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PubMedDate not supplied

Selenium in cardiology and angiology.

The effect selenium in the form of sodium selenite on central hemodynamic conditions and coronary artery flow was studied in pig hearts infarcted by a ligature of the ramus interventricularis anterior. Infusions of sodium selenite solutions at levels of 1-3 mg/kg body wt improved the survival of infarcted pigs. Both short-term and long-term protective effects of selenite could be demonstrated. It is of potential therapeutic importance that sodium selenite administration suppresses the electrical vulnerability of the cell membrane, notably the occurrence of ventricular late potentials in the ischemic border zone. Coronary blood circulation, as evidenced by an increase of heart rate and coronary artery dilatation and peripheral vasodilation was also improved. The pulsatile coronary blood flow thus is altered, increasing total perfusion of the infarcted heart. Initial observations with human subjects suggest that selenium deficiency is a factor in the pathogenesis of ischemic and arteriosclerotic heart disease. In 54 hospitalized patients with clinical diagnosis of acute myocardial infarction, serum selenium levels were 670 +/- 266 nmol/L, as compared to 981 +/- 209 nmol/L in 93 healthy controls. In 32 patients with general arteriosclerosis, the serum Se level was 375 +/- 85 nmol/L, in 64 patients with arteriosclerotic occlusional disease in the leg region, 366 +/- 85 nmol/L, respectively. Serum selenium levels of healthy subjects were found to be age- and sex dependent. In men, the selenium concentrations reached maximum levels of 1083 nmol/L in the 41-50 y age group. In women in the same age group, the serum Se level was 1385 nmol/L. Evidence is presented to suggest that selenium is preventing oxidative damage of heart cell membranes by lipid peroxidation.

Adolescent↗
PubMedDate not supplied

Selenium in chronic neurologic diseases. Multiple sclerosis and Batten's disease.

The selenium levels in whole blood and the activity of glutathione peroxidase in hematogenous cells of normal Danes have been defined taking into account sex and confounding factors such as smoking and aging. No differences related to sex could be found with regard to the selenium level, and peroxidase activity assayed with hydrogen peroxide. However, the peroxidase activity assayed with t-butyl hydroperoxide was higher in females than in males (p less than .05). The peroxidase activities are dependent on age. Thus, the peroxidase levels assayed with both substrates show a minimum value in the age group from 40 to 50 yr for both smokers and nonsmokers. Smokers did show more homogeneous values as a function of age than nonsmokers. Smokers had significantly lower selenium values than nonsmokers, but glutathione peroxidase values identical with those of nonsmokers. Multiple sclerosis (MS) patients suffer from a chronic relapsing/remitting demyelinating disease. A theory explaining the pathogenesis of MS concerns increased stickiness of cellular plasma membranes, hampering normal vascular function of the brain. In agreement with that theory, the present communication demonstrates significantly lowered selenium values and lowered glutathione peroxidase activities of major types of hematogenous cells. In close agreement with these findings, hematogenous cells in MS show increased peroxidation rates. A nonblinded biochemical dietary experiment on MS patients showed that all abnormalities could be normalized by daily intake of selenium, vitamin E, and vitamin C. Batten's disease is a recessive inherited neurodegenerative disorder clinically characterized by progressive loss of vision, epilepsy, and dementia. Neuropathologically, this disease is characterized by storage of lipofuscin in nervous tissue. We have in a few cases documented a low selenium status and low glutathione peroxidase activities of hematogenous cells. As in MS, we normalized the biochemical abnormalities by an antioxidative treatment. Like in similar Finnish studies, the biochemical parameters can be normalized. Further, the Finnish studies indicate it possible by an antioxidative treatment to inhibit progression of the mental deterioration. The data presented will be discussed in relationship both to specific pathological parameters of the diseases and to the low dietary energy expenditures of handicapped immobile patients.

Adult↗
PubMed2006

Understanding the importance of selenium and selenoproteins in muscle function.

Selenium is an essential trace element. In cattle, selenium deficiency causes dysfunction of various organs, including skeletal and cardiac muscles. In humans as well, lack of selenium is associated with many disorders, but despite accumulation of clinical reports, muscle diseases are not generally considered on the list. The goal of this review is to establish the connection between clinical observations and the most recent advances obtained in selenium biology. Recent results about a possible role of selenium-containing proteins in muscle formation and repair have been collected. Selenoprotein N is the first selenoprotein linked to genetic disorders consisting of different forms of congenital muscular dystrophies. Understanding the muscle disorders associated with selenium deficiency or selenoprotein N dysfunction is an essential step in defining the causes of the disease and obtaining a better comprehension of the mechanisms involved in muscle formation and maintenance.

