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Selenium (pronounced /sɨˈliːniəm/ sə-LEE-nee-əm) is a chemical element with the atomic number 34, represented by the chemical symbol Se, an atomic mass of 78.96. It is a nonmetal, chemically related to sulfur and tellurium, and rarely occurs in its elemental state in nature.

Isolated selenium occurs in several different forms, the most stable of which is a dense purplish-gray semi-metal (semiconductor) form that is structurally a trigonal polymer chain. It conducts electricity better in the light than in the dark, and is used in photocells (see section Allotropes below). Selenium also exists in many non-conductive forms: a black glass-like allotrope, as well as several red crystalline forms built of eight-membered ring molecules, like its lighter cousin sulfur.

Selenium is found in economic quantities in sulfide ores such as pyrite, partially replacing the sulfur in the ore matrix. Minerals that are selenide or selenate compounds are also known, but are rare. The chief commercial uses for selenium today are in glassmaking and in chemicals and pigments. Uses in electronics, once important, have been supplanted by silicon semiconductor devices.

Selenium salts are toxic in large amounts, but trace amounts of the element are necessary for cellular function in most, if not all, animals, forming the active center of the enzymes glutathione peroxidase and thioredoxin reductase (which indirectly reduce certain oxidized molecules in animals and some plants) and three known deiodinase enzymes (which convert one thyroid hormone to another). Selenium requirements in plants differ by species, with some plants apparently requiring none.[3]

History and global demand

Selenium (Greek σελήνη selene meaning "Moon") was discovered in 1817 by Jöns Jakob Berzelius,[4] who found the element associated with tellurium (named for the Earth). It was discovered as a byproduct of sulfuric acid production.

It came to medical notice later because of its toxicity to humans working in industry. It was also recognized as an important veterinary toxin. In 1954 the first hints of specific biological functions of selenium were discovered in microorganisms. Its essentiality for mammalian life was discovered in 1957. In the 1970s it was shown to be present in two independent sets of enzymes. This was followed by the discovery of selenocysteine in proteins. During the 1980s, it was shown that selenocystine was encoded by the codon TGA. The recoding mechanism was worked out first in bacteria and then in mammals (see SECIS element).

Growth in selenium consumption was historically driven by steady development of new uses, including applications in rubber compounding, steel alloying, and selenium rectifiers. Selenium is also an essential material in the drums of laser printers and copiers. By 1970, selenium in rectifiers had largely been replaced by silicon, but its use as a photoconductor in plain-paper copiers had become its leading application. During the 1980s, the photoconductor application declined (although it was still a large end-use) as more and more copiers using organic photoconductors were produced. Currently, the largest use of selenium worldwide is in glass manufacturing, followed by uses in chemicals and pigments. Electronics use, despite a number of continued applications, continues to decline.[5]

In the late 1990s, the use of selenium (usually with bismuth) as an additive to plumbing brasses to meet no-lead environmental standards became important. At present, total world selenium production continues to increase modestly.
Native selenium

Selenium occurs naturally in a number of inorganic forms, including selenide, selenate, and selenite. In soils, selenium most often occurs in soluble forms such as selenate (analogous to sulfate), which are leached into rivers very easily by runoff.

Selenium has a biological role, and it is found in organic compounds such as dimethyl selenide, selenomethionine, selenocysteine and methylselenocysteine. In these compounds selenium plays a role analogous to that of sulfur.

Selenium is most commonly produced from selenide in many sulfide ores, such as those of copper, silver, or lead. It is obtained as a byproduct of the processing of these ores, from the anode mud of copper refineries and the mud from the lead chambers of sulfuric acid plants. These muds can be processed by a number of means to obtain free selenium.

Natural sources of selenium include certain selenium-rich soils, and selenium that has been bioconcentrated by certain plants. Anthropogenic sources of selenium include coal burning and the mining and smelting of sulfide ores.[6]

See also Selenide minerals.
Production and allotropic forms
Structure of trigonal selenium

Native selenium is a rare mineral, which does not usually form good crystals, but when it does they are steep rhombohedrons or tiny acicular (hair-like) crystals.[7] Isolation of selenium is often complicated by the presence of other compounds and elements.

