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PubMed1983

Absorption, distribution, and retention of inhaled selenious acid and selenium metal aerosols in beagle dogs.

We studied the distribution and retention of inhaled selenious acid and selenium metal aerosols which were similar in size and chemical form to selenium aerosols that may be produced during fossil fuel combustion. Beagle dogs were given 10 to 61 micrograms Se/kg of body weight by inhalation. Aerosols generated for the inhalation exposures were also collected and instilled into the upper respiratory tracts or stomachs of additional dogs to measure systemic absorption at these sites. Selenium-75, incorporated into the aerosols, was used to determine the Se content in the whole animal, excreta, and individual tissues as a function of time. Virtually all of the inhaled selenious acid aerosol was rapidly absorbed into the blood from the lungs, gastrointestinal tract, and the nasal membranes. Selenium metal aerosols were less rapidly absorbed. Selenium that was absorbed into the blood was translocated to the liver, kidney, spleen, and heart. Selenium-75 in these organs had a biological half-life of 30 to 40 days. Approximately 50% of the deposited Se was eliminated with a biological T1/2 of 1.2 days. Urine was the major route of excretion, accounting for 70 to 80% of the excreted Se. The long-term component of the whole-body retention function for both inhaled aerosols had a half-life of about 34 days and accounted for about 20% of the initial Se dose. The data suggested that although absorption of selenious acid into blood following inhalation was more rapid than absorption of selenium metal, once absorbed the disposition of both compounds was similar.

Aerosols↗

PubMed1987

Selenium contamination of the Grasslands, a major California waterfowl area.

In a recent study at Kesterson Reservoir in California, selenium was shown to cause mortality and deformities in embryos of aquatic birds. The present study was conducted to determine if selenium or other contaminants in agricultural drainwater used for marsh management were likely to cause similar adverse effects in the nearby Grasslands area. Selenium concentrations were elevated (greater than 15 ppm, dry-weight) in livers of some birds of all species collected from the Grasslands. Mean selenium concentrations in all species sampled in the South Grasslands were significantly higher (P less than 0.05) than those from the "control site", the Volta Wildlife Area. Mean selenium levels in black-necked stilts (Himantopus mexicanus) from the South Grasslands (35.6 ppm) were similar (P greater than 0.05) to levels in stilts from Kesterson (46.4 ppm), but means for American avocets (Recurvirostra americana) from the South Grasslands (67.3 ppm) were higher (P less than 0.05) than those from Kesterson (28.4 ppm). Bird eggs and fish from the Grasslands also contained elevated levels of selenium. Concentrations of eight heavy metals in fish generally reflected those patterns previously found in water entering the study areas. Of the organochlorines detected in fish, only DDE occurred at concentrations potentially harmful to birds (6.1 and 3.0 ppm, wet weight, at two South Grassland sites). The effect on avian health or reproduction of the other contaminants, singly or in combination, could not be determined. However, selenium levels were apparently sufficiently elevated in 1984 to have caused adverse effects on avian reproduction in the South Grasslands.

Animals↗

PubMed1991

Sewage sludge as a source of environmental selenium.

Information is presented on the impact of land application of municipal sewage sludge on the selenium content and speciation in soil, groundwater and edible vegetation. Sources and typical concentrations of selenium in sludge are documented. A discussion of selenium uptake by agricultural crops from sludge-amended soil includes results from greenhouse and field studies. A comparison is made with crop selenium uptake from fly ash application. The effect of sludge treatment on animal and human dietary selenium intake is quantitatively evaluated and selenium guidelines for sludge application are summarized. The conclusion is made that future widespread use of sludge on agricultural land will result in increased selenium uptake by food crops and human dietary intake. While this may not present an increased human health risk, long-term risks are identified and recommendations are made to minimize them.

Agriculture↗

PubMed1994

Have high selenium concentrations in wading birds their origin in mercury?

The relationship between selenium and mercury in marine waders from the Wadden Sea (known to have high tissue selenium concentrations), was investigated in the framework of the possibility that high mercury concentrations may have induced parallel selenium accumulation to detoxify the mercury. The selenium and mercury concentrations are shown to be negatively correlated in both the liver and kidneys of these birds. In the tissues and red blood cells of oystercatchers, positive correlations between the two elements are found. The atom increment Se/Hg ratio in the pooled oystercatcher tissue and red cell data is 32:1. This ratio greatly exceeds the 1:1 ratio found when selenium is accumulated to detoxify mercury. Furthermore, breeding females are able to excrete mercury independently of selenium from the red blood cells, probably into the eggs; the whole egg mercury concentrations of the local breeding populations are low. From these results it is concluded that the high selenium concentrations in waders do not have their origin in elevated levels of mercury.

