Methods of Selenium Supplementation: Bioavailability and Determination of Selenium Compounds.

Selenium, a "dual-surface" element, maintains a very thin line between a level of necessity and harmfulness. Because of this, a deficiency or excess of this element in an organism is dangerous and causes health-related problems, both physically and mentally. The main source of selenium is a balanced diet, with a proper selection of meat and plant products. Meanwhile, the proper assimilation of selenium into these products depends on their bioavailability, bioaccessibility, and/or bioactivity of a given selenium compound. From the time when it was discovered that selenium and its compounds have a significant influence on metabolic processes and in many countries throughout the world, a low quantity of selenium was found in different parts of the environment, pressure was put upon an effective and fast method of supplementing the environment with the help of selenium. This work describes supplementation methods applied with the use of selenium, as well as new ideas for increasing the level of this element in various organisms. Based on the fact that selenium appears in the environment at trace levels, the determination of total amount of selenium or selenium speciation in a given sample demands the selection of appropriate measurement methods. These methods are most often comprised of a sample preparation technique and/or a separation technique as well as a detection system. The work presents information on the subject of analytical methods used for determining selenium and its compounds as well as examples in literature of their application.

Teratogenic effects and monetary cost of selenium poisoning of fish in Lake Sutton, North Carolina.

Selenium pollution from coal ash wastewater was investigated in Lake Sutton, NC. This lake has been continuously used as a cooling pond for a coal-fired power plant since 1972. Historic and recent levels of contamination in fish tissues (14-105µg Se/g dry weight in liver, 24-127 in eggs, 4-23 in muscle, 7-38 in whole-body) exceeded toxic thresholds and teratogenic effects were observed in fish collected in 2013. A high proportion (28.9 percent) of juvenile Lepomis spp. exhibited spinal and craniofacial malformations that were consistent with selenium poisoning. Teratogenic Deformity Index values indicated population-level impacts on the fishery. The partially monetized cost of resultant fishery losses was calculated at over $US 8.6 million annually, and over $US 217 million for the entire period of damage, which dates back to 1987 when chemical and biological monitoring began.

Sudden death associated with myocardial contraction band necrosis in Boer goat kids.

Parenteral selenium (Se) and vitamin E (Vit E) were administered to all newborn kids at a Boer goat farm where there was previous high neonatal mortality assumed to be due to nutritional myopathy. All treated kids were affected by severe respiratory distress and died within 8 hours of Se/Vit E administration. Gross lesions included severe pulmonary edema, hydrothorax, and hydropericardium. The primary histopathologic finding was severe, acute, and monophasic myocardial contraction band necrosis. The diagnosis was accidental acute selenosis based on trace mineral analysis of the liver. This case highlights an important differential diagnosis in cases of acute myocardial contraction band necrosis and sudden death in goats and emphasizes the need for caution when administering parenteral Se/Vit E preparations.

Selenium toxicosis in a white-tailed deer herd.

Chronic selenium (Se) toxicosis was found in a herd of white-tailed deer showing signs of anorexia, weight loss, and lameness. Concentration of Se in the liver ranged from 2.7 to 8.97 mg/kg wet weight. Myocardial necrosis, mineralization, and fibroplasia were seen histologically. This is the first report of this toxicosis in white-tailed deer.

[Feed-related selenium poisoning in swine]. / Fütterungsbedingte Selen-Vergiftung beim Schwein.

The following case report describes a selenium toxicosis in a pig-fattening farm of two finisher groups. The diseased animals partly showed ataxia and paresis or intense lameness in connection with band-like ablation of the epidermis at the coronary band. Some of them suffered from alopecia. Foot-and-mouth disease and swine vesicular disease were excluded by serological tests. Dissection revealed a multifocal bilateral symmetric poliomyelomalacia. Histological changes in the claws ranged from severe cell-decay in the germinative layer to distinctive decay of the stratum corneum. Due to damage of the claw epidermis the corium was partly exposed. Feed analysis revealed 100-fold increased selenium content in the finishing premix from the feed mill and as a result 20- to 60-fold increased selenium values in feed samples from the farm-made finisher mixture. Selenium concentration in the blood of diseased animals was 4- to 10-fold higher than normal values, which confirmed the tentative diagnosis of a selenium toxicosis.

Selenosis in Ruminants.

Selenium (Se) is a metalloid that exists as a red amorphous powder, reddish crystal, silver-gray crystal, or brown-black solid. Its potency as a nutrient and a toxicant is such that few people have seen the pure element. It is easy to lose sight of the narrow margin between too little and too much. The most common cause of selenosis is accidental or intentional overuse of supplements. Many target organs and effects of Se toxicity are similar to those of Se deficiency, so laboratory confirmation is necessary. Prevention consists of minimizing exposure to seleniferous feedstuffs and optimizing dietary factors that might aggravate selenosis.

