significantly (P < 0.05) elevated and lowered plasma concentrations of ceruloplasmin and urea nitrogen, respectively, More importantly, plasma concentrations of estradiol and progesterone were decreased markedly (P < 0.05) in the BSO-treated animals. The hormonal results suggest that investigations on the role of BSO-induced GSH depletion in the treatment of malignancies both with and without hormone dependence in women should be undertaken.

Alkaline Phosphatase↗

Dietary folate affects the response of rats to nickel deprivation.

Because vitamin B12 and Ni are known to interact and because of the similar metabolic roles of vitamin B12 and folate, an experiment was performed to determine the effect of dietary folate on Ni deprivation in rats. A 2 x 2 factorially arranged experiment used groups of nine weanling Sprague-Dawley rats. Dietary variables were Ni, as NiCl(2) 6H(2)0, 0 or 1 mu g/g; and folic acid, 0 or 2 mg/kg. The basal diet, based on skim milk, contained less than 20 ng Ni/g. After 54 d, an interaction between dietary Ni and folate affected several variables including erythrocyte folate, plasma amino acids, and femur trace elements. For example, folate deprivation decreased erythrocyte folate; folate supplementation to the Ni-supplemented rats caused a larger increase in erythrocyte folate concentration than did folate supplementation to the Ni-deprived rats. Also, dietary Ni affected several plasma amino acids important in one-carbon metabolism (e.g., Ni deprivation increased the plasma concentrations of glycine and serine). This study shows that dietary Ni, folate, and their interaction can affect variables associated with one-carbon metabolism. This study does not show a specific site of action of Ni but it indicates that Ni may be important in processes related to the vitamin B12-dependent pathway in methionine metabolism, possibly one-carbon metabolism.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗

The use of fuzzy logic in nutrition.

Fuzzy logic is a mathematical approach to deal with systems that can not be defined precisely. Nutrient requirements fall into this category. Dietary intakes of nutrients are such that if a nutrient is given in graded amounts, with all other nutrients constant, there is no definitive border where, for example, one intake is deficient and another, slightly higher intake, adequate. Thus, fuzzy sets were developed that describe the range of intakes of a nutrient, ranging from deficiency to excess. On the basis of these fuzzy sets and the known nutrient composition of the food, an index is derived that reflects how closely the diet of an individual meets all the nutrient requirements set by the German Society of Nutrition. Because this is a computer-based system, alterations in the diet are suggested if the diet does not meet requirements. The suggested dietary alterations are usually small but nevertheless allow the diet to meet recommendations. It is important that the suggested alterations be small because the fewer the suggested changes in a diet, the greater the change a person will accept the changes. Thus nutrient intake can be described and evaluated by using fuzzy decision making. This has present applicability in nutrition education and could possibly be used as a tool in determining recommended dietary allowances.

Fuzzy Logic↗

Deliberations and evaluations of the approaches, endpoints and paradigms for dietary recommendations of the other trace elements.

Circumstantial evidence suggests that aluminum, arsenic, bromine, cadmium, germanium, lead, lithium, nickel, rubidium, silicon, tin and vanadium are essential. The evidence is most compelling for arsenic, nickel, silicon and vanadium. The estimated daily dietary intakes for these elements are arsenic, 12-50 micrograms; nickel, 100 micrograms; silicon, 20-50 mg and vanadium, 10-20 micrograms. By extrapolation from animal studies, the daily dietary intakes of these elements needed to prevent deficiency or to provide beneficial action in humans are arsenic, 12-25 micrograms; nickel, 100 micrograms; silicon, 2-5 mg (based on 10% bioavailability in natural diets) and vanadium, 10 micrograms. Thus, the postulated need by humans for these elements can be met by typical diets. Because there may be situations, however, where dietary intake does not meet the postulated requirements, research is needed to derive status indicators in humans and to further study the relationships of low intake or impaired bioavailability of these ultratrace elements to various diseases.

Animals↗

Diethyl maleate, an in vivo chemical depletor of glutathione, affects the response of male and female rats to arsenic deprivation.

An experiment was performed to determine the effect of diethyl maleate (DEM), an in vivo depletor of glutathione, on the response of male and female rats to arsenic deprivation. A 2 x 2 x 2 factorially arranged experiment used groups of six weanling Sprague-Dawley rats. Dietary variables were arsenic at 0 or 0.5 microgram/g and DEM at 0 or 0.25%; the third variable was gender. Animals were fed for 10 wk a casein-ground corn based diet that contained amounts of calcium, phosphorus, and magnesium similar to the AIN-76 diet. DEM supplementation increased blood arsenic in both male and female rats; female rats had the greatest amount of arsenic in whole blood. Although female rats in general had a lower concentration of glutathione in liver, those fed no supplemental DEM, regardless of their arsenic status, had the lowest amounts. Compared to males, female rats had a lower activity of liver glutathione S-transferase (GST). Arsenic deprivation decreased, and DEM supplementation increased liver GST activity in both male and female rats. Lung GST activity was also increased by DEM supplementation in male, but not female, rats. The most striking finding of the study was that compared to males, females had extremely elevated kidney calcium concentrations, and that the elevation was exacerbated by arsenic deprivation. DEM supplementation also exacerbated the accumulation of calcium in the kidney of the female rats. The response of the rat to both DEM and arsenic was, for many variables, dependent on gender. This gender dependence may be explained by the differences in methionine metabolism between male and female rats. Thus, arsenic deprivation apparently can manifest itself differently depending on gender.