Animals↗

PubMed1995

Inter-individual variation of selenium in maternal plasma, cord plasma and placenta.

Selenium (Se) in high doses has been known to cause injury to the fetus and newborn. The major difficulty in assessing the effects of selenium on human reproduction stems from the need for a suitable means of estimating maternal and fetal exposure. The present investigation, therefore, examines the respective reliability of maternal plasma, cord plasma and placenta as epidemiological indicators as well as inter-individual variation of this trace element. An unselected population of 128 pregnancies was studied. Obstetrical characteristics were noted. Selenium concentrations were determined for maternal plasma, cord plasma, and placental tissue by fluorometric analysis. Maternal plasma selenium concentrations (Se-Bm) were significantly greater than fetal concentrations (Se-Bc). Placental selenium (Se-Pl) levels were four times that of fetal levels. Variability of Se-Bc is best explained by placental concentrations. Maternal weight and ethnic origin are significantly correlated with Se-Bc. Female newborn have higher selenium levels than male newborn. The present study demonstrates the significance of the placenta as an indicator of fetal selenium exposure.

Adult↗

PubMed1985

Subcellular distribution of selenium-containing proteins in the rat.

The subcellular distribution of selenium in rat tissues was studied by measuring 75Se in animals provided for 5 months with [75Se]selenite as the main dietary source of selenium. Equilibration of the animals to a constant specific activity allowed the measurement of 75Se to be used as a specific elemental assay for selenium. Of the whole-body selenium, 51% was in the soluble fractions and 48% was bound to the particulate fractions as follows: 21% in plasma membranes, 11% in microsomes, and 16% in mitochondria. Glutathione peroxidase was primarily a soluble enzyme, but part of the activity was associated with plasma membrane in liver, mitochondria in liver and kidney, and microsomes in testes. Selenium in glutathione peroxidase accounted for about one-third of the particulate-associated selenium. These results indicate that other selenium-containing proteins besides glutathione peroxidase are present in membranes.

Animals↗

PubMed1980

Unscheduled DNA synthesis and chromosome aberrations induced by inorganic and organic selenium compounds in the presence of glutathione.

Glutathione strongly enhanced the induction of unscheduled DNA synthesis (UDS) in cultured human cells by inorganic selenium compounds: sodium selenate, sodium selenite and sodium selenide. In the presence of 10(-3) M glutathione, high levels of UDS (74-114 grains per nucleus) were observed in cells treated with (i) selenate at 10(-3) M, (ii) selenite at 10(-5)-3 X 10(-4) 7, and (iii) selenide at 10(-5)-10(-3) M. Glutathione at 10(-3) M also enhanced the clastogenic and cytotoxic effects of selenite and selenate in Chinese hamster ovary (CHO) cells. Glutathione at 10(-4) M or 10(-2) M caused less enhancement of DNA damage and toxicity in both the UDS and chromosome aberration assays. In the absence of glutathione, these inorganic selenium compounds induced low levels of UDS (up to 13 grains per nucleus) and moderate frequencies of chromosome aberrations (up to 11%). 3 organic selenium compounds (selenocystine, selenocystamine and selenomethionine) were also examined for the induction of UDS. No unscheduled DNA synthesis was detected in cells treated with selenocystamine or selenomethione, with or without added glutathione. However, selenocystine alone at 10(-4)-10(-3) M induced a low level of UDS; glutathione enhanced the DNA-damaging effect of selenocystine. The maximum amount of UDS (22 grains/nucleus) occurred in the presence of 10(-2) M glutathione. This was about one-fifth of that detected in cells treated with inorganic selenium compounds and 10-fold lower concentrations of glutathione (10(-3) M). The results suggest that recution is involved in the conversion of selenium compounds to mutagenic forms. The active mutagens may be selenols, GS-Se- from inorganic selenium and R-Se- from organic selenium compounds.

Animals↗

PubMed1982

The effects of dietary selenium on the biotransformation of 7,21-dimethylbenz[a]anthracene.

