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The urinary excretion of selenium in sheep treated with a vasopressin analogue.

The renal excretion of selenium was investigated in ewes with an excretion of hypotonic urine (control group) and in ewes with a formation of highly concentrated urine. Chronic stimulation of the urinary concentrating activity of sheep kidneys was induced by a long-term treatment with 1-desamino-8-D-arginine vasopressin (dDAVP), a synthetic analogue of vasopressin with prolonged effects. Young animals with 22 to 25 kg b.w. were fed a normal protein diet providing a daily intake of 129.25 g of crude protein, 12.03 MJ of digestible energy and 0.18 mg of selenium for 3 weeks. The vasopressin treated sheep (n = 11) were given subcutaneous injections of 12.5 micrograms of dDAVP in glycerol twice daily for one week before the clearance measurement of renal functions. The control group (n = 11) was treated with glycerol only. The administration of dDAVP resulted in a highly significant decrease of the urinary flow rate (from 3.19 +/- 0.50 in control group to 0.33 +/- 0.03 mL.min-1 in dDAVP animals, P < 0.001) without changes in the glomerular filtration rate (80.18 +/- 6.36 in controls vs. 77.86 +/- 6.26 mL.min-1, NS). No effects on plasma selenium level were observed (0.17 +/- 0.03 in controls vs. 0.20 +/- 0.03 mumol.L-1, NS) but the amounts of selenium excreted were found to be highly significantly reduced (from 0.29 +/- 0.05 in controls to 0.03 +/- 0.01 nmol.min-1, P < 0.001) in dDAVP treated sheep. Despite a large reduction in urinary flow rate, the selenium concentration in urine was actually the same in both groups (0.09 +/- 0.01 mumol.L-1) resulting in a sharp fall in the renal clearance of selenium (2.20 +/- 0.54 in controls vs. 0.18 +/- 0.03 mL.min-1, P < 0.01) due to dDAVP. This seems to be a consequence of the large increase in the selenium solvent drag induced by a vasopressin treatment. The results presented suggest that vasopressin may contribute to maintenance of the selenium balance in sheep via its effects on renal function.

Animals↗
PubMed2003

Low selenium status is associated with the occurrence of the pregnancy disease preeclampsia in women from the United Kingdom.

OBJECTIVE: Because the trace element selenium behaves as an antioxidant and peroxynitrite scavenger when incorporated into selenoproteins, our objective was to determine whether low selenium status was associated with a greater risk of occurrence of preeclampsia. STUDY DESIGN: Fifty-three preeclamptic patients and 53 matched pregnant controls at the John Radcliffe Hospital, Oxford, gave clippings of their toenails (laid down from 3-12 months previously) for selenium determination by neutron activation analysis. Clinical characteristics of the women and their infants were recorded. Statistical analysis was by Wilcoxon signed rank test and odds ratios were calculated by the ratio of discordant pairs. RESULTS: Median toenail selenium concentrations in the preeclamptic subjects were significantly lower than in their matched controls (P=.001). Being in the bottom tertile of toenail selenium was associated with a 4.4-fold (95% CI 1.6-14.9) greater incidence of the condition. Within the preeclamptic group, lower selenium status was significantly associated (P=.029) with more severe expression of disease, as measured by delivery before 32 weeks. CONCLUSION: In the light of the reduction in selenium status in a number of European countries in recent years, this study raises the question of whether a small increase in selenium intake might help prevent preeclampsia in susceptible women.

Adult↗
PubMed1984

Occurrence of selenium-containing tRNAs in mouse leukemia cells.

Selenium incorporation into the polynucleotide structures of tRNAs has been documented in several microorganisms. In the present study, selenium-containing species were isolated from bulk tRNA preparations from 75Se-labeled mouse leukemia cells. The major 75Se-labeled species was similar in size and exhibited the same sensitivity to ribonuclease as did Escherichia coli tRNAs. The chromatographic properties of the intact major selenium-containing tRNA species indicated it to be very hydrophobic in character. The selenium component that is unstable at neutral-to-alkaline pH but is relatively stable at acid pH is not an esterified selenoamino acid. HPLC analysis of enzymic digests of the major selenium-containing species detected selenium-containing hydrophobic products (probably selenonucleosides ). These properties strongly suggest that the selenium in the mouse leukemia-cell tRNAs is present in the form of a selenium-modified nucleoside.

