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Biomedical subjects

O A Levander

Publications and source records attributed to O A Levander.

At least 91 records · Page 5Linked to original sources
PubMed1983

Bioavailability of selenium to Finnish men as assessed by platelet glutathione peroxidase activity and other blood parameters.

Three groups of 10 men of low selenium status were given 200 micrograms Se/day as Serich wheat, Se-rich yeast, or sodium selenate for 11 wk. Twenty unsupplemented subjects served as controls. Plasma Se levels increased steadily in the wheat and yeast groups for 11 wk without plateauing, whereas in the selenate group, plasma Se plateaued around 110 ng/ml after 4 wk. Platelet glutathione peroxidase (GSH-Px) activities increased rapidly in the wheat and selenate groups for 4 wk and then plateaued. Platelet GSH-Px increased more slowly in the yeast group. Ten weeks after the supplements were discontinued, platelet GSH-Px was higher in the wheat and yeast groups than in the selenate group. Assessment of Se bioavailability requires a short-term platelet GSH-Px measurement to determine immediate availability, a medium-term plasma Se measurement to estimate retention, and a long-term platelet GSH-Px measurement after supplements are discontinued to determine the covertibility of tissue Se stores to biologically active Se.

Adult↗
PubMed1983

Quantitative and qualitative aspects of selenium utilization in pregnant and nonpregnant women: an application of stable isotope methodology.

Selenium utilization of women in early and late pregnancy was compared to that of nonpregnant controls. A defined diet providing about 150 micrograms Se/day was fed for 20 days, and selenium balance was measured during the last 12 days. Net selenium retentions of the women in early and late pregnancy were 10 and 23 micrograms/day, respectively, but probably are inflated estimates of the increased selenium requirement during pregnancy. Apparent absorption of selenium was 80% for all three groups. Pregnant women tended to conserve selenium by decreasing urinary selenium excretion. Those observations were corroborated by monitoring the urinary and fecal excretion of 40 micrograms of a stable isotope of selenium (76Se) from intrinsically labeled egg. The isotope data also indicated that recent selenium intake was incorporated into a long-term selenium pool. Mean glutathione peroxidase activity was lower in plasma and higher in platelets in the pregnant women as compared to controls, but the physiological significance of those observations is unknown.

Adult↗
PubMed1983

Selenium and acute alcoholism.

Selenium status was investigated in nine inebriated alcoholic subjects by collecting serial samples of blood and urine during hospitalization for alcohol detoxification. The selenium content of various alcoholic beverages and samples of hospital diets was also determined. Mean plasma selenium level and mean urinary excretion of selenium were both significantly lower (p less than 0.01) in alcoholic subjects as compared to the control subjects at the time of admission. Furthermore, the daily dietary intake of selenium before hospitalization was estimated to be below the recommended safe and adequate range in the majority of the alcoholic subjects. The selenium content of various alcoholic beverages was determined to be very low (0.1 to 0.8 microgram/dl). These data suggest that selenium depletion does occur in alcoholic subjects most likely due to poor dietary intake. Selenium depletion in this group of patients is corrected by cessation of ethanol ingestion and adequate dietary intake without additional selenium supplementation.

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

Intrinsic labeling of chicken products with a stable isotope of selenium (76Se).

Chicken tissues were intrinsically labeled with a stable isotope of selenium (76Se) and were evaluated for use in a human feeding study. Laying hens were fed a low Se (0.06 ppm) basal diet for 39 days and then fed the basal diet supplemented with 0.3 ppm enriched 76Se (as selenite) for 35 days. Incorporation of 76Se into samples was determined by use of a double isotope dilution technique and a combined gas chromatography/mass spectrometry analysis. The 76Se content of the basal diet was increased by a factor of 9.7 with the addition of the enriched stable isotope. This maximal level of enrichment was approached in egg yolk (9.5-fold) and liver (9.0-fold). Enrichment was lower in egg white (7.2-fold) and breast meat (5.0-fold). Level of enrichment in a given tissue reflected both the turnover rate of the tissue and its natural selenium content. Selenium-depleted laying hens continuously fed 76Se at the 0.3 ppm level produced egg yolks and livers that were enriched sufficiently with the stable isotope for use in a human metabolic study.

Animals↗
PubMed1983

Considerations in the design of selenium bioavailability studies.

