Nutritional Se Research Articles

Influence of Dietary Vitamin E on Nutritional Pancreatic Atrophy in Selenium-Deficient Chicks

Studies were conducted to determine the relationship between dietary vitamin E (VE) and the development of nutritional pancreatic atrophy (NPA) in selenium (Se)-deficient chicks. Selenium- and VE-depleted chicks reared on a low Se, amino acid-based diet containing 100 KI VE (as all-rac-α-tocopheryl acetate) per kilogram were found to have exceedingly low pancreatic activities of Se-dependent glutathione peroxidase (SeGSHpx) at 8 d of age. Supplementation of the purified diet with 500 or 1000 KI VE/kg prevented both NPA and the associated growth depression. Use of graded dietary VE levels showed that addition of at least 300 KI/kg was required to overcome the growth depression associated with severe Se deficiency. Although tissue α-tocopherol concentrations increased linearly with increasing dietary levels of VE, the response in pancreas was less than (about one-half of) those in liver and heart and, unlike the response in heart, was not affected by dietary Se level. That protection against NPA involved the antioxidant action of VE was suggested by results showing that NPA is promoted by high dietary levels of linoleic acid, that high VE levels correct membrane unsaturated fatty acid losses due to Se deficiency and that NPA is prevented by high levels of other antioxidants. It is suggested that the normally low activities of SeGSHpx and concentrations of α-tocopherol in the pancreas may predispose that organ to lesions due to oxidative stress under conditions of severe nutritional Se deficiency that results in further depletion of SeGSHpx. This situation may be overcome by feeding VE at 15–20-fold excesses over the levels normally regarded as nutritionally required.

Response to Divergent Selection for Early Growth of Chickens Fed a Diet Deficient in Selenium

Three generations of divergent selection for 21-day growth response to a diet deficient in selenium (–Se) were bred using a meat-type chicken. The Athens-Canadian Randombred (AC) population of chickens served as the base population for this study. Mass selection was used to establish a –Se refractory line (SDR) and a –Se susceptible line (SDS). A genetic control line was maintained during the selection process to facilitate evaluation of the responses of the selected lines.The SDR males and females had an average of 17% increase in weight gain at 21 days of age when fed the –Se diet compared with the control line males and females fed the same diet for the three generations of selection. The SDS line had an average reduction in weight gain of 27% during the same period of selection. A difference of 25 g was observed between the mean body weights of SDR males and females and between the SDS males and females after one generation of selection. By the third generation of selection, the difference between SDR and SDS males had increased to 31 g, whereas the SDR and SDS females differed by 41 g.Early response to selection was asymmetrical because the response was greater in the SDS than in the SDR line. Response to selection, however, generally declined after the first generation. Realized heritability estimates for individual generations for this trait were variable (ranging from –.26 to .95), but cumulative estimates (.15 to .39) for growth through three generations were similar to those reported for chickens and quail. Females had larger estimates of heritability than males, which suggests the possiblity of sex-linked effects for this trait. This study establishes the response of the chick to nutritional Se deficiency as an heritable trait.

The role of selenium in Keshan disease.

Since the discovery of the essentiality of selenium (Se) for rats by Schwarz and Foltz (1957) and for chicks by Patterson et al. (1957), several naturally occurring animal diseases related to Se and vitamin E (VE) deficiency have been reported (Muth et al., 1958; Hartley and Grant, 1961). Since the recognition of Se as an essential nutrient for animals, suggestions that Se may also be essential in human nutrition have been based upon three kinds of findings. One was the demonstration of certain uncomplicated Se-deficiency diseases produced in the laboratory chick (Thompson and Scott, 1970) and rat (McCoy and Weswig, 1969; Wu et al., 1979), with the assumption that a similar specific requirement should occur in humans. Second was the isolation of glutathione peroxidase (GSHpx) from human erythrocytes (Awasthi et al., 1975) and human placenta (Awasthi and Dao, 1978). There was also the finding that Se is required for the growth of human fibroblasts in culture (McKeehan et al., 1976). It was, therefore, reasonable to assume that some human disorders may be related to nutritional Se deficiency. The association of Se with protein-rich foods prompted the early investigation of its possible relation to the pathogenesis of protein-calorie malnutrition (Schwarz, 1965a; Burk et al., 1967). Moreover, the detrimental effects of Se deficiency on heart function observed in animals (Godwin, 1965;) Godwin and Frash, 1966) led some relationship between Se deficiency and human cardiovascular disease.