Animals↗
PubMed2000

Effects of continuous supplementations of ascorbic acid, aspirin, vitamin E and selenium on some haematological parameters and serum superoxide dismutase level in broiler chickens.

1. This study was conducted using male broiler chickens to determine the effects of ascorbic acid, aspirin, ascorbic acid+aspirin, vitamin E+selenium and ascorbic acid+aspirin+vitamin E+selenium supplementations on haematological parameters and serum superoxide dismutase concentration. 2. One hundred and twenty day-old male Hubbunt broiler chicks were randomly divided into 6 experimental groups of 20 chicks each and placed in different pens. Groups 2, 3, 4, 5 and 6 were given a diet supplemented with ascorbic acid, aspirin (in water), ascorbic acid+aspirin, vitamin E+selenium and ascorbic acid+aspirin+vitamin E+selenium, respectively for 45 d while group 1 was given a commercial broiler diet. 3. There was no significant effect of ascorbic acid, aspirin, ascorbic acid+aspirin, vitamin E+selenium supplementations on any of the haematological parameters (red blood cell, haemoglobin, haematocrit, mean corpuscular volume, mean corpuscular haemoglobin concentration, mean corpuscular haemoglobin) in broilers but ascorbic acid+aspirin+vitamin E+selenium supplementation significantly decreased the white blood cell counts. 4. In addition to this, ascorbic acid, aspirin, ascorbic acid+aspirin and ascorbic acid+aspirin+vitamin E+selenium supplementations had no significant effect on the serum superoxide dismutase level, but vitamin E+selenium supplementation increased the serum superoxide dismutase level.

Animals↗
PubMed1994

Effect of dietary phytate on growth and selenium status of chicks fed selenite or selenomethionine.

1. An experiment was conducted to study the effect of dietary phytate on the selenium status of chicks fed on a semi-purified diet with or without supplements of sodium selenite or selenomethionine (200 micrograms Selenium/kg). 2. Assessment included measurement of growth and activity of glutathione peroxidase (GSHPx) (EC.1.11.1.9), an enzyme that limits damage by free radical species arising from oxygen metabolism by catalysing the reduction of hydrogen peroxide and lipid hydroperoxides. In addition, information was obtained on forms of selenium in blood, liver, kidney, heart and muscle, distinguishing between selenide-Se, reducible-Se and non-reducible-Se. 3. Phytate caused significant reductions in growth, food consumption and food conversion efficiency. Supplementary selenium was without effect on growth but significantly increased GSHPx activity in all tissues. Phytate also increased GSHPx activity in blood and heart, and in muscle in the absence of supplementary selenium, but decreased the activity in kidney. 4. Concentrations of all forms of tissue selenium were significantly increased by supplementary selenium. In general, there was greater deposition from selenomethionine than from selenite and most was in non-reducible form. 5. Phytate increased selenium in all tissues except muscle; it is not clear if this resulted from increased absorption or increased retention. It increased reducible-Se in blood, liver and heart and non-reducible-Se in blood and kidney. Tissue concentrations of selenide-Se were highly variable: presence or absence of phytate contributed to some significant interactions. 6. The results suggest that there is a positive relationship between phytate and selenium status in chicks, in contrast to its negative effect on growth.

Animals↗
PubMed1987

Low plasma selenium as a risk factor for cancer death in middle-aged men.