Most elemental selenium comes as a byproduct of refining copper or producing sulfuric acid.[8][9]

Industrial production of selenium often involves the extraction of selenium dioxide from residues obtained during the purification of copper. Commonly, production begins by oxidation with sodium carbonate to produce selenium dioxide. The selenium dioxide is then mixed with water and the solution is acidified to form selenous acid (oxidation step). Selenous acid is bubbled with sulfur dioxide (reduction step) to give elemental selenium.

Elemental selenium produced in chemical reactions invariably appears as the amorphous red form: an insoluble, brick-red powder. When this form is rapidly melted, it forms the black, vitreous form, which is usually sold industrially as beads. The most thermodynamically stable and dense form of selenium is the electrically conductive gray (trigonal) form, which is composed of long helical chains of selenium atoms (see figure).[10] The conductivity of this form is notably light sensitive. Selenium also exists in three different deep-red crystalline monoclinic forms, which are composed of Se8 molecules, similar to many allotropes of sulfur.[11][12] Unlike sulfur, however, selenium does not exhibit the unusual changes in viscosity that sulfur undergoes when gradually heated.[12]
Main article: isotopes of selenium

Selenium has six naturally occurring isotopes, five of which are stable: 74Se, 76Se, 77Se, 78Se, and 80Se. The last three also occur as fission products, along with 79Se which has a half-life of 295,000 years. The final naturally occurring isotope, 82Se, has a very long half-life (~1020 yr, decaying via double beta decay to 82Kr), which, for practical purposes, can be considered to be stable. Twenty-three other unstable isotopes have been characterized.

See also Selenium-79 for more information on recent changes in the measured half-life of this long-lived fission product, important for the dose calculations performed in the frame of the geological disposal of long-lived radioactive waste.
Health effects and nutrition

Although it is toxic in large doses, selenium is an essential micronutrient for animals. In plants, it occurs as a bystander mineral, sometimes in toxic proportions in forage (some plants may accumulate selenium as a defense against being eaten by animals, but other plants such as locoweed require selenium, and their growth indicates the presence of selenium in soil).[3] It is a component of the unusual amino acids selenocysteine and selenomethionine. In humans, selenium is a trace element nutrient which functions as cofactor for reduction of antioxidant enzymes such as glutathione peroxidases[13] and certain forms of thioredoxin reductase found in animals and some plants (this enzyme occurs in all living organisms, but not all forms of it in plants require selenium).

Glutathione peroxidase (GSH-Px) catalyzes certain reactions that remove reactive oxygen species such as peroxide:

2 GSH + H2O2----GSH-Px → GSSG + 2 H2O

Selenium also plays a role in the functioning of the thyroid gland, by participating as a cofactor for the three known thyroid hormone deiodinases.[14] It may inhibit Hashimotos's disease, in which the body's own thyroid cells are attacked as alien. A reduction of 21% on TPO antibodies was reported with the dietary intake of 0.2 mg of selenium.[15]

Dietary selenium comes from nuts, cereals, meat, fish, and eggs. Brazil nuts are the richest ordinary dietary source (though this is soil-dependent, since the Brazil nut does not require high levels of the element for its own needs). In descending order of concentration, high levels are also found in kidney, tuna, crab, and lobster.[16][17]
Indicator plants

Certain species of plants are considered indicators of high selenium content of the soil, since they require high levels of selenium in order to thrive. The main selenium indicator plants are Astragalus species (including some locoweeds), prince's plume (Stanleya sp.), woody asters (Xylorhiza sp.), and false goldenweed (Oonopsis sp.)[18]

Although selenium is an essential trace element, it is toxic if taken in excess. Exceeding the Tolerable Upper Intake Level of 400 micrograms per day can lead to selenosis.[19] This 400 microgram Tolerable Upper Intake Level is primarily based on a 1986 study of five Chinese patients who exhibited overt signs of selenosis and a follow up study on the same five people in 1992.[20] The 1992 study actually found the maximum safe dietary Se intake to be approximately 800 micrograms per day (15 micrograms per kilogram body weight), but suggested 400 micrograms per day to not only avoid toxicity, but also to avoid creating an imbalance of nutrients in the diet and to account for data from other countries.[21] The Chinese people that suffered from selenium toxicity ingested selenium by eating corn grown in extremely selenium-rich stony coal (carbonaceous shale). This coal was shown to have selenium content as high as 9.1%, the highest concentration in coal ever recorded in literature.[22] A dose of selenium as small as 5 mg per day can be lethal for many humans.[23]
Reference ranges for blood tests, showing selenium in purple in center