The influence of dietary selenium on the mutagenic activation of 7,12-dimethylbenz[a]anthracene (DMBA) by rat liver S9 was studied using the Ames test. Rats received supplemental selenium, as sodium selenite, in the drinking water or in the diet. All rats additionally received 0, 20, 50, 100, or 500 mg Aroclor 1254 per kg body weight. Revertant counts decreased 72 and 31% at the 20- and 100-mg/kg induction levels, respectively, with S9 preparations from rats given selenium supplementation, compared to controls. No significant effects of selenium on S9 preparations was observed in rats treated with 500 mg/kg Aroclor. Preparations of S9 from rats receiving 2.5 ppm Se in their diet produced 46, 84 and 70% less revertants than controls at the 20-, 50- and 100-mg/kg induction levels. Increasing the selenium concentration in the diet to 5 ppm reduced the revertant counts by 71, 68 and 65%, at the 20-, 50- and 100-mg/kg induction level of Aroclor, respectively. Dietary selenium supplementation was shown to decrease the mutagenic activation of DMBA by liver microsomes. These studies indicate that in vivo selenium supplementation may reduce susceptibility to the action of various carcinogens.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1985

The effects of selenium on the emergence of aflatoxin B1-induced enzyme-altered foci in rat liver.

The effects of selenium on the emergence of aflatoxin B1 (AFB1)-induced enzyme-altered foci were studied in male Sprague-Dawley rats. Animals were fed a selenium-deficient diet and supplemented with 5.0, 2.0, and 0.2, or 0 ppm selenium in drinking water for 3 weeks prior to initiation with 2.0 mumol/kg AFB1. After a 1-week period of selenium normalization, the animals were placed on a diet of ordinary rat chow, and were administered a promoting regimen of 500 ppm phenobarbital in drinking water for 1 week, after which time each rat received a two-thirds partial hepatectomy. The promoting regimen of phenobarbital in tap water was then reduced to 100 ppm and continued for 7 weeks. Subsequently, the rats were sacrificed, their livers excised, and fresh frozen sections prepared and stained histochemically to demonstrate areas of gamma-glutamyl transpeptidase (GGT) activity. Selenium supplementation was observed to diminish the induction of GGT-positive foci, especially at the 5.0-ppm level. These data suggest that selenium is able to protect against the hepatocarcinogenic effects of AFB1 in the rat, and that the enzyme-altered foci bioassay may be a useful technique in assessing the interaction of selenium on the process of hepatocarcinogenesis.

Aflatoxin B1↗

PubMed1994

Translactational exposure of F1 mouse pups to selenium.

In an investigation of the modulation of certain neonatal xenobiotic-metabolizing enzymes in liver of mouse pups postnatally exposed to selenium through the transmammary route, sodium selenite was administered in drinking water to lactating dams at the dose levels of 1 or 5 ppm from day 1 of lactation and continued daily for 14 or 21 days. The higher dose of selenium was found to increase the hepatic acid-soluble sulfhydryl content significantly after 21 days of treatment in dams, their pups (P < 0.01) and in the 14-day-old male pups (P < 0.05). Cytochrome b5 content decreased in the livers of dams that received 5 ppm selenium (P < 0.01) and in the F1 pups (P < 0.01) translactationally exposed to selenium for 14 days. Cytochrome P-450 content decreased in dams and pups exposed to 5 ppm selenium for 14 days and either dose for 21 days (P < 0.01). Hepatic glutathione S-transferase decreased in the dam that had received 5 ppm selenium for 14 days (P < 0.05) and in the 14-day-old pups (P < 0.01). Glutathione reductase and glutathione peroxidase activities decreased in both dams and pups (P < 0.01). The overall suppression of neonatal hepatic detoxification enzymes demonstrates that selenium may have far-reaching consequences on neonatal growth, development and drug pharmacokinetics.

Animals↗

PubMed1993

Effect of vitamin B12 on performance and tissue selenium content in rats fed sub-toxic levels of selenite.

The effects of vitamin B12 status on growth and tissue selenium distribution were studied in Sprague-Dawley rats chronically exposed to subtoxic levels of selenite. Vitamin B12 status was monitored by urinary methylmalonic acid excretion and by liver and plasma vitamin B12 levels. Selenite absorption was unaffected by dietary level of vitamin B12. A significant (P < 0.05) interaction of vitamin B12 and selenium was found on growth of rats fed vitamin B12 deficient or control diets. In vitamin B12 depleted rats, there were significant histologic changes in the liver that were characterized by micronodules and regeneration, bile duct reduplication, mild cirrhosis, necrosis of individual hepatocytes and other minor histologic changes. There was no gross or histologic evidence of liver toxicity in rats supplemented with vitamin B12. Rats pair-fed 9 mg/kg selenium with vitamin B12 had significantly lower liver and kidney selenium levels and significantly higher blood selenium levels compared to rats fed the diet without vitamin B12. These results are consistent with the hypothesis that vitamin B12 deficiency limits selenium methylation and excretion, resulting in higher tissue selenium levels and subsequent toxicity.