Analysis of Variance↗

Effect of nitrous oxide on nickel deprivation in rats.

Because nickel may have a biological function in a pathway in which vitamin B12 is important, an experiment was performed to determine the effects of nitrous oxide exposure in rats deprived of nickel. Exposure to nitrous oxide (N2O) causes inactivation of cobalamin and a subsequent decrease in the vitamin B12-dependent enzymes methionine synthase and methylmalonyl CoA mutase. Rats were assigned to dietary groups of 12 in a factorially arranged experiment with dietary variables of nickel (0 or 1 microgram/g) and vitamin B12 (0 or 50 ng/g). After 6 wk, one-half of the rats from each dietary group were exposed to 50% N2O/50% O2 for 90 min/d for the last 28 d of the experiment. Vitamin B12, N2O, or their interaction had numerous effects; classical findings included N2O-induced reduction in plasma vitamin B12 and decreases in the vitamin B12-dependent enzymes. Inactivation of vitamin B12 by N2O, however, did not exacerbate signs of nickel deprivation, possibly because the rats were able to metabolically compensate to N2O exposure.

Alkaline Phosphatase↗

Dietary vitamin B12, sulfur amino acids, and odd-chain fatty acids affect the responses of rats to nickel deprivation.

An experiment was performed to ascertain whether changing the dietary intake of two substances, cystine and margaric acid (heptadecanoic acid), that affect the flux through pathways involving the two vitamin B12-dependent enzymes, methionine synthase and methylmalonyl-CoA mutase, would affect the interaction between nickel and vitamin B12. Rats were assigned to treatment groups of six in a fully crossed, four-factorial arrangement. The independent variables, or factors, were: per kg of fresh diet, nickel analyzed at 25 and 850 micrograms; vitamin B12 supplements of 0 and 50 micrograms; margaric acid supplements of 0 and 5 g; and L-cystine supplements of 0 and 12 g. The diet without cystine was marginally deficient in sulfur amino acids. Nickel affected growth, liver wt/body wt ratio (LB/BW), and a number of variables associated with iron, calcium, zinc, copper, and magnesium metabolism. Most of the effects of nickel were modified by the vitamin B12 status of the rat. In numerous cases, the interaction between nickel and vitamin B12 was dependent on, or altered by, the cystine or margaric acid content of the diet. Thus, the findings showed that the extent and the direction of changes in numerous variables in response to nickel deprivation varied greatly with changes in diet composition. These variables include those previously reported to be affected by nickel deprivation, including growth and the distribution or functioning of iron, calcium, zinc, copper, and magnesium. The findings also support the hypothesis that nickel has a biological function in a metabolic pathway in which vitamin B12 is important.

Animals↗

Effect of vanadium, iodine and their interaction on growth, blood variables, liver trace elements and thyroid status indices in rats.

A two-factor, two-by-three factorially arranged experiment was performed to ascertain whether iodine affects the response of rats to vanadium deprivation. Male weanling Wistar-Kyoto rats were fed a 16% casein 68% acid-washed ground corn diet for 8 weeks. The variables were supplemental vanadium at 0 or 1 microgram/g and supplemental iodine at 0, 0.33 or 25 micrograms/g. Vanadium deprivation increased thyroid weight and thyroid weight/body weight ratio and decreased the concentration of vanadium in liver. Vanadium and iodine interacted such that, as dietary iodine was increased, plasma glucose increased in the vanadium-deficient rats but decreased in the vanadium-supplemented rats. Also, as dietary iodine was increased, thyroid peroxidase activity decreased; the decrease was more marked in the vanadium-supplemented than the vanadium-deprived rats. The findings suggest that vanadium may have a physiological role affecting iodine metabolism and thyroid function.

Animals↗

Effects of arsenic deprivation in hamsters.

An experiment was conducted to ascertain the effects of arsenic deprivation in hamsters. Male weanling Golden Syrian hamsters were fed a casein-corn-based diet containing approximately 12 ng arsenic/g. Controls were fed 1 microgram arsenic/g of diet, as Na2HAsO4.7 H2O. After 6 weeks arsenic deprivation elevated heart weight/body weight ratio and the concentration of liver zinc and decreased the concentrations of the plasma amino acids alanine, glycine, phenylalanine and taurine. Although no biological role has been found for arsenic, the findings indicate that the hamster is a suitable animal for arsenic deprivation studies and support the hypothesis that arsenic may have a physiological role that influences methionine/methyl metabolism.

Amino Acids↗

Effects in rats of iron on lead deprivation.