Protection against Acute Paraquat Toxicity by Dietary Selenium in the Chick

Experiments were conducted to determine whether both dietary vitamin E and selenium (Se) affect the acute toxicity of paraquat in the chick. Paraquat significantly stimulated the rate of NADPH-supported consumption of oxygen by the microsomal fractions of chick liver and lung, and this stimulation was decreased by addition of superoxide dismutase and/or catalase. The acute oral LD50 of paraquat in the 8-day-old vitamin E- and Se-deficient chick (131 mg/kg body weight) was increased more than threefold by supplementing the diet with 0.10 ppm Se as Na2SeO3, (419 mg/kg body weight) but was not significantly affected by supplementing the diet with vitamin E (148 mg/kg body weight). A high fat (20%) diet did not alter the protective effect of Se against the acute toxicity of paraquat; however exposure to an oxygen-enriched atmosphere did reduce the protection by dietary Se. Dietary Se at 0.01 ppm protected against acute paraquat toxicity, whereas 0.08 ppm Se produced detectable increases in the Se-dependent glutathione peroxidase. These results indicate that the acute toxicity of paraquat in the chick is highly responsive to nutritional Se status and not vitamin E status.

Subject groups high and low in urinary selenium levels: workers exposed to heavy metals and patients with cancer and epilepsy.

Selenium was first recognized for its toxicity; its essential nature in animals was discovered and established later. That Se is essential to human nutrition has yet to be confirmed. Recently the selenoenzyme glutathione peroxidase (GSH-Px) was isolated from human erythrocyte and placenta. In order to discover the role Se plays in human health and disease, Thomson and Robinson emphasized a need for continuing studies of special needs of certain groups such as those exposed to heavy metals and those with certain disease and illness for example, cancer and cardiovascular disease. It is amongst these groups that Se deficiency or Se-responsive conditions may be found. Urinary Se excretion has been mainly used to assess the nutritional Se status. Recently estimation of urinary Se level in the form of its content per creatinine (abbreviated as CT) content using 24-h or random urine samples was shown to be more precise in reducing dilution and variation effects than that per urinary volume using 24-h urines (HOJO). The purpose of this study is to search the subject groups high or low in Se status by employing urinary Se content per CT content or per urine volume.

In vitro Uptake of Selenium-75 by Red Blood Cells from the Immature Ovine during Varying Selenium Intakes

Six crossbred wether lambs were used for preliminary study of the effect of varying Se intake upon uptake of 75Se in vitro by ovine red blood cells. In a second experiment, 16 crossbred wether lambs were equally allotted among 4 dietary Se levels of 0.014, 0.264, 0.514 and 5.014 ppm. The feeding trial lasted 104 and 107 days for experiments 1 and 2, respectively. Lambs receiving 0.264 and 0.514 ppm Se gained faster, consumed more feed and had a higher feed efficiency than lambs in other dietary groups. Lambs on 0.014 ppm Se performed better than with the 5.014 ppm level. Adequate vitamin E may have prevented deficiency syndromes in lambs fed the low level of Se. Two lambs on the 5.014 ppm level exhibited symptoms of chronic selenosis. The uptake of 75Se was significantly correlated with incubation time in the presence of an O2-CO2 mixture. The initial influx and rate of in vitro uptake of 75Se by ovine blood cells decreased with increasing Se level in the diet. The in vitro uptake of 75Se by red blood cells proved to be a promising technique to assess the nutritional Se status in the immature ovine.

Sulfur-selenium-vitamin E interrelations in ovine nutrition.

Three experiments were conducted to evaluate interrelationships between S, Se and vitamin E in the nutrition of the ovine. In the initial experiment, a daily intake of 7.62 gm. S as sodium sulfate was found to be readily absorbed and excreted in large quantities (51.4% of ingested S) in the urine. The amount of water excreted via the urine was found to be greatly increased due to sulfate supplementation of the ration. Hence sodium sulfate was considered an excellent source of S as a potential competitor with Se in nutrition of the pregnant ewe. Hematocrits of ewes at 27–38 days prepartum appeared to be greater when ewes were fed a final level of 12.1 gm. S per head daily than when fed 3.0 or 21.3 gm. per head daily. The hematocrits of ewes fed 3.0 or 21.3 gm. S per head daily appeared to be below normal. Serum tocopherol levels were significantly affected by treatment and dietary Se depressed levels in what may have been a sparing action of Se in mobilizing tissue tocopherols. Serum tocopherol levels appeared to be increased as a result of feeding the intermediate level of S (final level, 12.1 gm. per head daily). Administration of vitamin E at 89 days or less of pregnancy appeared to exert a favourable effect on lambing percentage; the intermediate level of S also appeared to exert a favourable effect, but this was primarily a result of the 190% lamb crop that resulted when the ewes also were administered tocopherol. Five ewes fed the intermediate level of S and four fed the high level aborted in late pregnancy. These abortions occurred regardless of vitamin E or Se administration. Pathological changes in tissues of five lambs from ewes fed medium and high levels of sulfur were similar to those associated with WMD. There was no evidence that 0.75% to 1.32% dietary S in rations fed to ewes during late pregnancy were contributory to WMD in lambs born alive and surviving beyond 24 hr. of age. Administration of 1.5 mg. Se to 2- to 4-week old lambs creep fed diets containing less than 0.07 ppm Se and nursing ewes fed rations providing an equally low level of Se did not significantly increase gains over a 6 5-day feeding period.