Animals↗
PubMed1998

The vhuU gene encoding a small subunit of a selenium-containing [NiFe]-hydrogenase in Methanococcus voltae appears to be essential for the cell.

We developed a general method for the site-specific deletion of gene sequences to obtain new selectable markers in the archaeon Methanococcus voltae. Using a deletion in the hisA gene, a vector was integrated into the chromosome by homologous recombination, thereby reconstituting histidine prototrophy. The vector contained the beta-glucuronidase gene uidA of Escherichia coli as a reporter under the control of an M. voltae promoter that normally drives the expression of a selenium-free [NiFe]-hydrogenase after selenium deprivation. This construct has allowed us to check whether the selenium supply was sufficiently low to induce the transcription of the genes encoding the selenium-free hydrogenases. We tried to introduce a chromosomal deletion of the vhuU gene of the archaeon M. voltae by gene replacement and by keeping the cells under selenium deprivation. The gene vhuU encodes the very small, selenocysteine-containing subunit that is part of the primary reaction center of the Vhu hydrogenase. All transformants bearing the deletion also contained the vhuU wild-type gene. Therefore, the vhuU gene appears to be essential for the cell even under conditions that lead to the induction of the selenium-free homologue Vhc of the Vhu hydrogenase.

Aldose-Ketose Isomerases↗
PubMed1996

Selenium-mediated inhibition of transcription factor NF-kappa B and HIV-1 LTR promoter activity.

The eukaryotic transcription factor NF-kappa B is involved in the inducible expression of various inflammatory genes as well as in HIV-1 replication. Activation of NF-kappa B is induced by prooxidants and several stimuli eliciting oxidative stress, such as cytokines, lipopolysaccharide, UV irradiation and other mediators. Various antioxidants inhibit NF-kappa B activation in response to these stimuli. In this study, we have investigated the effects of selenium, an integral component of glutathione peroxidase (GPX), on NF-kappa B activation. In selenium-deprived Jurkat and ESb-L T lymphocytes, supplementation of selenium led to a substantial increase of GPX activity. Analysis of DNA binding revealed that NF-kappa B activation in response to TNF was significantly inhibited under these conditions. Likewise, reporter gene assays using luciferase constructs driven by the HIV-1 long terminal repeat showed a dose-dependent inhibition of NF-kappa B controlled gene expression by selenium. The effects of selenium were specific for NF-kappa B, since the activity of the transcription factor AP-1 was not suppressed. These data suggest that selenium supplementation may be used to modulate the expression of NF-kappa B target genes and HIV-1.

Cell Line↗
PubMed2005

Development and application of a simple routine method for the determination of selenium in serum by octopole reaction system ICPMS.

The aim of the study was to develop an inductively coupled plasma mass spectrometry (ICPMS) method for robust and simple routine determination of selenium in serum. Polyatomic interferences on 76Se, 77Se, and 78Se were removed by applying an octopole reaction system ICPMS with the reaction cell pressurized with H2 gas. We developed a novel simple optimization routine for the H2 gas flow based on a signal-to-noise ratio (SNR) calculation of the selenium signal measured in a single selenium standard. The optimum H2 flow was 2.9 mL min-1. The selenium content in serum was determined after a 50-fold dilution with 0.16 M HNO3 and quantified by using addition calibration and gallium as an internal standard. The method detection limit was 0.10 microg L-1 for 76Se and 78Se and 0.13 microg L-1 for 77Se. Human serum samples from a case-control study investigating if selenium was associated with risk of colorectal adenoma were analyzed. The average selenium concentration for the control group (n=768) was 137.1 microg L-1 and the range was 73.4-305.5 microg L-1. The within-batch repeatability (a batch is ten samples) estimated from 182 replicate analyses was 6.3% coefficient of variation (CV), whereas the between-batch repeatability was 7.4% CV estimated from 361 replicates between batches. The method accuracy was evaluated by analysis of a human serum certified reference material (Seronorm Serum level II, Sero A/S, Norway). There was a fairly good agreement between the measured average of 145+/-3 microg L-1 (n=36) and the certified value of 136+/-9 microg L-1. In addition the method was successfully applied for analysis of zinc serum concentrations without further optimization. For the Seronorm certified reference material a value of 911+/-75 microg L-1 (n=31) for zinc was obtained, which corresponds well to the certified zinc value of 920+/-60 microg L-1.