Symptoms of selenosis include a garlic odor on the breath, gastrointestinal disorders, hair loss, sloughing of nails, fatigue, irritability, and neurological damage. Extreme cases of selenosis can result in cirrhosis of the liver, pulmonary edema, and death.[24] Elemental selenium and most metallic selenides have relatively low toxicities because of their low bioavailability. By contrast, selenates and selenites are very toxic, having an oxidant mode of action similar to that of arsenic trioxide. The chronic toxic dose of selenite for human beings is about 2400 to 3000 micrograms of selenium per day for a long time.[25] Hydrogen selenide is an extremely toxic, corrosive gas.[26] Selenium also occurs in organic compounds such as dimethyl selenide, selenomethionine, selenocysteine and methylselenocysteine, all of which have high bioavailability and are toxic in large doses. Nano-size selenium has equal efficacy, but much lower toxicity.[27]

On April 19, 2009, twenty-one polo ponies began to die shortly before a match in the United States Polo Open. Three days later, a pharmacy released a statement explaining that the horses had received an incorrect dose of one of the ingredients used in a vitamin compound, with which the horses had been injected. Such vitamin injections are common to promote recovery after a match. The pharmacy did not initially release the name of the specific ingredient due to ongoing law-enforcement and other investigations. Analysis of inorganic compounds of the vitamin supplement indicated that selenium concentrations were ten to fifteen times higher than normal in the horses' blood samples and 15 to 20 times higher than normal in their liver samples. It was later confirmed that selenium was the ingredient in question.[28]

Selenium poisoning of water systems may result whenever new agricultural runoff courses through normally dry undeveloped lands. This process leaches natural soluble selenium compounds (such as selenates) into the water, which may then be concentrated in new "wetlands" as the water evaporates. High selenium levels produced in this fashion have been found to have caused certain congenital disorders in wetland birds.[29]
Main article: selenium deficiency

Selenium deficiency is relatively rare in healthy, well-nourished individuals. It can occur in patients with severely compromised intestinal function, those undergoing total parenteral nutrition, and also[30] on advanced-aged people (over 90). Also, people dependent on food grown from selenium-deficient soil are also at risk. However, although New Zealand has low levels of selenium in its soil, adverse health effects have not been detected.[31]

Selenium deficiency may only occur when a low selenium status is linked with an additional stress such as chemical exposure or increased oxidant stress due to vitamin E deficiency.[32]

There are interactions between selenium and other nutrient such as iodine and vitamin E. The interaction is observed in the etiology of many deficiency diseases in animals and pure selenium deficiency is in fact rare. The effect of selenium deficiency on health remains uncertain, particularly in relation to Kashin-Beck disease.[33]
Controversial health effects


Several studies have suggested a possible link between cancer and selenium deficiency.[34][35][36][37] One study, known as the NPC, was conducted to test the effect of selenium supplementation on the recurrence of skin cancers on selenium-deficient men. It did not demonstrate a reduced rate of recurrence of skin cancers, but did show a reduced occurrence of total cancers, although without a statistically significant change in overall mortality.[38] The preventative effect observed in the NPC was greatest in those with the lowest baseline selenium levels.[39] In 2009 the 5.5 year SELECT study reported that selenium and vitamin E supplementation, both alone and together, did not significantly reduce the incidence of prostate cancer in 35,000 men who "generally were replete in selenium at baseline".[39] The SELECT trial found that vitamin E did not reduce prostate cancer as it had in the Alpha-Tocopherol, Beta Carotene (ATBC) study, but the ATBC had a large percentage of smokers while the SELECT trial did not.[39]. There was a slight trend toward more prostate cancer in the SELECT trial, but in the vitamin E only arm of the trial, where no selenium was given.