In two fully crossed, two-factor experiments, F1 generation male rats were fed a basal diet supplemented with lead (lead acetate) at 0 or 2 micrograms/g and iron (ferric sulfate) at 50 or 250 micrograms/g (Experiment 1). Supplements in Experiment 2 were lead at 0 or 1 micrograms/g and iron at 50, 250, or 1000 micrograms/g. After 28 or 50 d in Experiment 1, and 35 d in Experiment 2, a relationship between lead and iron was found. Body weight was lower in low-lead than lead-supplemented 28-d-old rats regardless of dietary iron, whereas hematocrit and hemoglobin were lower in low-lead than lead-supplemented rats fed 50 micrograms iron/g diet. A similar finding was obtained with hematocrit and hemoglobin in 35-d-old rats. Dietary lead did not affect rats fed 250 or 1000 micrograms iron/g diet. Also, feeding low dietary lead did not affect 50-d-old rats regardless of dietary iron. Liver and bone concentrations of lead were markedly affected by dietary lead and iron. The concentration of lead in liver and bone was lower in low-lead than lead-supplemented rats. Compared to rats fed 50 micrograms iron/g diet, rats fed 250 micrograms iron/g diet exhibited a decreased lead concentration in liver and bone. This decrease was accentuated by lead supplementation. The findings suggest that lead acted pharmacologically to affect iron metabolism in rats.

Aging↗

Dietary magnesium, manganese and boron affect the response of rats to high dietary aluminum.

Studies were done to ascertain whether dietary magnesium, manganese and boron affect the response of the rat to high dietary aluminum. Four factorially arranged experiments of 7 weeks duration were performed with weanling Sprague-Dawley male rats. The variables were the following supplements (microgram/g fresh diet): boron as boric acid, 0 and 3; aluminum as aluminum chloride, 0 and 1,000; and magnesium as magnesium acetate, 100 and 400 (experiments 1 and 4) or 100, 200 and 400 (experiments 2 and 3). In experiments 1 and 2, the diet was supplemented with 20 micrograms manganese/g as manganese acetate, in experiments 3 and 4 the supplement was 50 micrograms/g. High dietary aluminum seemed most toxic when dietary magnesium was low enough to cause a marked growth depression (100 micrograms/g). High dietary aluminum elevated the spleen weight/body weight and liver weight/body weight ratios in magnesium-deficient, but not in magnesium-adequate rats. High dietary aluminum depressed the concentrations of magnesium in bone more markedly in magnesium-deficient than adequate rats. On the other hand, aluminum seemed most toxic when dietary boron was not low. Aluminum more markedly depressed growth in boron-supplemented than boron-deprived rats. In the boron-deprived rats fed 400 micrograms magnesium/g of diet, high dietary aluminum (1,000 micrograms/g) apparently was beneficial, in experiments 2 and 3, hematocrit, and hemoglobin were actually normalized by high dietary aluminum. Plasma magnesium was significantly depressed by high dietary aluminum when the manganese supplement was 50 micrograms/g diet but not when it was 20 micrograms/g diet. On the other hand, growth was more markedly depressed by high dietary aluminum in boron-supplemented rats when the manganese supplement was 20 rather than 50 micrograms/g diet. The findings indicate that the response of rats to high dietary aluminum is influenced by magnesium, boron, and manganese nutriture.

Aluminum↗

Interactions between essential trace and ultratrace elements.

Fully crossed, factorially arranged experiments showed that, under defined conditions, interactions occur between nickel and iron, nickel and copper, arsenic and zinc, and possibly vanadium and chromium. Nickel and iron interacted when dietary iron was supplemented as ferric sulfate only. Signs of nickel deprivation were more severe when dietary iron was low; or the signs of moderate iron deficiency were more severe when dietary nickel was deficient. When iron was supplemented to the diet as a 60% ferric-40% ferrous sulfate mixture, nickel and iron apparently did not interact. The findings suggested a synergistic relationship between nickel and iron when dietary iron was in a relatively unavailable form. An antagonistic interaction between nickel and copper was found when dietary iron was supplemented as a 60% ferric-40% ferrous sulfate mixture. Signs of copper deficiency were more severe in nickel-supplemented than in nickel-deprived rats. When the rats were made severely iron deficient by feeding of low levels of ferric sulfate only, no apparent interaction between nickel and copper was found. The interaction between arsenic and zinc apparently was noncompetitive. When dietary zinc was 40 microgram/g, arsenic-deprived chicks exhibited depressed growth and elevated hematocrits. In zinc deficiency, growth was more markedly depressed and hematocrits more markedly elevated in arsenic-supplemented than in arsenic-deficient chicks. Arsenic might be necessary for the efficient utilization or metabolism of zinc. Findings indicating an interaction between vanadium and chromium were tentative. In one experiment, the addition of 500 microgram of chromium/g of diet apparently made 5 micrograms of vanadium/g of diet toxic for chicks. Thus, the interactions between essential trace and ultratrace elements might be of nutritional significance.

Anemia↗