SELENIUMSELENIUM

3 levels of biological activity:3 levels of biological activity:

1) Trace concentrations required for normal growth and development

2) Moderate concentrations can be stored

3) Elevated concentrations result in toxic effects

1) Trace concentrations required for normal growth and development

2) Moderate concentrations can be stored

3) Elevated concentrations result in toxic effects

CHEMICAL PROPERTIESCHEMICAL PROPERTIES Atomic number 34 Chemical symbol: Se Essential trace element

Component of glutathione peroxidase

4 oxidative states Elemental Se (0) Selenide(-2) Selenite (+4) Selenate (+6)

Inorganic forms: selenate, selenite (found in water) Organic forms: selenomethionine, selenocysteine(found

in veggies and cereal)

Atomic number 34 Chemical symbol: Se Essential trace element

Component of glutathione peroxidase

4 oxidative states Elemental Se (0) Selenide(-2) Selenite (+4) Selenate (+6)

Inorganic forms: selenate, selenite (found in water) Organic forms: selenomethionine, selenocysteine(found

in veggies and cereal)

PHYSICAL PROPERTIESPHYSICAL PROPERTIES

-Found in various forms ranging from a grey metallic to a reddish glassy appearance -Found in various rocks and minerals, coal, and oil-Melting point 494 K(221°C, 430°F)Boiling point 958 K(685°C, 1265°F)

-Found in various forms ranging from a grey metallic to a reddish glassy appearance -Found in various rocks and minerals, coal, and oil-Melting point 494 K(221°C, 430°F)Boiling point 958 K(685°C, 1265°F)

- Heavy metal Selenides(-2) and elemental Se = INSOLUBLE in water

-Inorganic alkali selenites(+4), and selenates (+6) = soluble in water

greater bioavailability

-selenites less soluble than selenates (both predominate in water)

- Heavy metal Selenides(-2) and elemental Se = INSOLUBLE in water

-Inorganic alkali selenites(+4), and selenates (+6) = soluble in water

greater bioavailability

-selenites less soluble than selenates (both predominate in water)

HISTORY, USES, andAPPLICATIONS

HISTORY, USES, andAPPLICATIONS

1817- Jons Jacob Berzelius- isolated and identified Se

Marco Polo- recorded first observation of toxicity “hoof rot”

Medical use: dietary supplement Applications:

manufacturing of ceramics, glass, pigments, semiconductors, and steel

Used in photography and pharmaceutical production

1817- Jons Jacob Berzelius- isolated and identified Se

Marco Polo- recorded first observation of toxicity “hoof rot”

Medical use: dietary supplement Applications:

manufacturing of ceramics, glass, pigments, semiconductors, and steel

Used in photography and pharmaceutical production

MODE OF ENTRYInto the Environment:

MODE OF ENTRYInto the Environment:

Water:-Through surface and subsurface draining-Wet and dry deposition from the atmosphere-Selenates and selenites predominate

Sea water :[Se]: low .04-.12µg/lGround, surface water: .06-400µg/l

Air:-Natural source: Volcanic gas-Combustion of fossil fuels and Coal- attaches to fly ash

-Also incineration of rubber, municipal waste and paper.

Water:-Through surface and subsurface draining-Wet and dry deposition from the atmosphere-Selenates and selenites predominate

Sea water :[Se]: low .04-.12µg/lGround, surface water: .06-400µg/l

Air:-Natural source: Volcanic gas-Combustion of fossil fuels and Coal- attaches to fly ash

-Also incineration of rubber, municipal waste and paper.

Soil:

-weathering and leaching of parent bedrock

-Se in sediment can be cycled into food chain for decades from the soil

Industrial and agricultural activity has hastened release of Se from geological stores making it available to fish and wildlife

Soil:

-weathering and leaching of parent bedrock

-Se in sediment can be cycled into food chain for decades from the soil

Industrial and agricultural activity has hastened release of Se from geological stores making it available to fish and wildlife

MODE OF ENTRYinto the OrganismMODE OF ENTRYinto the Organism

PLANTS:-Absorb via high affinity sulfate permeases.