In a population study, 10,000 men (aged 46-48 years) were invited to a health screening program. At follow-up, which was up to eight years later, 61 subjects had died from cancer; from 35 of these subjects, plasma samples were available that were obtained at the initial screening. These samples, together with samples from two living controls for each case, were analyzed for selenium, retinol, cholesterol, triglyceride, and a number of plasma proteins. Plasma selenium was significantly lower (p less than 0.05) in cases than in controls (means: 1.06 vs. 1.12 mumol/l). The proportion of cases increased significantly from the highest to the lowest quintile of plasma selenium, and the relative risk for cancer death was 3.8 times higher in the lowest quintile compared with the highest. Mean plasma retinol was similar in cases (2.53 mumol/l) and controls (2.56 mumol/l). Cases and controls also had similar values for plasma cholesterol, triglyceride, uric acid, apolipoprotein B, orosomucoid, prealbumin, retinol-binding protein, and beta 2-microglobulin. Apolipoprotein AI in plasma was lower among cases (p less than 0.025). Cases smoked significantly more than controls did (p less than 0.05). Data indicate that low plasma selenium was a risk factor for cancer death in middle-aged men who lived in the same area. Further studies are necessary to establish whether differences in selenium intake, selenium metabolism, or other factors related to selenium are responsible for the relations observed. At present, the available data do not justify selenium supplementation programs in the whole population.

Apolipoprotein A-I↗
PubMed1991

Inhibition by selenium of intrahepatic cholangiocarcinoma induction in Syrian golden hamsters by N'-nitrosobis(2-oxopropyl)amine.

The effects of selenium supplementation on induction of cholangiocarcinomas and related precancerous lesions in female Syrian Golden hamsters by N'-nitrosobis(2-oxopropyl)amine (BOP) were investigated. Four-week-old animals were divided into two groups according to the selenium level contained in the drinking water (0.1 ppm or 4.0 ppm) and fed a purified diet containing less than 0.05 ppm of the trace element. Starting at Week 4 of the experiment, hamsters were administered 10 weekly injections of BOP (10 mg/kg body wt) and then killed 18 weeks after the last carcinogen administration. Animals receiving physiological saline alone served as controls. Cholangiocellular carcinomas tended to be reduced, and putative preneoplastic lesions of cholangiofibrosis were significantly decreased in the high-as opposed to the low-selenium groups in terms of both incidence rate and number per effective animal. The respective high and low selenium values for incidence and number were 24/38% and 0.34/0.66, respectively, for cholangiocarcinomas and 50/89% and 1.21/8.44, respectively, for cholangiofibroses. Proliferation of intrahepatic bile ducts was also significantly inhibited in the high-selenium group along with cyst formation. Biochemical investigation revealed both selenium level and glutathione peroxidase activity to be significantly greater in the high-than in the low-selenium group livers. The results thus suggest that selenium may inhibit BOP-induction of bile duct lesions, possibly via glutathione peroxidase-mediated alteration of carcinogenesis.

Adenoma, Bile Duct↗
PubMed1990

Selenium status in workers handling aromatic nitro-amino compounds in a chemical factory.

The selenium status of workers handling aromatic nitro-amino (ANA) compounds was evaluated by measurement of their blood and urinary selenium concentrations and blood glutathione peroxidase (GSH-Px) activities. Forty-seven healthy Japanese male workers (42.7 +/- 12.1 yr) handling ANA compounds routinely in a chemical factory were studied as exposed workers, and 107 nonindustrial healthy Japanese males (39.3 +/- 10.0 yr) in the same region served as a control group. Urinary diazoreaction-positive metabolites and methemoglobin, both of which have been used as indices of exposure to ANA compounds, were significantly elevated in the exposed workers. Both plasma and erythrocyte selenium in the exposed workers showed 20% lower values compared to the control group. GSH-Px activities in plasma and erythrocytes were also significantly decreased in the exposed workers, but urinary selenium excretions were similar between the two groups. Questionnaire information obtained from each subject regarding intake habits of selenium-rich foods (bread, eggs, meat, and fish) indicated that the average dietary selenium intake was similar for the control group and the exposed workers. These results indicate that (1) the workers handling ANA compounds were surely exposed to these chemicals; (2) their selenium status was lower than that of the nonindustrial controls; and (3) the low selenium status was not associated with any dietary factor.

