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.