Dietary selenium prevents chemically induced carcinogenesis in many rodent studies.[40] It has been proposed that selenium may help prevent cancer by acting as an antioxidant or by enhancing immune activity. Not all studies agree on the cancer-fighting effects of selenium. One study of naturally occurring levels of selenium in over 60,000 participants did not show a significant correlation between those levels and cancer.[41] The SU.VI.MAX study[42] concluded that low-dose supplementation (with 120 mg of ascorbic acid, 30 mg of vitamin E, 6 mg of beta carotene, 100 µg of selenium, and 20 mg of zinc) resulted in a 30% reduction in the incidence of cancer and a 37% reduction in all-cause mortality in males, but did not get a significant result for females.[43] However, there is evidence that selenium can help chemotherapy treatment by enhancing the efficacy of the treatment, reducing the toxicity of chemotherapeutic drugs, and preventing the body's resistance to the drugs.[44] Studies of cancer cells in vitro showed that chemotherapeutic drugs, such as Taxol and Adriamycin, were more toxic to strains of cancer cells grown in culture when selenium was added.[45][46]

In March 2009, Vitamin E (400 IU) and selenium (200 micrograms) supplements were reported to affect gene expression and can act as a tumor suppressor.[47] Eric Klein, MD from the Glickman Urological and Kidney Institute in Ohio said the new study “lend credence to the previous evidence that selenium and vitamin E might be active as cancer preventatives”.[48] In an attempt to rationalize the differences between epidemiological and in vitro studies and randomized trials like SELECT, Klein said that randomized controlled trials “do not always validate what we believe biology indicates and that our model systems are imperfect measures of clinical outcomes in the real world”.[48]


Some research has indicated a geographical link between regions of selenium-deficient soils and peak incidences of HIV/AIDS infection. For example, much of sub-Saharan Africa is low in selenium. However, Senegal is not, and also has a significantly lower level of AIDS infection than the rest of the continent. AIDS appears to involve a slow and progressive decline in levels of selenium in the body. Whether this decline in selenium levels is a direct result of the replication of HIV[49] or related more generally to the overall malabsorption of nutrients by AIDS patients remains debated.

Low selenium levels in AIDS patients have been directly correlated with decreased immune cell count and increased disease progression and risk of death.[50] Selenium normally acts as an antioxidant, so low levels of it may increase oxidative stress on the immune system leading to more rapid decline of the immune system. Others have argued that T-cell associated genes encode selenoproteins similar to human glutathione peroxidase. Depleted selenium levels in turn lead to a decline in CD4 helper T-cells, further weakening the immune system.[51]

Regardless of the cause of depleted selenium levels in AIDS patients, studies have shown that selenium deficiency does strongly correlate with the progression of the disease and the risk of death.[52][53][54]


Some research has suggested that selenium supplementation, along with other nutrients, can help prevent the recurrence of tuberculosis.[55]


A well-controlled study showed that selenium intake is positively correlated with the risk of developing type 2 diabetes. Because high serum selenium levels are positively associated with the prevalence of diabetes, and because selenium deficiency is rare, supplementation is not recommended in well-nourished populations such as the U.S.[56]


Experimental findings have demonstrated a protective effect of selenium on methylmercury toxicity, but epidemiological studies have been inconclusive in linking selenium to protection against the adverse effects of methylmercury.[57]
Non-biologic applications


Selenium is a catalyst in many chemical reactions and is widely used in various industrial and laboratory syntheses, especially organoselenium chemistry. It is also widely used in structure determination of proteins and nucleic acids by X-ray crystallography (incorporation of one or more Se atoms helps with MAD and SAD phasing.)

Manufacturing and materials use

The largest use of selenium worldwide is in glass and ceramic manufacturing, where it is used to give a red color to glasses, enamels and glazes as well as to remove color from glass by counteracting the green tint imparted by ferrous impurities.

Selenium is used with bismuth in brasses to replace more toxic lead. It is also used to improve abrasion resistance in vulcanized rubbers.


Because of its photovoltaic and photoconductive properties, selenium is used in photocopying, photocells, light meters and solar cells. It was once widely used in rectifiers. These uses have mostly been replaced by silicon-based devices, or are in the process of being replaced. The most notable exception is in power DC surge protection, where the superior energy capabilities of selenium suppressors make them more desirable than metal oxide varistors.

Sheets of amorphous selenium convert x-ray images to patterns of charge in xeroradiography and in solid-state, flat-panel x-ray cameras.


Selenium is used in the toning of photographic prints, and it is sold as a toner by numerous photographic manufacturers including Kodak and Fotospeed. Its use intensifies and extends the tonal range of black and white photographic images as well as improving the permanence of prints.