Adenoma↗
PubMed2005

Analysis of the selenium species distribution in cow blood by size exclusion liquid chromatography-inductively coupled plasma collision cell mass spectrometry (SEC-ICPccMS).

A method for performing rapid semiquantitative screening of the distribution of Se species in the blood of cows fed with a diet enriched in selenized yeast was optimized. The method was based on direct injection of a blood sample onto a high resolution size exclusion chromatographic column and fractionation of the selenium species. Selenium was detected on-line by ICP-MS with a collision cell. The concentrations of selenized haemoglobin and free selenomethionine were estimated using the chromatogram. The method was applied to a study involving 15 control and 15 treated dairy cows at four different supplementation time points. The increase in the selenomethionine and selenized haemoglobin was a linear function of the total selenium concentration. A threshold value of 600 ng ml(-1) of total Se was established beyond which selenomethionine could not be incorporated into the protein. No inorganic selenium was found to be present. The total selenium in cow blood correlated well with that in milk. The selenium supplementation did not change the protein distribution profiles for other essential elements (Cu, Fe, Mn, Zn).

Animals↗
PubMed2002

Mercury and selenium concentrations in livers and eggs of common loons (Gavia immer) from Minnesota.

Mercury and selenium act as mutual antagonists in mature birds, but their toxicity is additive or synergistic in avian embryos and immature birds. Twenty eggs and livers from 18 mature and 9 immature common loon carcasses found in Minnesota were collected. Livers and eggs were analyzed for mercury and selenium by atomic emission and atomic absorption spectroscopy. Liver mercury concentrations were significantly higher in mature loons compared to those of immature loons and eggs. Liver selenium concentrations were significantly higher in mature loons than those of immature loons, and selenium concentrations in immature loon livers were significantly higher than levels in eggs. There was a significant positive correlation between mercury and selenium in loon livers. There was a negative correlation between mercury and selenium in eggs.

Age Factors↗
PubMed2003

Encephalopathy in megacystis-microcolon-intestinal hypoperistalsis syndrome patients on long-term total parenteral nutrition possibly due to selenium deficiency.

This report concerns two patients (female, 9 and 6 years) who were diagnosed with megacystis-microcolon-intestinal hypoperistalsis syndrome (MMIHS). Although they exceeded the usual life expectancy of patients diagnosed with MMIHS because of total parenteral nutrition (TPN), they demonstrated progressive neurological deficits and showed histopathological features in the brain. Both patients were diagnosed with MMIHS in the neonatal period and were fed by TPN. The first patient developed visual and gait disturbances at the age of 7 years. Two months later, she developed dysarthria and muscular weakness, and could not maintain her posture. The level of serum selenium was extremely low. The second patient developed flexion and spasticity of the extremities followed by decorticate posture at the age of 3 years. Both patients died of sepsis. The brain weights of the two cases were 880 g and 715 g. In both cases, severe neuronal loss and gliosis were present in the medial convolutions of the occipital lobe, including the visual cortex. The postcentral gyrus and temporal transverse gyrus were also involved. In addition, extensive loss of Purkinje cells and granular neurons, and gliosis were observed in the cerebellum. We measured the selenium content of the brains and livers using the graphite furnace atomic absorption spectrometry method. Selenium was not detected in either brain, although the livers of both cases contained a low level of selenium. On immunohistochemical examination of the anti-oxidative enzymes, histiocyte-macrophage lineage cells in MMIHS cases, including microglia and Kupffer cells, showed only a weak reaction for glutathione peroxidase, of which selenium is an essential component. However, the cells in the control cases were strongly positive. In cases of MMIHS and methylmercury intoxication, the brain features similar lesions, in both their topographical and histopathological aspects. We considered that the brain lesions of the MMIHS patients mainly resulted from oxidative damage of the brain related to the low levels of glutathione peroxidase and other selenoproteins due to selenium deficiency.

Abnormalities, Multiple↗
PubMed2003

A study on soluble intercellular adhesion molecule-1 and selenium in patients with rheumatoid arthritis complicated by vasculitis.