Scalp hair mercury concentrations in Pakistan.

The presence of mercury in the environment is widespread and persistent, but the extent of exposure of Pakistanis to mercury is virtually unknown. We collected toenail and scalp hair samples from 158 subjects (83 males and 75 females) residing in Lahore and its suburbs. We also conducted a questionnaire survey and personal interviews to obtain information on demographic factors, lifestyles, and socioeconomic factors, among others. Mercury concentration in hair samples was measured by cold vapor atomic absorption spectrometry (CVAAS). In addition, the concentration of selenium in the toenail and hair samples was determined by inductively coupled plasma mass spectrometry (ICP-MS). The mean hair mercury concentration was 0.45 ppm (95% CI = 0.34-0.60) and did not show correlation with fish consumption, age, area of origin, or present residence. Mercury concentration was higher (p = 0.021) in females than in males, and was also higher in subjects with 11 or more years of education (p for trend = 0.013). There were 13 subjects with mercury concentration higher than 10 ppm. Most of them were young females and a few were middle-aged males. When the analysis was confined to subjects with mercury concentrations lower than 0.6 ppm, the amount of fish consumed showed correlation with hair mercury concentration with a marginal statistical significance (p = 0.065). The geometric means of selenium in hair and toenails were 0.87 and 1.01 ppm, respectively. Mercury and selenium concentrations in hair showed no correlation (correlation coefficient = 0.057, p = 0.478). This study shows that mercury exposure levels among residents in Lahore and its suburban areas are relatively low, except among outliers, wherein mercury exposure might be brought about by the use of mercury-containing soaps.

Chemical Speciation of Selenium and Mercury as Determinant of Their Neurotoxicity.

The antagonism of mercury toxicity by selenium has been well documented. Mercury is a toxic metal, widespread in the environment. The main target organs (kidneys, lungs, or brain) of mercury vary depending on its chemical forms (inorganic or organic). Selenium is a semimetal essential to mammalian life as part of the amino acid selenocysteine, which is required to the synthesis of the selenoproteins. This chapter has the aim of disclosing the role of selenide or hydrogen selenide (Se-2 or HSe-) as central metabolite of selenium and as an important antidote of the electrophilic mercury forms (particularly, Hg2+ and MeHg). Emphasis will be centered on the neurotoxicity of electrophile forms of mercury and selenium. The controversial participation of electrophile mercury and selenium forms in the development of some neurodegenerative disease will be briefly presented. The potential pharmacological use of organoseleno compounds (Ebselen and diphenyl diselenide) in the treatment of mercury poisoning will be considered. The central role of thiol (-SH) and selenol (-SeH) groups as the generic targets of electrophile mercury forms and the need of new in silico tools to guide the future biological researches will be commented.

Modulation of urinary siderophores by the diet, gut microbiota and inflammation in mice.

Mammalian siderophores are believed to play a critical role in maintaining iron homeostasis. However, the properties and functions of mammalian siderophores have not been fully clarified. In this study, we have employed Chrome Azurol S (CAS) assay which is a well-established method for bacterial siderophores study, to detect and quantify mammalian siderophores in urine samples. Our study demonstrates that siderophores in urine can be altered by diet, gut microbiota and inflammation. C57BL/6 mice, fed on plant-based chow diets which contain numerous phytochemicals, have more siderophores in the urine compared to those fed on purified diets. Urinary siderophores were up-regulated in iron overload conditions, but not altered by other tested nutrients status. Further, germ-free mice displayed 50% reduced urinary siderophores, in comparison to conventional mice, indicating microbiota biotransformation is critical in generating or stimulating host metabolism to create more siderophores. Altered urinary siderophores levels during inflammation suggest that host health conditions influence systemic siderophores level. This is the first report to measure urinary siderophores as a whole, describing how siderophores levels are modulated under different physiological conditions. We believe that our study opens up a new field in mammalian siderophores research and the technique we used in a novel manner has the potential to be applied to clinical purpose.

Evaluation of the Content of Antimony, Arsenic, Bismuth, Selenium, Tellurium and Their Inorganic Forms in Commercially Baby Foods.

Baby foods, from the Spanish market and prepared from meat, fish, vegetables, cereals, legumes, and fruits, were analyzed to obtain the concentration of antimony (Sb), arsenic (As), bismuth (Bi), and tellurium (Te) as toxic elements and selenium (Se) as essential element. An analytical procedure was employed based on atomic fluorescence spectroscopy which allowed to obtain accurate data at low levels of concentration. Values of 14 commercial samples, expressed in nanograms per gram fresh weight, ranged for Sb 0.66-6.9, As 4.5-242, Te 1.35-2.94, Bi 2.18-4.79, and Se 5.4-109. Additionally, speciation studies were performed based on data from a non-chromatographic screening method. It was concluded that tellurium and bismuth were mainly present as inorganic forms and selenium as organic form, and antimony and arsenic species depend on the ingredients of each baby food. Risk assessment considerations were made by comparing dietary intake of the aforementioned elements through the consumption of one baby food portion a day and recommended or tolerable guideline values.

