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PubMedDate not supplied

Chemical stability of selenious acid in total parenteral nutrition solutions containing ascorbic acid.

Reduction of selenious acid (H2SeO3) to elemental Se by ascorbic acid was investigated in regard to the stability of selenite in total parenteral nutrition (TPN) solutions. [75Se] H2SeO3 (100 micrograms Se/liter) was incubated at 25 degrees C with pure ascorbic acid (100 or 500 mg/liter) or added to complete TPN solutions containing similar levels of ascorbate. The mixtures were subjected to thin layer electrophoresis at pH 5.3 to separate HSeO3- from Se degree. In complete TPN formulas, little or no reduction of HSeO3- to Se degree occurred over a 24-hr period, whereas complete reduction occurred with pure ascorbic acid. Further experiments showed that the amino acid component of the TPN formula was preventing the reduction of selenite, and that reduction of selenite by ascorbate did not occur in buffered solutions having a pH of 5 or greater. These results show that reduction of selenite is strongly influenced by pH. At the concentrations of H2SeO3 and ascorbic acid commonly used, reduction to elemental Se is unlikely to be a practical problem in TPN solutions in the near-neutral pH range.

Ascorbic Acid↗
PubMedDate not supplied

Systemic absorption of selenious acid and elemental selenium aerosols in rats.

Absorption of Se from the nasal passages, lungs, gastrointestinal tract, and skin was studied in Fischer-344 rats. Radiolabeled selenious acid and elemental Se particles were administered by inhalation, gavage, nasal instillation, and iv injection. Selenious acid was always absorbed into the general circulation more rapidly and to a greater extent than elemental Se. By 4 h after inhalation of selenious acid and elemental Se aerosols, 94% of the selenious acid and 57% of the elemental Se deposited in lungs was absorbed into blood. Of the selenious acid instilled into nasal passages, 18% was absorbed into blood; 16% of the elemental Se was absorbed. Gastrointestinal absorption was 87% for selenious acid and 50% for elemental Se. Selenious acid solutions were also painted onto the pelts of rats. From 10 to 30% of the selenious acid was absorbed through the skin. Following inhalation or injection of either Se compound, most of the Se was excreted in the urine. Significantly more Se appeared in feces of animals receiving elemental Se by gavage than animals receiving selenious acid. Results indicate that if people were to absorb inhaled Se from the upper respiratory tract in a manner similar to that of rats, one-third more selenious acid would be absorbed into the general circulation than elemental Se. All Se deposited in the lungs would be absorbed into blood. However, selenious acid would be absorbed more rapidly than elemental Se.

Absorption↗
PubMed1984

A double isotope method for characterizing hygroscopic selenious acid aerosols used in inhalation exposures.

Methods of generating and characterizing selenious acid aerosols for use in deposition and toxicity studies are described. Selenious acid aerosols were nebulized and heat treated at varied temperatures. Because selenious acid is hygroscopic, a solution containing 3H2O and 75Se was nebulized to determine the water content in selenium aerosols after generation. The stable aerosol was a hydrate of selenious acid, H2SeO3 X 1/2 H2O, at New Mexico ambient relative humidity (ca. 20%). The mass median aerodynamic diameter of the collected droplets was 0.6 micron with a geometric standard deviation of 1.3.

Aerosols↗
PubMed1984

Utilizing selenious acid to reverse selenium deficiency in total parenteral nutrition patients.

The ability of selenious acid to reverse selenium deficiency in eight adult home TPN patients was assessed. Initially, deficiency was documented by comparing both plasma selenium levels in patients (means = 0.035 micrograms/g) to those of 10 controls (means = 0.117 micrograms/g) (p less than 0.001) and by comparing erythrocyte glutathione peroxidase (GSHPx) activity, as mumol NADPH oxidized/g Hb/min, in patients (means = 8.93) to controls (means = 31.76) (p less than 0.002). Subsequently, patients added 100 micrograms/day of selenious acid to their total parenteral nutrition solutions. Postsupplementation selenium status demonstrated a mean plasma level of 0.101 micrograms/g and a mean erythrocyte GSHPx activity of 17.56. Statistically, patients' plasma selenium levels were significantly different (p less than 0.001) when compared to pretreatment levels. Additionally, there was no significant difference between the restored levels and the levels of the controls. Postsupplementation erythrocyte GSHPx activity (means = 17.56) was not significantly different from the initial patient values, although activity did double. Additionally, there existed a significant difference between the postsupplementation enzyme activity and the controls (p less than 0.03). We conclude that selenious acid is able to normalize deficient plasma levels but not deficient erythrocyte GSHPx activity.

Female↗
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↗
PubMed1991

The recovery of selenious acid aerosols on glass fiber filters.

Previous workers have shown that selenium is only partially trapped on a filter during air sampling. In some cases, these losses have been attributed to volatilization of selenium dioxide. Our results demonstrate that selenium dioxide, in the presence of moist air, is completely recovered (apparently as selenious acid aerosols) and that the previous shortfalls must be due to other selenium species as yet unidentified. Selenious acid aerosols in our study were formed by volatilizing selenium dioxide (approximately 3 mg) into a stream of moist ambient air (relative humidity, greater than 50%), and trapped on glass fiber filters using a high-volume air sampler. Selenium(IV) was ultrasonically extracted from the filter with water and analyzed by atomic absorption spectrometry. Selenious acid aerosols were trapped on the filters with high efficiency (105 +/- 5 percent) using a 50 minute sampling period. With an extended sampling period (24 hours) the recovery was 103 +/- 6 percent.