Clinical manifestations of vasculitis, as a complication of rheumatoid arthritis (RA), can be postulated as a consequence of immune response abnormalities and endothelial cell dysfunction. In this study we searched for the relationship between the extent of vascular involvement and either serum sICAM-1 or selenium concentrations. We also explored the possible interaction of serum selenium with sICAM-1 to provide a greater understanding of their role in rheumatoid vasculitis (RV). For the study, we measured the serum titers of sICAM-1 using an ELISA assay and the serum selenium concentrations using the ETAAS method in 37 women suffering from RA and 18 normal women serving as controls. All the RA patients were evaluated by extensive clinical, laboratory and capillaroscopic studies. In all patients with extra-articular manifestations, severe or moderate changes in nailfold capillaroscopy were found. Serum sICAM-1 titers in RA patients with mild vasculitis on nailfold capillaroscopy did not differ significantly from those of the healthy subjects, whereas a higher sICAM-1 level seemed to reflect the more intensive vascular changes in capillaroscopy. These data suggest that sICAM-1 serum levels may reflect the extent of the microvascular involvement in RA patients. Compared with controls, all the RA patients had markedly lower serum selenium concentrations, irrespective of the degree of the capillaroscopic vascular changes. A significant inverse correlation between sICAM-1 and selenium was found in the controls (r = -0.54; P<0.02). By contrast, no correlation was noted in RA patients (r=0.10, P not significant). This suggests that the sICAM-1 shedding in RV does not appear to be influenced by selenium, presumably owing to its low serum concentration.

Adult↗
PubMed2005

Selenium in the Blackfoot, Salt, and Bear river watersheds.

Nine stream sites in the Blackfoot River, Salt River, and Bear River watersheds in southeast Idaho, USA were sampled in May 2001 for water, surficial sediment, aquatic plants, aquatic invertebrates, and fish. Selenium was measured in these aquatic ecosystem components, and a hazard assessment was performed on the data. Water quality characteristics such as pH, hardness, and specific conductance were relatively uniform among the nine sites. Of the aquatic components assessed, water was the least contaminated with selenium because measured concentrations were below the national water quality criterion of 5 microg/L at eight of the nine sites. In contrast, selenium was elevated in sediment, aquatic plants, aquatic invertebrates, and fish from several sites, suggesting deposition in sediments and food web cycling through plants and invertebrates. Selenium was elevated to concentrations of concern in fish at eight sites (> 4 microg/g in whole body). A hazard assessment of selenium in the aquatic environment suggested a moderate hazard at upper Angus Creek (UAC) and Smoky Creek (SC), and high hazard at Little Blackfoot River (LiB), Blackfoot River gaging station (BGS), State Land Creek (SLC), upper (UGC) and lower Georgetown Creek (LGC), Deer Creek (DC), and Crow Creek (CC). The results of this study indicate that selenium concentrations from the phosphate mining area of southeast Idaho were sufficiently eleated in several ecosystem components to cause adverse effects to aquatic resources in southeastern Idaho.

Animals↗
PubMed2005

Heavy metals and selenium in grebe eggs from Agassiz National Wildlife Refuge in northern Minnesota.

Metal levels in eggs can often be used as an indicator of exposure and of potential effects. In previous work at Agassiz National Wildlife Refuge, northwestern Minnesota, the levels of several heavy metals were shown to be significantly higher in the eggs of eared grebes (Podiceps nigricollis) compared to those in the eggs of Franklin's gulls (Larus pipixcan), black-crowned night-herons (Nycticorax nycticorax) and double-crested cormorants (Phalacrocorax auritus, except for mercury). In the present study we test the hypothesis that there are no differences in the levels of heavy metals in eggs of three species of grebes nesting at Agassiz National Wildlife Refuge (1997, 1999). There were significant differences in levels of selenium, manganese and mercury in the eggs of the grebes collected in 1997, with pied-billed grebe (Podilymbus podiceps) having significantly higher levels of manganese and mercury, and significantly lower levels of selenium, than eared or red-necked grebes (Podiceps grisegena). In 1999, pied-billed grebes had significantly higher levels of mercury, but lower levels of selenium and tin than the other species. The only pattern that was significant and consistent among years was selenium; in both years pied-billed grebes had lower levels than the other species. For eared grebes, there was a decline from 1997 to 1998, and again to 1999 for arsenic, cadmium, and selenium. Levels of mercury in the eggs of grebes were not as high, however, as those found in cormorants or night-herons sampled in 1994 at Agassiz National Wildlife Refuge. There were few consistent patterns in the relationships among metals in eared grebe eggs (with the largest sample sizes). The possible reasons for the high levels of some metals in eggs of grebes are unknown, but presumably egg levels represent exposure on the wintering grounds or migratory routes. In comparison to eggs of other birds: 1) the mean levels for manganese were at the high end of the range, and the mean was an order of magnitude higher than the median for the studies examined, 2) mean levels were above the median in the eggs of other birds for lead (red-necked grebe), mercury (pied-billed grebe) and selenium (eared and red-necked grebe).