Animals↗

PubMed1986

Effect of dietary selenium levels on methylbenzylnitrosamine-induced esophageal cancer in rats.

Male Sprague-Dawley rats fed selenium deficient diets received either 0 ppm, 0.15 ppm or 4.0 ppm selenium in the drinking water. Animals were treated with methylbenzylnitrosamine (MBN). Dietary selenium deficiency had no effect on MBN-induced esophageal carcinogenesis. Animals treated with 4 ppm selenium in the drinking water during the initiation and post-initiation period had the same number of tumors as the group which received 0.15 ppm selenium for the entire experimental period. The incidence and frequency of carcinomas was lowest in the group which was supplemented with extra selenium (4.0 ppm) during the period of carcinogen administration and highest in the group which received 4.0 ppm selenium during the post-initiation period.

Animals↗

PubMed1996

Four cases of selenium deficiency in postoperative long-term enteral nutrition.

Because selenium is seldom added to formulations for enteral nutrition (EN), postoperative patients who are supported with EN are at risk for selenium deficiency. This report describes four cases of suspected selenium deficiency in long-term EN. Two patients underwent pancreaticoduodenectomy, one underwent total gastro-pancreatectomy, and one underwent esophageal resection and reconstruction with jejunal autotransplantation. They all developed malabsorption syndrome within 2 yr after operation. Enteral nutritional support with an elemental diet was provided continuously for 7-11 yr. Over the past 1-2 yr they experienced increasing bilateral muscular pain and weakness in the legs, gait disturbance, palpitation, and shortness of breath. Investigation for possible trace element deficiency revealed very low levels of selenium in the blood. After 10-20 d of supplementation with daily intravenous administration of selenious acid 0.16 mg/d (100 micrograms/d of selenium), their blood levels of selenium rose and their symptoms resolved. They were then continued on a maintenance regimen of oral sodium selenite 0.13 mg/d (60 micrograms/d of selenium).

Aged↗

PubMed2005

Commentary: selenium study on endangered razorback sucker is flawed.

The razorback sucker (Xyrauchen texanus) is listed as federally endangered throughout its range. A massive recovery effort by the Recovery Implementation Program for Endangered Fish Species in the Upper Colorado River Basin has focused its efforts in the upper Colorado River. The upper Colorado River basin also has two locations that have been identified by the National Irrigation Water Quality Program as having substantial selenium contamination. Selenium is toxic to fishes, affecting reproductive success. Thus, there is concern about potential effects of selenium on the endangered razorback sucker. Two sets of studies have investigated the effects of selenium on razorback suckers, but study results are conflicting. This commentary evaluates studies that claim selenium is not a problem for razorback sucker. We find that study bias was so pervasive that purported conclusions were unwarranted. Contaminated control water, older life stages of fish tested, lack of methodology for analysis of selenium in water, diet, or fish, use of rotifer food, low feeding rates, low growth rates of fish, and improper storage of site waters resulted in an apparent erroneous linkage of high selenium in whole-body residues with no adverse effects.

Age Factors↗

PubMed2004

Effects of selenium on histopathological and enzymatic changes in experimental liver injury of rats.

The most important antioxidant aspect of selenium is its function in the active site of selenoenzyme glutathione peroxidase. Glutathione peroxidase not only allows the removal of the toxic radicals but also permits the regeneration of lipid molecules through reacylation in the cellular membrane. Thus, GSHPx may prevent the harmful effects of free radicals and may reduce the formation of the reactive metabolites of carbon tetrachloride. Carbon tetrachloride is a hepatotoxic agent which generates haloalkane radicals during its biotransformation in the liver and is widely used to make the experimental model of hepatic damage. Therefore, the aim of the present study is to investigate the possible protective role of selenium on the experimental liver cirrhosis and some enzyme activities in blood plasma from rats. While the activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were significantly increased (p < 0.05, p < 0.05 and p < 0.01, respectively), gamma-glutamyle transferase (GGT) activity was not statistically affected (p < 0.05) with carbon tetrachloride-injection. The levels of AST, ALT and GGT in carbon tetrachloride-group decreased to nearly the enzyme values in control-group after the selenium-injection but the ALP was increased (p<0.01). On the other hand, it was noticed that selenium significantly decreased the hepatic injury. In conclusion, our results showed that carbon tetrachloride caused an increase in the activities of liver enzymes in plasma and selenium application decreased the hepatic injury. Plasma levels of the liver enzymes were decreased after selenium-injections. Based upon these results, selenium may play an important role in the preventive indication of hepatic cellular injury inducted by carbon tetrachloride.