Evaluating selenium poisoning.

Selenium poisoning in humans is reviewed from the perspective of the clinical laboratory. While evaluation of selenium poisoning is straightforward when the analytic results are markedly elevated and the patient is acutely symptomatic, distinguishing toxic from non-toxic elevations is a more frequent issue and more challenging. A significant problem is that selenium is determined as its total concentration in spite of the fact that different chemical forms of selenium have different toxic potentials. In the published reports reviewed herein, serum selenium concentrations span the following ranges: 400-30,000 micro g/L associated with acute toxicity, 500-1400 micro g/L associated with chronic toxicity, and <1400 micro g/L free of toxicity; the category is determined by signs and symptoms in the patient. Most reports that describe acute selenium poisoning involve ingestion of inorganic compounds such as selenious acid, found in gun-bluing agents, and fatalities that occur within the first day are associated with postmortem blood selenium levels >1400 micro g/L. Tissue selenium levels show a complex pattern and significant elevations in organs such as kidney are not always indicative of toxicity. As with many trace elements, measuring selenium concentrations in body fluids and tissues tends to be easier than understanding what the results mean.

Selenium Health Benefit Values: Updated Criteria for Mercury Risk Assessments.

Selenium (Se)-dependent enzymes (selenoenzymes) protect brain tissues against oxidative damage and perform other vital functions, but their synthesis requires a steady supply of Se. High methylmercury (CH3Hg) exposures can severely diminish Se transport across the placenta and irreversibly inhibit fetal brain selenoenzymes. However, supplemental dietary Se preserves their activities and thus prevents pathological consequences. The modified Se health benefit value (HBVSe) is a risk assessment criterion based on the molar concentrations of CH3Hg and Se present in a fish or seafood. It was developed to reflect the contrasting effects of maternal CH3Hg and Se intakes on fetal brain selenoenzyme activities. However, the original equation was prone to divide-by-zero-type errors whereby the calculated values increased exponentially in samples with low CH3Hg contents. The equation was refined to provide an improved index to better reflect the risks of CH3Hg exposures and the benefits provided by dietary Se. The HBVSe provides a biochemically based perspective that confirms and supports the FDA/EPA advice for pregnant and breast-feeding women regarding seafoods that should be avoided vs. those that are beneficial to consume. Since Se can be highly variable between watersheds, further evaluation of freshwater fish is needed to identify locations where fish with negative HBVSe may arise and be consumed by vulnerable subpopulation groups.

A critical review of the biogeochemistry and ecotoxicology of selenium in lotic and lentic environments.

Anthropogenic activities resulting in elevated selenium (Se) levels in aquatic ecosystems can result in teratogenic and reproductive effects in fish and waterfowl. However, relationships between observed effects and exposure concentrations or body burdens are ambiguous. Therefore, it is critical to identify factors that affect Se ecotoxicity before defining adequate protective environmental regulations. One important political debate questions if Se ecotoxicity differs between standing (lentic) and flowing (lotic) waters and, if so, how this should be incorporated into the definition of protective criteria. In the present review, we compile and discuss the scarce literature regarding Se ecotoxicity in lotic systems, and we compare it to the substantial body of evidence for lentic systems. General differences between lentic and lotic systems with respect to ecology, hydrology, and biogeochemistry are identified and related to Se ecotoxicity. The limited knowledge regarding Se speciation in the biomagnification process is reviewed and put in context. Fundamental considerations suggest that Se ecotoxicity in lotic systems should be reduced compared to lentic systems, but we conclude that this statement is not substantiated by the existing data. Additionally, we identify critical gaps of knowledge that must be resolved in future studies before the argument can be decided conclusively.

Acute selenium poisoning: suicide by ingestion.

Selenium is a ubiquitous element in the environment essential to the human diet and widely utilized in industrial processes. Fatal human selenium intoxication is rare. The authors report a case in which investigators recovered a bottle of gun-bluing agent beside a 24-year-old man. He exhibited signs and symptoms typical of acute selenium intoxication presenting with nausea and vomiting, followed by pulmonary edema and rapid cardiovascular collapse approximately 3 to 4 h after ingestion. Classic electrocardiographic (EKG) changes, which have been reported to occur in acute selenium intoxication, included sinus tachycardia with ST wave alteration. Toxicological results confirmed elevated blood and tissue concentrations. The cause of death was ascribed to acute selenium intoxication, which ensued rapidly after oral consumption. The manner of death was suicide. This case report, which presents an overview of acute and chronic selenium poisoning, underscores the value of thorough toxicologic analyses of tissue and body fluids in humans.