Animals↗
PubMed2006

Influence of selenium (antioxidant) on gliclazide induced hypoglycaemia/anti hyperglycaemia in normal/alloxan-induced diabetic rats.

Oxidative stress is involved in diabetes mellitus and its complications. Since diabetes is a stress-related disorder, supplementation with antioxidants may improve the condition. The purpose of this study is to know the effect of oral administration of selenium on blood glucose and its influence on gliclazide induced hypoglycaemia/antihyperglycaemia in normal and alloxan-induced diabetic rats. Albino rats of either sex were divided into three groups of six each. Group-I/II/III were treated with selenium 1/2 TD (0.9 microg/200 g rat)/TD (1.8 microg/200 g rat)/2TD (3.6 microg/200 g rat), respectively. Later group II was treated with gliclazide TD (1.44 mg/200 g rat)/selenium TD + gliclazide TD with a washout period of 1 week between the treatments. Diabetes was induced by alloxan monohydrate 100 mg/kg body weight i.p. A group of six rats showing fasting blood glucose levels ranging from 175-250 mg/dl were selected for the study. Rats were treated with selenium TD, gliclazide TD and selenium TD + gliclazide TD with a washout period of 1 week between the treatments. Selenium 1/2 TD and TD produced hypoglycaemia while 2TD produced hyperglycaemia. The combination of selenium TD with gliclazide TD, significantly enhanced the glucose lowering effect of gliclazide in normal and diabetic rats.

Administration, Oral↗
PubMed1987

Effects of selenium-deficient diets on the production of prostaglandins and other oxygenated metabolites of arachidonic acid and linoleic acid by rat and rabbit aortae.

Selenium is an essential component of glutathione peroxidase, which reduces free and esterified hydroperoxides of polyunsaturated fatty acids. Adequate glutathione peroxidase activity could be important for the maintenance of prostacyclin synthesis by blood vessels, since hydroperoxides can inhibit the formation of this substance. We have investigated the effects of dietary selenium deficiency on glutathione peroxidase activity and the synthesis of 6-oxoprostaglandin F1 alpha and monohydroxy and trihydroxy metabolites of polyunsaturated fatty acids by aorta. The latter products can be formed either by the actions of cyclooxygenase or lipoxygenase or by lipid peroxidation. Aortic glutathione peroxidase activity was reduced by over 80% by feeding rats a selenium-deficient diet for 4 weeks, and to undetectable levels after 6 weeks. There were no appreciable differences in the levels of free and esterified oxygenated metabolites of linoleic acid or arachidonic acid between the control and treated groups after 4 weeks. However, after 6 weeks, there were modest, but statistically significant reductions in the formation of 6-oxoprostaglandin F1 alpha and monohydroxy products formed by cyclooxygenase. On the other hand, the amounts of esterified 18:2 metabolites appeared to be higher in aortae from animals on the selenium-deficient diet, although only the increase in esterified 9-hydroxy-10,12-octadecadienoic acid was statistically significant. These results suggest that selenium deficiency can affect the formation of prostacyclin and other oxygenated metabolites of polyunsaturated fatty acids by aorta, possibly by increasing lipid peroxidation. However, the differences between control and selenium-deficient rats after 6 weeks were not very dramatic, in spite of the fact that glutathione peroxidase activity was undetectable. It would therefore appear that additional mechanisms are also involved in controlling the levels of lipid hydroperoxides in aorta.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

The alpha-tocopherol and phospholipid fatty acid content of rat liver subcellular membranes in vitamin E and selenium deficiency.