Alanine Transaminase↗

PubMed2005

Mechanistic aspects of the interaction between selenium and arsenic.

Selenium is an essential trace element for humans and other animals, and there is mounting evidence for the efficacy of certain forms of selenium as cancer-chemopreventive compounds. However, over the years, numerous elements such as As, Cu, Zn, Cd, Hg, Sn, Pb, Ni, Co, Sb, Bi, Ag, Au, and Mo have been found to inhibit anti-carcinogenic effects of selenium, which may affect the anti-carcinogenic activity of selenium. The interaction between selenium and arsenic has been one of the most extensively studied. The proposed mechanisms of this interaction include the increase of biliary excretion and direct interaction/precipitation of selenium and arsenic, and their effects on zinc finger protein function, cellular signaling and methylation pathways. This article focuses on these proposed mechanisms and how anti-carcinogenic effects of selenium may be affected by arsenic.

Animals↗

PubMed2004

Dietary selenium supplementation prolongs pentobarbital induced hypnosis.

The present studies characterized the influence of dietary selenium (Na2SeO3) on the duration of pentobarbital (PB) induced hypnosis (sleep) in the rat. Rats were fed semipurified diets varying from 0.01 to 2.0 mg Se/kg for up to 4 weeks. Consumption of diets containing 1.0 and 2.0 mg Se/kg significantly prolonged PB induced hypnosis. Hepatic selenium, but not hepatic glutathione peroxidase activity, correlated with the length of PB induced hypnosis. The prolongation of hypnosis caused by diets containing 1.0 mg Se/kg was substantially reduced or eliminated by repeated exposure to PB. Although single exposure to increasing quantities of PB (60-100 mg/kg body weight) led to a progressive increase in sleep duration, the proportional increase caused by supplemental selenium (2.0 vs 0.1 microg Se/g) remained relatively constant (approximately 25%). Increasing maturity was inversely related to the duration of PB induced hypnosis, regardless of dietary selenium provided. Consumption of the 2.0 mg Se/kg diet prolonged PB induced hypnosis to a greater degree in immature than in mature rats (P < 0.05). Consumption of the selenium enriched diet (2 microg Se/g) resulted in an increase in cytochrome 2B, but had no effect on cytochrome 1A compared to controls (0.1 microg Se/g). Pretreatment of rats with P450 enzymes activators (i.e., PB, Aroclor 1254, or 3-methylcholanthrene) shortened the duration of PB induced sleep and masked the effects of dietary selenium. The current studies document that dietary selenium can influence the response to pentobarbital induced hypnosis and likely relates to changes in drug detoxification enzymes.

Age Factors↗

PubMed2006

Factors associated with longitudinal plasma selenium decline in the elderly: the EVA study.

Selenium status decreases in elderly populations. Cardiovascular diseases are the primary cause of death in the French elderly, and selenium may protect against cardiovascular diseases. The present work aims to evaluate the relationships between cardiovascular-related risk factors and plasma selenium variability in an elderly population during a 9-year period. Seven hundred fifty-one subjects from the EVA ("Etude du Vieillissement Artériel") study, aged 59 to 71 at baseline, were followed for 9 years. Clinical examinations and lifestyle questionnaires were repeated every 2 years. Plasma selenium determinations were performed at baseline and at the end of the study. The association between the 9-year plasma selenium variability and studied risk factors at baseline or occurring during the follow-up was evaluated by using multivariate linear regression models. After controlling all potential associated factors, age of subjects (P<.01), obesity (P=.02) and occurrence of cardiovascular disease during follow-up (P=.03) increased the longitudinal decline in plasma selenium, whereas gender, education, smoking, alcohol intakes, dyslipidemia, diabetes, hypertension had no effect (P>.05). It may be postulated that obesity and occurrence of cardiovascular events are the main factors associated with plasma selenium fall during ageing. The respective roles played by nutritional and metabolism changes in the mechanism of these associations still need to be explored.

Aged↗