PubMed HealthSearch

SEARCH · PubMed Health

Results for “Selenium”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Selenium and cancer: effects of selenium and of the diet on the genesis of spontaneous mammary tumors in virgin inbred female C3H/St mice.

Inbred female C3H/St mice exhibit the normal incidence of spontaneous mammary adenocarcinoma of 80--100% if they are maintained on a standard commercial laboratory diet containing 0.15 ppm of selenium with meat and dried skimmed milk as major sources of protein. The tumor incidence drops to 42% if animals of the same strain are kept on a diet containing 0.45 ppm of selenium, with fishmeal as the main source of protein. The tumor incidence declines further to 25, 19 and 10% if the animals in addition receive 0.1, 0.5, and 1.0 ppm of selenium in the drinking water. Selenium supplementation at these levels has no noticable adverse effects on weight-grains and survival of the mice. Selenium supplmented groups of animals also remained tumor-free for longer periods than the unsupplemented controls. The results of this study indicate that a diet rich in seafoods and cereals provides more selenium and may in turn lower the probability of cancer development. Reference is made to the average human diet in the U.S.A., which only contains 0.07--0.15 ppm of selenium due to the comparatively low consumption of cereals and seafoods. An equivalent mouse diet would not have any cancer-protecting effect in the C3H/St mice of our study. Australian workers have reported significantly lower tumor incidence in a different strain of C3H mice if it was kept in Australia rather than in the U.S.A. We have found that the Australian feed contained three times more selenium than that employed in the U.S.A. and propose that this difference in selenium content was primarily responsible for these previous observations.

Animals

Hepatic cytosolic non selenium-dependent glutathione peroxidase activity: its nature and the effect of selenium deficiency.

Recent work had indicated the presence of a non selenium-dependent glutathione peroxidase activity in rat liver in addition to the selenium-dependent activity. The present study was undertaken to learn whether the glutathione S-transferases are reponsible for the non selenium-dependent glutathione peroxidase activity and to study the effect of selenium deficiency on those enzymes. Glutathione S-transferase B was purified by an established method using carboxymethyl cellulose ion exchange chromatography and studied. It exhibited glutathione peroxidase activity toward cumene hydroperoxide and t-butyl hydroperoxide. A limiting Km of 0.55 mM was determined for cumene hydroperoxide. Sulfobromophthalein was found to be a competitive inhibitor with respect to cumene hydroperoxide of the glutathione peroxidase activity of glutathione S-transferase B. Selenium deficiency caused an increase in glutathione S-transferase activity. These results establish that glutathione S-transferase B contributes to the non selenium-dependent glutathione peroxidase activity in rat liver and show that it increases in selenium deficiency when the selenium-dependent glutathione peroxidase is decreased.

Animals

Selenium content of tissues in Finnish infants and adults with various diseases, and studies on the effects of selenium supplementation in neuronal ceroid lipofuscinosis patients.

A low blood selenium level has previously been observed in healthy inhabitants of Finland (WESTERMARCK et al. 1977). In this study even lower blood selenium values were observed in patients with acrodermatitis enteropathica, dystrophia musculorum progressiva (Duchenne), infantile and juvenile type of neuronal ceroid lipofuscinosis (NCL), severe mental retardation caused by various factors, and myocardial infarction. The selenium content of the brain, heart, kidney and liver in patients of different ages was also determined. The highest selenium level was found in the kidney. The mean liver selenium concentrations in stillborn, premature and full-term neonates were 1.11 +/- 0.23 (8), 1.21 +/- 0.17 (12) and 0.93 +/- 0.16 microgram/g dry weight (12) respectively (the number of subjects in parentheses). The selenium values are considerably higher than those in infants of from one to nine months of age and adults, whose liver selenium values were 0.58 +/- 0.21 (8) and 0.67 +/- 0.08 microgram/g dry weight (8) respectively. The vitamin E levels of serum in patients with NCL, as well as in subjects with severe mental retardation (controls), were low compared with values in healthy normal subjects. Sodium selenite supplementation in patients with NCL produced at least a transitory improvement without causing any toxic effects during one year of administration.

Acrodermatitis

The selenium state of children. II. Selenium content of serum, whole blood, hair and the activity of erythrocyte glutathione peroxidase in dietetically treated patients with phenylketonuria and maple-syrup-urine disease.

The selenium content of serum, whole blood and hair was measured by neutron activation analysis in dietetically treated patients with phenylketonuria (PKU) and maple-syrup-urine disease (MSUD). Follow-up studies showed a decrease of the serum selenium content and the glutathione peroxidase activity of erythrocytes--a selenoenzyme--from normal values at the beginning of the diet to 20% (selenium) and 50% (gluthione peroxidase) of normal within 10--12 weeks of dietary treatment. In 36 patients the serum selenium content was lower at 6.7--28 X 10(-9) g/ml, independent of the age of the patients (0.5 to 10 years). The selenium content of whole blood was reduced: median = 98 X 10(-9) g/g dry weight; range 75 to 165 X 10(-9) g/g dry weitht (healthy children: median = 381 X 10(-9) g/g dry weight; range 245 to 588 X 10(-9) g/g dry weight). The selenium content of hair was markedly lower in the patients (median = 62 X 10(-9) g/g; range 13--140 X 10(-9) g/g) than in healthy children (median = 429; range 213 to 720 X 10(-9) g/g). The mean glutathione peroxidase activity of erythrocytes was reduced to 4.6 +/- 0.64 U37/g Hb, comparison to normal values (mean = 8.8 +/- 0.88 U37/g Hb).