(1) Rats were given a diet deficient in vitamin E and selenium, or diets supplemented with either or both of these nutrients. The livers were subfractionated by standard procedures, and the purity of the fractions was assessed by marker enzyme techniques. alpha-Tocopherol was measured and profiles of phospholipid fatty acids were determined. (2) All the organelles studied were severely depleted of alpha-tocopherol in the rats deprived of vitamin E: no organelle was particularly severely depleted. There was a large rise in the alpha-tocopherol content in organelles of rats deprived of selenium but given adequate amounts of vitamin E, suggesting an increased uptake or mobilization of tocopherol to compensate for the detrimental effects of selenium deficiency. (3) The following general conclusions were reached from the results of the phospholipid fatty acid analyses. (i) vitamin E deficiency caused a consistent fall in the polyunsaturated fatty acid (PUFA) content (13-66% of the control level); (ii) selenium deficiency alone caused no consistent effect on phospholipid PUFA in the fractions studied; (iii) double deficiency of vitamin E and selenium caused a consistent rise in the proportion of PUFA in the fractions studied, ranging from 11 to 311%. (4) The result given in 3(i) is consistent with peroxidative destruction of membrane phospholipid PUFA during vitamin E deficiency. The result in 3(iii) is paradoxical: a possible explanation is that during severe disruption of antioxidant defences, there is an overshoot in the increased incorporation of unsaturated fatty acids into the membrane phospholipids, or in the chain-elongation and desaturation process required for the formation of PUFA, which may require vitamin E and/or selenium for its regulation.

Animals↗
PubMed1983

In vitro hemolysis of rat erythrocytes by selenium compounds.

Rat erythrocytes were incubated in vitro with various selenium compounds at 37 degrees. Hemolysis occurred with some selenium compounds but not with corresponding sulfur analogues. Selenite induced more rapid loss of intracellular glutathione (GSH) than did selenocystine but was less hemolytic. Cystine caused neither loss of intracellular GSH nor hemolysis. Addition of GSH to the incubation medium enhanced hemolysis by selenite and selenium dioxide but inhibited hemolysis by selenocystine. Inclusion of glucose in the incubation medium also inhibited selenocystine-induced lysis of erythrocytes from both selenium-supplemented rats and selenium-deficient rats. The results suggest a relationship between the oxidation of intracellular GSH and the hemolysis by selenocystine, selenite and selenium dioxide.

Animals↗
PubMed1985

Structural and functional assembly of rat intestinal cytochrome P-450 isozymes. Effects of dietary iron and selenium.

We have reported previously that both dietary iron and selenium regulate intestinal cytochrome P-450 content by modulating the synthesis of its prosthetic heme moiety. Whether these elements are required for synthesis and/or viability of its apocytochrome moiety is unknown. We have examined the effects of intraluminal deprivation of these elements on the apocytochrome moieties of the constitutive (P-450) and the beta-naphthoflavone inducible (P-448) intestinal isozymes. The relative content of intestinal apocytochrome P-450 moieties generated by dietary deprivation of iron and/or selenium was assessed indirectly by complexing with exogenous heme in vitro, to reassemble the holocytochromes which could be monitored spectrally and catalytically. We now report that, whereas both intraluminal iron and selenium are required for maintenance of the prosthetic apocytochrome moiety of the constitutive intestinal isozyme, only intraluminal selenium is required for the viability of apocytochrome P-448. The latter apparently survives in the absence of intraluminal iron and can be assembled to the holocytochrome, with exogenously added heme. The mechanistic basis of the critical requirement of intestinal apocytochromes for intraluminal selenium is unclear. It is intriguing, however, that the deleterious effects of selenium deprivation are principally exerted in cell systems actively synthesizing protein and inexorably dependent on their extracellular milieu for their nutriment.

Animals↗
PubMed1989

Modulation of the induction of rat hepatic cytochromes P-450 by selenium deficiency.

The induction by phenobarbital of liver microsomal cytochrome P-450 has been demonstrated to be impaired in rats fed a selenium-deficient diet. Cytochrome P-450 isozyme specific immunologic and molecular techniques were used in the present study to better define the role of selenium in the induction of cytochrome P-450 by phenobarbital. Phenobarbital treatment of the selenium-deficient rats resulted in an increase in the level of total cytochrome P-450 50% of that observed with control rats and in a 10-fold increase in microsomal heme oxygenase. Quantitative immunoblot analyses demonstrated that the levels of cytochromes P-450b + e and P-450p in the phenobarbital-treated selenium-deficient rats were approximately 50% of those found in the phenobarbital-treated control rats. Finally, RNA hybridization studies using cDNA probes to cytochromes P-450b + e or P-450p demonstrated that the accumulations of the RNAs encoding these cytochromes P-450 were unaffected by the selenium status of the rats. These studies suggest that the impaired phenobarbital induction of the cytochromes P-450 in the selenium-deficient rats is the result of an increase in the degradation of the cytochromes P-450 or a decrease in the translation of the mRNAs coding for them.

Animals↗