Endemic selenium intoxication of humans in China.

An endemic disease was discovered in 1961 in parts of the population of Enshi County, Hubei Province of the People's Republic of China. During the years of the highest prevalence, from 1961 to 1964, the morbidity was almost 50% in the 248 inhabitants of the five most heavily affected villages; its cause was determined to be selenium intoxication. The most common sign of the poisoning was loss of hair and nails. In areas of high incidence, lesions of the skin, nervous system, and possibly teeth may have been involved. A case is reported of a middle-aged, female hemiplegic, whose illness and death apparently were related to selenosis. Daily dietary intakes of selenium, estimated after the peak prevalence had subsided, averaged 4.99 (range 3.20 to 6.69) mg and hair and blood selenium levels averaged 32.2 and 3.2 micrograms/ml, respectively. Up to 1000x differences occurred when selenium contents of vegetables, cereals, scalp hair, blood, and urine from the selenosis areas were compared with those from Keshan disease (selenium deficiency) areas. The ultimate environmental source of selenium was a stony coal of very high selenium content (average more than 300 micrograms/g; one sample exceeded 80,000 micrograms/g). Selenium from the coal entered the soil by weathering and was available for uptake by crops because of the traditional use of lime as fertilizer in that region. This particular outbreak of human selenosis was due to a drought that caused failure of the rice crop, forcing the villagers to eat more high-selenium vegetables and maize and fewer protein foods.

Labeling of the neurons of origin of zinc-containing pathways by intraperitoneal injections of sodium selenite.

Intraperitoneal injections of sodium selenite result in the formation of zinc-selenium complexes in zinc-containing axonal boutons ("Timm stainable boutons"), and the zinc-selenium precipitate can be rendered visible in histological sections by silver enhancement. In this work we present evidence, in the rat, that zinc-selenium precipitates formed in vivo after intraperitoneal injections of sodium selenite are translocated by colchicine-sensitive retrograde transport to neural perikarya when animals are allowed to survive 12-24 h after the selenite administration. Silver enhancement renders the perikaryal precipitates visible and thus demonstrates the perikarya of all zinc-containing neurons in the CNS simultaneously. Large populations of zinc-containing neurons identified by the method are found in layers II, III, and VI of all neocortical areas, in the superficial and deep layers of the prepyriform areas and, with a high degree of regional differentiation, in the retrosplenial, entorhinal, para- and presubicular cortices, the hippocampal formation and the amygdaloid complex. Zinc-containing cells were absent from the caudate-putamen, nucleus accumbens and septal complex. Labeled zinc-containing cells are absent in non-telencephalic parts of the brain. The findings indicate that the zinc-containing circuitry of the brain mainly serves in telencephalic information processing.

Acute hydrogen selenide inhalation.

Acute exposure to selenium hydrochloride resulted in severe dyspnea and a pneumomediastinum in a young healthy man. Pulmonary function tests revealed restrictive and obstructive airways disease. Although the patient's pulmonary function slowly improved, subsequent studies revealed persistent impairment. Therefore, exposure to selenium gas may result acutely in severe coughing and wheezing and may lead to irreversible obstructive lung disease.

Selenium and lead: mutual detoxifying effects.

Antagonistic toxic effects of selenium and lead were studied in growing rats. Chronic lead intoxication was produced by cutaneous application of lead naphthenate solution (80-200 mg Pb/kg body weight) for a period of 8 weeks and chronic selenium intoxication was induced by giving 5 ppm, 10 ppm and 15 ppm selenium in drinking water. The growth rate and food consumption of rats receiving selenium in addition to lead approached normal rate while animals treated with only one of them showed hampered growth rate and lower food consumption. The enzymatic activity of delta-aminolevulinic acid dehydrase (ALA-D) in whole blood, liver and kidney and liver P-450 enzyme activity were normal in rats receiving both selenium and lead. The enzymic activities assayed were, however, depressed in the animals receiving either lead or selenium. Assay of lead and selenium in liver, brain, kidney and blood was carried out. Rats receiving both metals and higher concentrations of these metals in the organs studied, as compared to those only receiving one component. The data seem to indicate that the effect of selenium on the toxic effects of lead is similar to its protective role against methylmercury intoxication.

Influence of chronic intoxication with selenium on collagen and elastin content in tissues of rat.

Rats were intoxicated with sodium selenite (0.3 mg/kg body wt.) for 10 weeks. An increase in total collagen content in skin and a decrease in the lungs, liver and kidneys were observed. Enhanced serum and urine levels of collagen metabolites were found. Elastin content was shown to be increased in the lung, liver, heart muscle and kidney of selenium-intoxicated rats.