Adult↗
PubMed2002

The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health.

Several minerals and trace elements are essential for normal thyroid hormone metabolism, e.g., iodine, iron, selenium, and zinc. Coexisting deficiencies of these elements can impair thyroid function. Iron deficiency impairs thyroid hormone synthesis by reducing activity of heme-dependent thyroid peroxidase. Iron-deficiency anemia blunts and iron supplementation improves the efficacy of iodine supplementation. Combined selenium and iodine deficiency leads to myxedematous cretinism. The normal thyroid gland retains high selenium concentrations even under conditions of inadequate selenium supply and expresses many of the known selenocysteine-containing proteins. Among these selenoproteins are the glutathione peroxidase, deiodinase, and thioredoxine reductase families of enzymes. Adequate selenium nutrition supports efficient thyroid hormone synthesis and metabolism and protects the thyroid gland from damage by excessive iodide exposure. In regions of combined severe iodine and selenium deficiency, normalization of iodine supply is mandatory before initiation of selenium supplementation in order to prevent hypothyroidism. Selenium deficiency and disturbed thyroid hormone economy may develop under conditions of special dietary regimens such as long-term total parenteral nutrition, phenylketonuria diet, cystic fibrosis, or may be the result of imbalanced nutrition in children, elderly people, or sick patients.

Animals↗
PubMed1990

Iodine and selenium deficiency associated with cretinism in northern Zaire.

Selenium status was determined in an endemic-goiter area and in a control area of Zaire. Compared with the reference values of a noniodine-deficient area, serum selenium in subjects living in the core of the northern Zaire endemic-goiter belt (Karawa villages) was seven times lower in 52 school-children and similarly low in 23 cretins; erythrocyte glutathione peroxidase (RBC-GPX) was five times lower in schoolchildren and still two times lower in cretins (P = 0.004). In a less severely iodine-deficient city of the same endemia (Businga), selenium status was moderately altered. RBC-GPX activity was linearly associated with serum selenium concentration up to a value of 1140 nmol/L and leveled off at approximately 15 U/g Hb at greater selenium concentration. At Karawa villages, selenium supplementation normalized both the serum selenium and the RBC-GPX. This combined iodine and selenium deficiency could be associated with the elevated frequency of endemic myxedematous cretinism in Central Africa.

Adolescent↗
PubMed1991

Selenium in diet, blood, and toenails in relation to human health in a seleniferous area.

To determine whether high dietary selenium intake was associated with adverse effects, selenium in diet, blood, and toenails was studied in relation to human health in adults residing in western South Dakota and eastern Wyoming. Over a 2-y period 142 subjects were recruited from households selected at random and from ranches where unusually high selenium intakes were suspected. Subjects completed health questionnaires, underwent physical examinations, provided blood samples for clinical assessment, and provided blood, urine, toenails, and duplicate-plate food collections for selenium analysis. About half of the 142 free-living subjects had selenium intakes greater than 2.54 mumol/d (200 micrograms/d) (range 0.86-9.20 mumol/d, or 68-724 micrograms/d). Physical findings characteristic of selenium toxicity were not present nor were clinically significant changes in laboratory tests or frequency of symptoms related to selenium in the blood, toenails, or diet. We found no evidence of toxicity from selenium in subjects whose intake was as high as 9.20 mumol/d (724 micrograms/d).

Adult↗
PubMed1993

Indexes of selenium status in human populations.

This paper considers the factors that affect the bioavailability of selenium to human populations and describes briefly the consequences of an inadequate dietary intake of selenium in the Peoples' Republic of China and in Zaire. A review of human blood selenium concentrations worldwide reveals very large differences in the apparent dietary status of individuals in different areas. The question is raised as to whether blood selenium measurement is a reliable index of actual selenium status in terms of bioavailability and function of the element. It is concluded that the preferred indexes of human selenium status are blood, or plasma and/or serum, concentrations of the element and the level of activity of the selenium-dependent enzyme glutathione peroxidase in erythrocytes or in plasma. Several important caveats to this conclusion are mentioned and other means of assessing selenium status are also considered.