Recommendations for safe and adequate dietary intakes of selenium were recently established. The recommendations were based largely on data from animals, because few data for humans were available. Some information regarding the dietary selenium intake required by humans to replace excretory losses has now appeared, but the bioavailability to humans of selenium from different dietary sources has not been determined. Selenium bioavailability depends on several metabolic processes, including not only absorption but also conversion into a biochemically active form. Of the different forms of selenium in foods, probably not all are converted to biologically active selenium with equal ease. Therefore, determination of selenium absorption may not in itself yield an accurate estimate of selenium bioavailability. Rather, functional tests, such as measurement of the selenoenzyme glutathione peroxidase, apparently are more valid for determining selenium bioavailability. Various food sources of selenium for humans differ widely in their ability to restore hepatic glutathione peroxidase activity in selenium-depleted rats. Platelet glutathione peroxidase activity seems to be particularly promising for bioavailability studies because platelets are a convenient biopsy material and the platelet enzyme is sensitive to changes in dietary selenium intake. Work in progress should establish the feasibility of this approach for future research in this area.

Animal Nutritional Physiological Phenomena↗
PubMed1982

Clinical consequences of low selenium intake and its relationship to vitamin E.

Great differences in dietary selenium intake have resulted in naturally occurring human selenium deficiencies and toxicities in certain parts of the world. Most North American diets, however, provide levels of selenium that fall within the estimated safe and adequate range of intake (50 to 200 microgram/day for adults) as established by the U.S. National Research Council. Low selenium status may develop in individuals fed certain therapeutic diets or given total parenteral nutrition. Attempts have been made to link low selenium intake with cancer and heart disease, but additional research is needed in this area. Selenium, as a constituent of glutathione peroxidase, plays a role in the antioxidant defense systems of the body, but other metabolic roles for selenium may yet be discovered.

Adult↗
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↗
PubMed1981

Selenium in self-selected diets of Maryland residents.

The mean selenium level in six self-selected, daily diets chosen by each of 22 free-living Maryland residents was 81 +/- 41 microgram. per day. Diets that were higher in selenium also were significantly higher in copper, iron, magnesium, and manganese and slightly higher in zinc. However, in general, the levels of these minerals were low, probably because of low consumption of grains, legumes, and nuts. Diets higher in selenium contained more fish and less processed meat than other diets.

Diet↗
PubMed1979

Lead toxicity and nutritional deficiencies.

Under appropriate conditions, deficiencies of certain minerals and vitamins as well as high intakes of dietary fat increase the toxicity of a given dose of lead in experimental animals. The severity of lead poisoning can also be increased by the consumption of either deficient or excessive levels of protein. Mineral deficiencies appear to have some of the most profound effects on lead toxicity, since the consequences of plumbism can be exaggerated by feeding diets low in calcium, phosphorus, iron, zinc, and in some cases, copper. Evidence for an antagonism between lead and nutritional levels of selenium is inconclusive. Vitamin E deficiency and lead poisoning interact to produce an anemia in rats that is more severe than that caused by either treatment alone. Lead apparently exerts a pro-oxidant stress on the red cell, thereby causing its accelerated destruction. One of the biochemical mechanisms of lead poisoning may be the disruption of normal membrane architecture, thereby leading to peroxidative damage. Epidemiological surveys have suggested a negative correlation between the poor nutritional status of children with regard to calcium and the concentration of lead in blood. Other examples of potential interactions of mineral status and lead poisoning in humans include the hypothesized hazards of soft water to public health in areas with lead plumbing and the possible role of mineral deficiencies in the etiology of pica. Experimental studies have shown that in some situations combined nutritional deficiencies can have an additive effect in potentiating lead toxicity.

Animals↗
PubMed1978

Metabolic interactions between metals and metalloids.

The experimental evidence obtained with laboratory animals which shows that the toxicities of lead, cadmium, and mercury can be increased by deficiencies of certain essential nutrients such as calcium, iron, zinc, and selenium is briefly reviewed. An idealized theoretical model which indicates the possible influence of multiple nutritional deficiencies on the toxicity of a heavy metal is presented. It is suggested that multiple marginal nutritional deficiencies may be of importance in determining the response of humans to the toxic effects of various heavy metal pollutants.

Animals↗