Aerosols↗
PubMed1985

Acute poisoning by selenious acid.

A 2 yo male child ingested approximately 15 ml of a Gun Blue solution containing selenious acid, nitric acid and copper nitrate. He was immediately given milk and vomited spontaneously blood-stained food with a garlic smell. He was admitted to our Centre less than 3 hr following ingestion. An esophago-gastroscopy showed a second degree burn of both esophagus and stomach. He became comatose and had to be ventilated mechanically. Metabolic acidosis, leucocytosis, hyperglycemia and hemoconcentration were also observed. During the following day he developed a severe intestinal distension, a cardiomyopathy (CPK = 1,302, cardiac arrhythmia), and moderate hepatic, renal and pulmonary dysfunctions. Plasma selenium concentration was 285 micrograms/L and the maximum urinary concentration was 28,459 micrograms/L. After 4 days, his condition had improved considerably and he was about to be extubated when he suddenly developed acute respiratory distress. A similar episode occurred 24 hr later. His lung function progressively deteriorated; later he required the use of an extracorporeal membrane lung. Legionella dumofii was found the causative agent. He died 17 d after ingestion despite aggressive treatment. Acute selenious acid poisoning and its relation to Legionnaire's disease is discussed.

Acid-Base Imbalance↗
PubMed1986

An autopsy case of acute selenium (selenious acid) poisoning and selenium levels in human tissues.

A case of fatal suicidal ingestion of "Super Blue (Gun Blue)" (gun-blueing) is presented. Post-mortem examination of the patient revealed pulmonary edema with pleural effusion and congestion of the kidney. Necrosis of proximal tubules was found in the kidney by histological examination. "Super Blue" contains 4% selenious acid and 2.5% cupric sulfate in HCl. Levels of selenium and copper in tissues of the toxic case and normal individuals were determined. The selenium levels of tissues of the patient were 9-90-fold higher than that of normal subjects, whereas concentrations of copper were about 2-fold compared to that of control levels. The highest levels of selenium in the tissues of the patient were found in the lung, kidney and stomach contents.

Adult↗
PubMedDate not supplied

[Thioamine compound content in urine determined by using an iodine-azide reagent and selenious acid reaction].

Iodine-azide reagent enabled to evaluate quantitatively content of thioamines excreted within a day. Concentration of thioketons in urine of patients was 11-15 microgram/eqv of thiourea per 1 ml, at the same time their excretion within a day accounted for 13.06 +/- 0.56 mg/eqv in women and 22.11 +/- 1.1 mg/eqv in men. Neither concentration of thioketones in urine nor their excretion in patients with various tumors studied were distinct from these patterns in urine of non-oncologic patients. Comparison of these two methods suggests that development of color on addition of selenous acid to urine is not due to reaction with thioamines present but to interaction with other unknown substances.

Amides↗
PubMedDate not supplied

Toxicity of selenium compounds to alveolar macrophages.

Selenium compounds released into urban atmospheres as a result of fossil fuel combustion may pose an inhalation hazard to people. Two chemical forms of selenium produced during coal combustion and present in combustion effluent are selenious acid. H2SeO3, and elemental selenium, Se. In an attempt to determine the toxicity of selenium compounds relative to other trace elements, the cytotoxicity of H2SeO3 and Se to rabbit alveolar macrophages in vitro was investigated. Macrophages were obtained by lung lavage and exposed in tissue culture after 20 h. Neither selenious acid nor elemental selenium caused cell lysis at concentrations which decreased total cell viability. Selenious acid was an order of magnitude more toxic then elemental selenium. Elemental selenium was similar in toxicity to environmental contaminants such as CdCl2 and V2O5. These in vitro cytotoxicity data can be used to predict the risk posed to people inhaling selenium compounds at levels found in urban atmospheres.

Animals↗
PubMed1989

Plasma selenium-dependent glutathione peroxidase. Cell of origin and secretion.