Biological Availability↗
PubMed2000

Antioxidant and thyroid hormone status in selenium-deficient phenylketonuric and hyperphenylalaninemic patients.

BACKGROUND: Subjects consuming protein-restricted diets, such as patients with phenylketonuria (PKU) or milder hyperphenylalaninemias (HPAs) are at risk of selenium deficiency. Selenium is a cofactor of the antioxidant enzyme glutathione peroxidase and of the thyroid hormone converting enzyme thyroxine deiodinase. OBJECTIVE: Our goal was to investigate the effects of low plasma selenium on antioxidant and thyroid hormone status. DESIGN: We assessed plasma selenium, plasma total antioxidant status and the individual components thereof, erythrocyte antioxidant status, and plasma thyroid hormones in 24 PKU and 10 HPA patients and in 42 age-matched control subjects. RESULTS: Selenium was significantly lower in both PKU and HPA patients than in control subjects and the PKU patients had lower values than did the HPA patients. Total antioxidant status was lower in both patient groups than in the control group, whereas alpha-tocopherol, albumin, and uric acid were not significantly different among groups. Plasma selenium correlated well (r = 0.76) with erythrocyte glutathione peroxidase. PKU patients had lower glutathione peroxidase activity than did HPA patients and control subjects and lower glutathione concentrations than did control subjects. Both patient groups had lower superoxide dismutase activity than did control subjects. Free triiodothyronine was higher in both patient groups than in control subjects, whereas free thyroxine was higher in the PKU patients only. Free thyroxine and reverse triiodothyronine were inversely correlated with selenium. CONCLUSION: Supplementation with selenium seems to be advisable for patients consuming diets low in natural protein.

Adolescent↗
PubMed2007

Glutathione, glutathione peroxidase, and selenium status in HIV-positive and HIV-negative adolescents and young adults.

BACKGROUND: Antioxidant nutrient deficiencies may hasten the progression of HIV disease by impairing antioxidant defenses. OBJECTIVE: The objective of the study was to determine whether HIV infection is associated with poor selenium status and low antioxidant protection by glutathione and glutathione peroxidase (GPX). DESIGN: In a cross-sectional study of 365 HIV-positive and HIV-negative adolescents and young adults, we examined the relation of plasma selenium, whole-blood glutathione, and whole-blood GPX to HIV status, disease severity, immune activation, and oxidative damage. RESULTS: Selenium deficiency (plasma selenium < 0.070 microg/mL) was not seen in any subjects, and plasma selenium in 244 HIV-positive subjects (0.120 +/- 0.0013 microg/mL) did not differ significantly (P = 0.071) from that in 121 HIV-negative subjects (0.125 +/- 0.0020 microg/mL) . However, multiple regression analysis after adjustment for covariates showed a significant (P = 0.002) negative association between HIV-associated immune activation (plasma neopterin) and plasma selenium concentrations. GPX activity was highest in HIV-positive subjects taking antiretroviral therapy (median: 14.2; 25th, 75th percentiles: 11.1, 18.7 U/mL; n = 130), intermediate in HIV-positive subjects not taking antiretroviral therapy (11.8; 9.4, 15.1 U/mL; n = 114), and lowest in HIV-negative subjects (10.6; 8.6, 12.7 U/mL; n = 121; P < 0.05 for all comparisons). GPX was also positively associated with malondialdehyde, a marker of oxidative damage. CONCLUSIONS: Subjects had adequate selenium status, although HIV-related immune activation was associated with lower plasma selenium concentrations. GPX activity appears to have been induced by the oxidative stress associated with HIV infection and use of antiretroviral therapy. Thus, young, well-nourished subjects can mount a compensatory antioxidant response to HIV infection.

Adolescent↗
PubMed1989

Supplementation with selenium, vitamin E and their combination in gynaecological cancer during cytotoxic chemotherapy.

