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A Toxicological Report of SELENIUM PHYSICAL & CHEMICAL PROPERTIES ‘Selene”, moon in Greek. Discovered in 1817. Non-metal element , Group 6, the chalcogens. Stable elemental forms in room temperature: Grey, Black, and Red. PHYSICAL & CHEMICAL PROPERTIES Chemical properties are similar to sulfur. Bind to many metals and nonmetals directly in aqueous solution Chalcogen, Greek words ‘copper-ore former’, refers to the tendency to form selenide minerals. PRODUCTION AND APPLICATION Naturally found in rocks and soils. Photographic devices, production of plastics, paints, rubber, dietary supplements, glass, pesticides, and anti-dandruff shampoos! Byproduct of copper refining, sulfuric acid production and production/burning of fossil fuels. PRODUCTION AND APPLICATION Essential micronutrient for organisms. Important in forming antioxidant enzymesGlutathione peroxidases and thioredoxin reductases. Selenocystein ( Se-Cys) acts as the site of reaction. Involved in regulation of Thyroid hormones (T3 and T4 ) 2 GSH + H2O2----GSH-Px → GSSG + 2 H2O ENTRY INTO THE AQUATIC ENVIRONMENT Anthropogenic sources: Burning of fossil fuels; metal refinery, end-product manufactures, sewage, agricultural , and industrial waste water runoff. Natural: Leaching and weathering of rocks; volcanic activity, and votilization by plants and bacteria. Greatest proportion of emission: Coal fly ash. ENTRY INTO THE AQUATIC ENVIRONMENT Local Example: Agricultural Run-off in San Joaquin Valley CHEMISTRY IN WATER Ph sensitive Under aerobic and alkaline conditions, the soluble and mobile forms dominate: Selenite and Selenate (SeO32− and SeO42- ) Elemental selenium is stable Under acidic condition, metal selenides’ formation is favored. TOXICITY TO AQUATIC LIFE Easily bioaccumulated, mainly through diet Potential high level of accumulation in bivalves (>500x in some cases) Responsible for multi-species die-off of fish, mainly in enclose freshwater lakes. Deformed embryos in water birds and ducks Also bioaccumulated in mammals. TOXIC EFFECTS Acute, large dose result in death. Chronic exposure: In Humans: Selenosis- brittle hair, deformed nails, lost of sensation in extremities. In Aquatic organisms: Impaired reproduction in birds. TOXIC EFFECTS Numbers! Numbers! 10 mg/L of seawater, thought to cause fish dieoff in fresh water lake In San Francisco bay particulate material ranged from 0.5 to 2.0 ug Se per g dry weight, and 0.29 g/L in sea water. Teratogenetic effects Local Mytilus 2.7 ug/dry tissue. In humans, 1,270 μg/day caused selenosis. TOXIC EFFECTS The Institute of Medicine of the National Academy of Sciences has set a tolerable upper intake level (UL) for selenium at 400 ug/day FDA recommended DA is 70 ug/day. Dried Brazil nuts 544 ug/ounce Canned Tuna 63/ 3 ounces Asian Clam Potamocorbula amurensis 20ug/g dry weight TOXIC EFFECTS Our Colorado Lagoon Bivalves ~ 13 ug/g dry weight With conversion factor of approximately 1:9… A pound of bivalves contains 585 ug of selenium. MOLECULAR INTERACTION Selenium Metabolism Pathway The toxicity of the selenium is mainly focused on the organic form: CySeH, selenocystine (CySeSeCy) a , and the inorganic forms :Selenite and selenate Selenite Selenite is metabolized by glutathione (GSH) or glutathione reductase to hydrogen selenide (H2Se) via selenodiglutathione and glutathionyselenol intermediates. Hydrogen Selenide (H2Se) is enzymatically methylated by S-adenosylmethionine (SAM) as methyl donor, resulting in the formation of mono-, di-, and tri-methylated derivatives. The trimethylselenomium ion (3 methyl selenium) is excreted in urine, dimethyl selenide (2 methyl selenium) is a volatile product and is exhaled via the lung. These methylated compounds are less toxic than the parent compound, thus the methylation process is regarded as detoxification mechanism of selenium. CySeH, selenocystine CySeH, selenocystine (CySeSeCy) After oral administration of CySeSeCy, selenocysteineglutathione selenenyl sulfide (CySeSG), selenocysteine– containing metabolite, is first produced by the reaction between CySeSeCy and GSH in the small intestine. In the second step, CySeSG is nonenzymatically reduced to CySeH by excess GSH in the liver. It was also recognized that CySeSG was enzymatically reduced to CySeH by glutathione reductase in the presence of NADPH. In the third step, CySeH is de composed by selenocysteine β-lyase to H2Se. Then H2Se undergoes the similar process described above. Mechanism METABOLISM AND BREAKDOWN Methylation, and extracted via urine, feces, expired air and sweat. Shown in lab animals that increased dietary intake resulted in increased excretion. LITERATURE CITED Literature Cited Katsuhiko Nakamuro, Tomofumi Okuno, and Tatsuya Hasegawa. 2000. Metabolism of Selenoamino Acids and Contribution of Selenium Methylation to Their Toxicity. Journal of Health Science 46(6)418-421.