Human plasma glutathione peroxidase (GSHPx) has been shown to be a glycosylated selenoprotein distinct enzymatically, structurally, and antigenically from known cellular glutathione peroxidases. The extracellular location of the enzyme and the fact that it is glycosylated suggested that it is a secreted protein. Utilizing mutually non-cross-reactive antibodies to human cellular and plasma GSHPx, we conducted a search to determine the tissue of origin for plasma GSHPx. The cells screened were endothelial cells because they are the main source of extracellular superoxide dismutase, HL-60 cells (myeloid cell line) because they are the main source of extracellular H2O2, and Hep G2 cells (hepatic cell line) because they are the source of many plasma proteins. Human umbilical vein endothelial cells were metabolically labeled with either [35S]methionine or [75Se]selenious acid, and HL-60 cells and Hep G2 cells were metabolically labeled with [75Se]selenious acid. Proteins were immunopurified from the labeled cells and their media with either anti-red blood cell (RBC) GSHPx IgG or with anti-plasma GSHPx IgG. Utilizing anti-RBC GSHPx IgG, only the cellular form of the enzyme was precipitated from all the cells tested but not from their media. When anti-plasma GSHPx IgG was applied to the cells and their media, a selenoprotein was precipitated only from the media of Hep G2 cells. When Hep G2 cells were incubated in the presence of the carboxylic ionophore monensin, an intracellular selenoprotein could be detected using anti-plasma GSHPx IgG. The precipitation of the cellular form from all three cell types was partially inhibited by preincubation of the anti-RBC GSHPx IgG with purified RBC GSHPx while the precipitation of the selenoprotein from the medium of Hep G2 cells by anti-plasma GSHPx IgG was prevented by preincubation of the antibody with purified plasma GSHPx. We suggest that plasma GSHPx is synthesized by and secreted from hepatic cells. This is, to the best of our knowledge, the only known selenoprotein with a defined function that has been shown to be synthesized for secretion by mammalian cells.

Cell Line↗
PubMed1986

Proximal muscle weakness and selenium deficiency associated with long term parenteral nutrition.

A 33-yr-old white female with short bowel syndrome secondary to trauma was maintained on home parenteral nutrition for 4 yr when her plasma, red cell, white cell, and platelet glutathione peroxidase (GSHPx) activities were found to be extremely low, as were her plasma and red cell selenium levels. During her first year on parenteral nutrition she noted the onset of an inability to rise from a squatting position, rapid tiring when stair climbing, and weakness when attempting to lift large or moderately heavy objects. Treatment with 400 micrograms/d of selenious acid intravenously was associated with a disappearance of her symptoms and an increase in proximal muscle strength within 6 wk. The plasma and red cell selenium levels, and the plasma and white cell GSHPx activities rose to normal levels within 6 wk. Red cell GSHPx activity returned to normal by 3 mo.

Adult↗
PubMed1985

Fatal acute selenium toxicity.

Selenium is used widely in industry and as a dietary supplement. Reports of acute selenium toxicity are infrequent, however, and the relationship of toxicity to selenium concentrations in blood and tissues has not been established. We describe a patient who died eight days after ingesting selenious acid in the form of gun blueing. The patient's clinical course demonstrated many of the features of inorganic selenium toxicity described in animals; hypotension as a result of both vasodilation and decreased cardiac output, adult respiratory distress syndrome, severe myopathy which contributed to respiratory failure, and a garlicky odor to the breath. Four days after ingestion the serum selenium concentration was twenty times normal and urinary excretion seventy times normal. Postmortem tissue selenium concentrations were up to 40 times normal.

Female↗
PubMed1988

Interactions of gold with cytosolic selenium-containing proteins in rat kidney and liver.

Rats injected with aurothioglucose (ATG) for 5 days were subsequently injected with [75Se]selenious acid and killed after 3 days. Kidney and liver cytosols were chromatographed on Sephadex G-150. 75Se in kidney was associated with high molecular weight (HMW), 85,000 Mr, 26,000 Mr, and 10,000 Mr proteins and with a nonprotein fraction. The elution profile of liver cytosol was similar to that of kidney, but without a 26,000 Mr protein. ATG injection increased the association of 75Se with all fractions of kidney cytosol except the 85,000 Mr fractions, which contained Se-glutathione peroxidase (SeGSHPx) activity; 75Se in liver was increased only in HMW fractions. Unfractionated kidney cytosolic SeGSHPx activity was decreased 14% by ATG injection, but liver enzyme activity was not changed. However, Sephadex G-150 chromatography showed that total and specific activities, respectively, were decreased 28 and 23% in kidney and 25 and 16% in liver. Au coeluted with HMW and 10,000 Mr 73Se-containing kidney proteins; the latter contained 50% of the Au eluted from the column. DEAE Sephacel chromatography of the 10,000 Mr kidney protein showed that both Au and 75Se were tightly associated with metallothionein-like proteins. This study demonstrates the interaction of Au with rat liver and kidney 75Se-containing proteins.

Animals↗
PubMed1979

Mineral metabolism of the healing arterial wall.

The mineral metabolism of healing arterial walls was studied by measuring the accumulation of several radioisotopes at the site of vascular repair in rats. Each rat was subjected to a 1-cm full-thickness aortotomy and then immediately injected by tail vein with c 5 muCi of one of the following radioisotopes: chromic chloride Cr 51 or sodium chromate Cr 51; ferrous chloride Fe 59 or ferric chloride Fe 59; manganous chloride Mn 54; selenious acid Se 75; strontium chloride Sr 85; or zinc chloride Zn 65. At intervals of 1, 2, 4, 6, and 10 days after operation and injection, groups of four rats for each radioisotope were killed, aortas dissected, and the specific radioactivity of healing vascular tissue compared with that of adjacent normal artery. There were sharp and statistically significant differences in the preferential accumulation of the radioisotopes in healing compared with normal aorta. Zinc appeared to be the element most involved in vascular repair, followed by selenium and chromium.

Animals↗