The biochemical responses to 8-week supplementary treatment with selenium and/or vitamin E were evaluated in 41 patients with gynaecological cancer during cytotoxic chemotherapy, in Finland, a selenium-deficient country. After the control course of 1-day treatment with cytostat agents, 11 patients received a combination of selenium and vitamin E (sodium selenate, 200 micrograms/day + vitamin E, 300 mg/day), 11 received selenium (sodium selenate, 200 micrograms/day) and seven received vitamin E (300 mg/day) as supplementary therapy, while 12 patients had no supplementary drugs. Sodium selenate alone and combined with vitamin E significantly increased the serum selenium levels, but the activity of serum glutathione peroxidase (GSH-Px) increased significantly only in the selenium- and vitamin E-treated patients with low initial GSH-Px activity. The cytotoxic chemotherapy did not change the activity of GSH-Px, while the concentrations of lipid peroxides decreased. Sodium selenate alone or with vitamin E did not modify this decrease. Sodium selenate alone significantly decreased the capacity of the platelets to produce thromboxane A2; it increased high-density lipoprotein cholesterol levels and prevented the cytotoxic-chemotherapy-associated increase of creatine kinase. Selenium supplementation might thus be beneficial during cytotoxic chemotherapy in ovarian cancer patients with low selenium levels.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1995

Evaluation of chemopreventive effect of dietary selenium-rich egg on mouse skin tumor induced by 2'-(4-nitrophenoxy)oxirane and 12-O-tetradecanoylphorbol-13-acetate.

Chemoprotective effect of dietary selenium (as sodium selenite or as Se-rich egg) on mouse skin tumor induced by topical application of 2'-(4-nitrophenoxy)oxirane (NPO) as tumor initiator and 12-O-tetradecanoylphorbol-13-acetate (TPA) as tumor promoter was evaluated in relation to the dietary source and levels of selenium. Selenium supplementation (0.3 p.p.m.) to the basal diet (0.07 p.p.m. Se) as sodium selenite or as Se-rich egg brought about a 40 or 37% reduction respectively, in the incidence of papilloma formation at 12 weeks after NPO treatment. Tumor yield (number of papillomas per mouse) at 14 weeks after NPO treatment in the basal diet group, basal diet supplemented with 0.3 p.p.m. Se as sodium selenite group and basal diet supplemented with 0.3 p.p.m. Se as Se-rich egg group were 7.5 +/- 2.1, 2.7 +/- 2.3 and 4.1 +/- 3.5 respectively. Dietary supplementation of 1.0 p.p.m. See as Se-rich egg to the basal diet reduced the incidence and the multiplicity of papillomas during the early phase of promotion (11 weeks) but its antitumor activity decreased thereafter, indicating that the accumulation of tissue selenium above the saturated level may not be beneficial. Selenium concentrations in blood, liver and skin tissue of mice in basal diet group (0.33 +/- 0.02, 0.54 +/- 0.10 and 0.21 +/- 0.03 p.p.m. respectively) increased significantly ( P < 0.05) by the supplementation of 0.3 p.p.m. Se as selenite (0.58 +/- 0.02, 1.17 +/- 0.10 and 0.31 +/- 0.05 p.p.m. respectively), 0.3 p.p.m. Se as Se-rich egg (0.59 +/- 0.02, 1.25 +/- 0.11 and 0.33 +/- 0.06 p.p.m. respectively) and 1.0 p.p.m. Se as Se-rich egg (1.20 +/- 0.05, 2.32 +/- 0.28 and 0.51 +/- 0.01 p.p.m. respectively). Glutathione peroxidase activity in blood of mice of the basal diet group (2.4 +/- 0.4 EU/mg) increased significantly (P < 0.05) by dietary selenium supplementation (3.8 +/- 0.6 EU/mg in 0.3 p.p.m. Selenite; 3.7 +/- 0.8 EU/mg in 0.3 p.p.m. Se as Se-rich egg; 4.9 +/- 0.9 EU/mg in 1/0 p.p.m. Se as Se-rich egg) and the enzyme activities in liver and skin tissue also increased by 0.3 p.p.m. Se (as selenite or Se-rich egg) supplementation, but no further increases in their activities were obtained by 1.0 p.p.m. Se (as Se-rich egg). It is, therefore, concluded that a moderate level of dietary selenium (0.3 p.p.m.) has an efficient chemopreventive activity at the promotional stage of carcinogenesis and that dietary selenium rich egg as well as dietary selenite exerted antitumor activity.