Child

Selenium proteins in ovine tissues: III. Distribution of selenium and glutathione peroxidases in tissue cytosols.

Three 6 week-old lambs were injected with carrier-free selenium-75 as sodium selenite initially and again after 6 days. One lamb received no further injections whereas the other two received injections of either vitamin E or unlabeled Na2SeO3 when the first selenium-75 injection was given. Selected tissues were removed at autopsy 10 days after the first injection. The cytosol from homogenates of these tissues was subjected to gel chromatography, and the elution profiles determined for radioactivity, protein content, and glutathione peroxidase activity using either hydrogen peroxide or cumene hydroperoxide as substrates. The selenium-75 was found to be distributed mainly between 2 different MW peaks. The larger MW seleno-peak (90,000) possessed both glutathione:hydrogen peroxide oxidoreductase, and glutathione:cumene hydroperoxide oxidoreductase activities, but the smaller MW seleno-peak (about 10,000) possessed no glutathione peroxidase activity. A peak of about 60,000 daltons containing only glutathione:cumene hydroperoxide oxidoreductase activity and no selenium-75 was found primarily in the liver and kidney. Vitamin E had no effect on the elution profiles. Selenium status of the animal had only a minor effect on the selenium-75 distribution in the cytosol, but had a marked effect on the absolute amount of the label taken up by tissues.

Animals

[Glutathione peroxidase activity in erythrocytes and selenium concentration in blood of untreated and selenium-treated rabbits].

White New Zealander rabbits were tested for erythrocyte-borne reference values of glutathion peroxidase Px activity, with correlations being established between that activity and selenium content of the blood. The average glutathion peroxidase Px activity in untreated clinically intact rabbits was 11.8 K/g Hb. That value doubled following five selenium applications in therapeutic dosage. The values empirically determined were well adapted to normal distribution. Selenium concentrations recorded from organs of control animals were in fair agreement with values established in earlier studies (Wiesner et al., 1978). The correlation coefficient was r = 0.7117 (n = 44, alpha less than 0.001). The equation of regressive straight line Y oder X (ŷ) was ŷ = -5.3 + 59.94x, and that of X over Y (ŷ) was ŷ = 0,27 + 0,0095y, when Y defined the activity of glutathion peroxidase Px and X the selenium level in the blood.

Animals

Selenium protection against mercury toxicity: high binding affinity of methylmercury by selenium-containing ligands in comparison with sulfur-containing ligands.

In determining the protection of selenium against mercury toxicity, the binding affinity of methylmercury by various selenium-containing ligands was investigated by proton magnetic resonance (PMR) spectroscopy. The most striking feature was the small J199Hg-1H value of the selenocysteamine- and selenocysteine-methylmercury complexes, namely, the high affinity of the selenohydryl group to the mercury in comparison with those of the sulfhydryl and amino groups. The order of binding affinity of the coordination groups toward methylmercury is clearly SeH greater than SH greater than or equal to Se-Se greater than NH2 greater than S-S, SeCH3, SCH3. A definite correlation was found to exist between the mercury-proton coupling constants and the chemical shifts of methyl groups of the methylmercury complexes. A relationship between the order (Se greater than S greater than NH2) of affinity for methylmercury and the basicity (or electronegativity and covalent radius) of the donor groups was also discussed. These results suggest the high covalency of the CH3Hg-Se bond, which involves dpi-dpi back bonding.

Chemical Phenomena

Inhibitory effects of selenium on 1,2-dimethylhydrazine and methylazoxymethanol colon carcinogenesis: correlative studies on selenium effects on the mutagenicity and sister chromatid exchange rates of selected carcinogens.

Selenium (Se) inhibition of either the activation of test compounds and/or mutagenic events elicited by activated compounds is suggested by experimental rat assays, mutagenesis assays, and assays with human lymphocytes in culture. The colon tumor incidence in 1,2-dimethylhydrazine (DMH)-treated rats was reduced from 87% to 40% by 4 ppm Se supplements in the drinking water. Supplemental Se decreased the total number of colon tumors induced by DMH more than three-fold and by methylazoxymethanol (MAM) almost two-fold. Coexposure of Salmonella typhimurium TA 1538 to an effective molar ratio of Se/2-acetylaminofluorene=10, Se/N-OH-acetylaminofluorene=10 and SE/N-OH-aminofluorene=300 reduced the mutagenicity to 65, 68, and 61% of their respective controls with mutagen alone. With a molar ratio of Se/N-OH-AAF=100, Se reduced the activity to 28% of the mutagenicity of N-OH-AAF alone. Preliminary data indicating MAM is mutagenic in S. typhimurium TA 1535 and His G 46(6837) are presented. In toxicity studies exposure of human lymphocyte cultures to 1.3 X 10(-9) to 1.6 X 10(-5) M Se yielded sister chromatid exchange (SCE) rates equivalent to background levels of 6--7 SCE per cell. The SCE frequencies of lymphocytes cultured with Se and selected carcinogens are discussed.

Animals