Do not actively absorb selenites

-Preferentially accumulate selenates (less bound to soil particles)

ANIMALS:-In vitro studies show organic selenium (selenomethionine) more readily accumulated in organisms vs. selenate and selenite

PLANTS:-Absorb via high affinity sulfate permeases.

Do not actively absorb selenites

-Preferentially accumulate selenates (less bound to soil particles)

ANIMALS:-In vitro studies show organic selenium (selenomethionine) more readily accumulated in organisms vs. selenate and selenite

MODE OF ENTRYinto Organism

MODE OF ENTRYinto Organism

-Uptake from Diet or from water

-Accumulated in the food chain

-Water-soluble Se by fish and wildlife through: -gills-epidermis-gut

-Dietary uptake- dominant pathway

Sandholm et al. (1973)-first to determine Se accumulation from dietary sources greater than accumulation from the water

Fish: Planktonic and detrital food pathways: 770 and 510-1395X waterborne exposure route

Se has surfaced as an element of primary concern due to its ability to bioaccumulate within base of food webs

-Uptake from Diet or from water

-Accumulated in the food chain

-Water-soluble Se by fish and wildlife through: -gills-epidermis-gut

-Dietary uptake- dominant pathway

Sandholm et al. (1973)-first to determine Se accumulation from dietary sources greater than accumulation from the water

Fish: Planktonic and detrital food pathways: 770 and 510-1395X waterborne exposure route

Se has surfaced as an element of primary concern due to its ability to bioaccumulate within base of food webs

MOLECULAR MODE OF TOXIC INTERACTION

MOLECULAR MODE OF TOXIC INTERACTION

Toxicity occurs from a flaw in protein synthesis.

Recall that sulfur is a key component of proteins. Sulfur disulfide bonds required for proper folding of protein

(tertiary structure) Disulfide bonds are between strands of amino acids Structure=Function

Cells do not discriminate well between Se and Sulfur during protein synthesis

Toxicity occurs from a flaw in protein synthesis.

Recall that sulfur is a key component of proteins. Sulfur disulfide bonds required for proper folding of protein

(tertiary structure) Disulfide bonds are between strands of amino acids Structure=Function

Cells do not discriminate well between Se and Sulfur during protein synthesis

MOLECULAR MODE OF TOXIC INTERACTION 2

MOLECULAR MODE OF TOXIC INTERACTION 2

Se is substituted for sulfur

formation of triselenium linkage (SE-SE-SE) or a selenotrisulfide linkage (S-Se-S)

-Prevent the formation of necessary disulfide bonds

-Results in distorted, dysfunctional enzymes and proteins

impairs normal cellular biochemistry

Se is substituted for sulfur

formation of triselenium linkage (SE-SE-SE) or a selenotrisulfide linkage (S-Se-S)

-Prevent the formation of necessary disulfide bonds

-Results in distorted, dysfunctional enzymes and proteins

impairs normal cellular biochemistry

TOXICITYTOXICITY

Teratogenic biomarker of Se toxicity in birds and fish at

embryo/larval stage Acute- fatal: hypertension, respiratory

depression Chronic: change in hair, nails, garlic odor on

breath (expiration of dimethyl selenide) Selenite more toxic than selenate (fish

selenomethionine more toxic)

Teratogenic biomarker of Se toxicity in birds and fish at

embryo/larval stage Acute- fatal: hypertension, respiratory

depression Chronic: change in hair, nails, garlic odor on

breath (expiration of dimethyl selenide) Selenite more toxic than selenate (fish

selenomethionine more toxic)

TOXICITYTOXICITY

-[Se] >2-5µg of dissolved Se/L water may cause bioaccumulation in food chain with potential to cause adverse effects

-Greatest increase in Se occurs at lower end of the food chain (between algae and water)

-[Se] >2-5µg of dissolved Se/L water may cause bioaccumulation in food chain with potential to cause adverse effects

-Greatest increase in Se occurs at lower end of the food chain (between algae and water)

Study on marine fish showed:

.5µg sodium selenite/kg body weight injected: half lives equaled

Liver 2.1 days Gills 2.1 days Skin 5.3 days

Inhalation of selenious acid:

excrete about 50%(mostly in urine) with a half life of 1.2 days

Study on marine fish showed:

.5µg sodium selenite/kg body weight injected: half lives equaled

Liver 2.1 days Gills 2.1 days Skin 5.3 days

Inhalation of selenious acid:

excrete about 50%(mostly in urine) with a half life of 1.2 days

Fish: reduced growth or survival 3µg/g

G.pseudolimnaeus LC50=1180µg/l

G.lacustris LC50=3054µg/l

H. azteca LC50=2480µg/l

D.pulex LC50= 8111-10123µg/l

D.magna LC50= 570-5300µg/l

Fish: reduced growth or survival 3µg/g

G.pseudolimnaeus LC50=1180µg/l

G.lacustris LC50=3054µg/l

H. azteca LC50=2480µg/l

D.pulex LC50= 8111-10123µg/l

D.magna LC50= 570-5300µg/l

ELIMINATIONELIMINATION

1) Reduction of selenite by cellular glutathione to selenide

2) Incorporation of selenide into selenoproteins(glutathione peroxidase, type I 5’iodothyronine deiodinase) via selenocysteine

3) Methylation of selenide to metabolites(dimethyl diselenide, dimethyl selenide (excreted into expired air), trimethylselenonium)

eliminated through urine (mostly)

1) Reduction of selenite by cellular glutathione to selenide

2) Incorporation of selenide into selenoproteins(glutathione peroxidase, type I 5’iodothyronine deiodinase) via selenocysteine

3) Methylation of selenide to metabolites(dimethyl diselenide, dimethyl selenide (excreted into expired air), trimethylselenonium)

eliminated through urine (mostly)

Belews LakeBelews Lake

Most extensive and prolonged case of Se poisoning in fresh water fish

19 out of 20 species of fish were eliminated (Mosquito fish survived)

Eggs-primary point of impact Se consumed in diet of adult fish deposited in eggs Metabolized by larval fish after hatching

1986 stopped draining into lake, 1996 still saw developmental abnormalities in young fish

Most extensive and prolonged case of Se poisoning in fresh water fish

19 out of 20 species of fish were eliminated (Mosquito fish survived)

Eggs-primary point of impact Se consumed in diet of adult fish deposited in eggs Metabolized by larval fish after hatching

1986 stopped draining into lake, 1996 still saw developmental abnormalities in young fish

ReferencesReferences

Barceloux, Donald G. Selenium. Clinical Toxicology 37(2) (1999):145-172.

Brix, Kevin V., Henderson, Douglas G., Adams, William J., Reash, Robin J., Carlton, Richard G., McIntyre, Dennis O. Acute Toxicity of Sodium Selenate to Two Daphnids and Three Amphipods. 2000:142-149.

Hamilton, Steven J., Review of selenium toxicity in the aquatic food chain. Science of the Total Environment 326 (2004):1-31.

Hoang, Tham C., Klaine, Stephen J. Characterizing the toxicity of pulsed selenium exposure to Daphnia magna. Chemosphere 71(2008) 429-439.

Lemly, A. Dennis. Symptoms and implications of selenium toxicity in fish: the Belews Lake case example. Aquatic Toxicology 57(2002): 39-49.

Barceloux, Donald G. Selenium. Clinical Toxicology 37(2) (1999):145-172.

Brix, Kevin V., Henderson, Douglas G., Adams, William J., Reash, Robin J., Carlton, Richard G., McIntyre, Dennis O. Acute Toxicity of Sodium Selenate to Two Daphnids and Three Amphipods. 2000:142-149.

Hamilton, Steven J., Review of selenium toxicity in the aquatic food chain. Science of the Total Environment 326 (2004):1-31.

Hoang, Tham C., Klaine, Stephen J. Characterizing the toxicity of pulsed selenium exposure to Daphnia magna. Chemosphere 71(2008) 429-439.

Lemly, A. Dennis. Symptoms and implications of selenium toxicity in fish: the Belews Lake case example. Aquatic Toxicology 57(2002): 39-49.