Animals↗
PubMed1996

Effects of dietary beta-carotene and selenium on initiation and promotion of pancreatic carcinogenesis in azaserine-treated rats.

In the present study the effects of 0.1 or 1.0 g beta-carotene/kg diet (L beta C or H beta C) and 1.0 mg or 2.5 mg selenium/kg diet (LSel or HSel), as well as combinations of the respective low and high concentrations of beta-carotene and selenium (LMix or HMix) on the initiation/early promotion phase or on the late promotion phase of pancreatic carcinogenesis in azaserine-treated rats, were investigated using cell proliferation and volumetric data of atypical acinar cell foci (AACF) as parameters. The present results indicate chemopreventive effects of dietary selenium, dietary beta-carotene and of their combination on the development of acinar pancreatic lesions induced in rats by azaserine. The inhibitory effect was most pronounced when beta-carotene and/or selenium were added to the diets during the late promotion phase of the carcinogenic process, although inhibition was also observed with these compounds when they were added to the diets during the first 5 weeks of the study only (initiation/early promotion phase). Neither in the initiation/early promotion phase nor in the late promotion phase was a dose-related trend observed. The multiplicities of AACF with a diameter over 1.0 mm and of carcinomas in situ (CIS), as well as the incidence of CIS were not significantly different among the groups. However, in the late promotion experiment a dose-related decline in multiplicity could be observed in the selenium supplemented groups and in the groups receiving combinations of beta-carotene and selenium. Cell proliferation in azaserine-induced AACF, as estimated by the bromodeoxyuridine (BrdU) labeling index, was significantly higher in H beta C, HSel, LMix and HMix groups (initiation/early promotion phase) as well as in H beta C, LSel, HSel, LMix and HMix groups (late promotion phase) than in high fat controls. From the present results it can be concluded that: (i) beta-carotene and selenium have inhibitory effects on pancreatic carcinogenesis induced in rats by azaserine; (ii) the most clear effects were observed when selenium was given as such, or in combination with beta-carotene during the late promotion phase; and (iii) beta-carotene and selenium stimulate cell proliferation in AACF.

Analysis of Variance↗
PubMed1977

Comparative effects of selenium and vitamin E in lead-poisoned rats.

Weanling male rats were fed a Torula yeast diet supplemented with selenium, vitamin E, or both for 3 months. Of rats fed each diet, one group received 250 ppm lead in the drinking water and another group did not. In rats not poisoned with lead, neither vitamin E nor selenium deficiency affected spleen weight, hematocrit value, or erythrocyte mechanical fragility. Vitamin E deficiency increased the splenomegaly, anemia, and mechanical fragility of red cells of lead-poisoned rats, whereas selenium deficiency did not. Addition of 0.5 ppm selenium to the vitamin E-supplemented diet increased slightly the splenomegaly and anemia in lead-poisoned rats. Excess levels of selenium (2.5 and 5 ppm) in the vitamin E-deficient diet had little or no effect on spleen size or hematocrit of rats not receiving lead, but partially prevented the splenomegaly and anemia of red cells from either non-poisoned or lead-oisoned vitamin E-deficient rats, but not as effectively as vitamin E. These results show that vitamin E status of rats is more important that selenium status in determining response to toxic levels of lead. Excess dietary selenium did protect partially against lead poisoning in vitamin E-deficient rats, but the levels of selenium used were toxic in themselves.

Anemia, Hemolytic↗