Early photographic light meters used selenium but this application is now obsolete.
Biologic applications

Medical use

The substance loosely called selenium sulfide (approximate formula SeS2) is the active ingredient in some anti-dandruff shampoos.[58] The selenium compound kills the scalp fungus Malassezia, which causes shedding of dry skin fragments. The ingredient is also used in body lotions to treat Tinea versicolor due to infection by a different species of Malassezia fungus.[59]


Selenium is used widely in vitamin preparations and other dietary supplements, in small doses (typically 50 to 200 micrograms per day for adult humans). Some livestock feeds are fortified with selenium as well.
Detection in biological fluids

Selenium may be measured in blood, plasma, serum or urine to monitor excessive environmental or occupational exposure, confirm a diagnosis of poisoning in hospitalized victims or to assist in a forensic investigation in a case of fatal overdosage. Some analytical techniques are capable of distinguishing organic from inorganic forms of the element. Both organic and inorganic forms of selenium are largely converted to monosaccharide conjugates (selenosugars) in the body prior to being eliminated in the urine. Cancer patients receiving daily oral doses of selenothionine may achieve very high plasma and urine selenium concentrations.[60]
Evolution in biology
Main article: Evolution of dietary antioxidants

Over three billion years ago, blue-green algae were the most primitive oxygenic photosynthetic organisms and are ancestors of multicellular eukaryotic algae.[61] Algae that contain the highest amount of antioxidant selenium, iodide, and peroxidase enzymes were the first living cells to produce poisonous oxygen in the atmosphere. Venturi et al. suggested that algal cells required a protective antioxidant action, in which selenium and iodides, through peroxidase enzymes, have had this specific role.[61][62] Selenium, which acts synergistically with iodine,[63] is a primitive mineral antioxidant, greatly present in the sea and prokaryotic cells, where it is an essential component of the family of glutathione peroxidase antioxidant enzymes (GSH-Px); seaweeds accumulate high quantity of selenium and iodine.[61] In 2008, Küpper et al. showed that iodide also scavenges reactive oxygen species (ROS) in algae, and that its biological role is that of an inorganic antioxidant, the first to be described in a living system, active also in an in vitro assay with the blood cells of today’s humans."[64]

From about three billion years ago, prokaryotic selenoprotein families drive selenocysteine evolution. Selenium is incorporated into several prokaryotic selenoprotein families in bacteria, archaea and eukaryotes as selenocysteine,[65] where selenoprotein peroxiredoxins protect bacterial and eukaryotic cells against oxidative damage. Selenoprotein families of GSH-Px and deiodinase of eukaryotic cells seem to have a bacterial phylogenetic origin. The selenocysteine-containing form occurred in green algae, diatoms, sea urchin, fish and chicken, too. One family of selenium-containing molecules as glutathione peroxidases repairs damaged cell membranes, while another (glutathione S-transferases) repairs damaged DNA and prevents mutations.[66]

At about 500 Mya, plants and animals began to transfer from the sea to rivers and land, the environmental deficiency of marine mineral antioxidants (as selenium, iodine, etc.) was a challenge to the evolution of terrestrial life.[61] Trace elements involved in GSH-Px and superoxide dismutase enzymes activities, i.e. selenium, vanadium, magnesium, copper, and zinc, may have been lacking in some terrestrial mineral-deficient areas.[65] Marine organisms retained and sometimes expanded their seleno-proteomes, whereas the seleno-proteomes of some terrestrial organisms were reduced or completely lost. These findings suggest that, with the exception of vertebrates, aquatic life supports selenium utilization, whereas terrestrial habitats lead to reduced use of this trace element.[67] Marine fishes and vertebrate thyroid glands have the highest concentration of selenium and iodine. From about 500 Mya, freshwater and terrestrial plants slowly optimized the production of “new” endogenous antioxidants such as ascorbic acid (Vitamin C), polyphenols (including flavonoids), tocopherols, etc. A few of these appeared more recently, in the last 50–200 million years, in fruits and flowers of angiosperm plants. In fact, the angiosperms (the dominant type of plant today) and most of their antioxidant pigments evolved during the late Jurassic period.

The deiodinase isoenzymes constituted the second family of eukaryotic selenoproteins with identified enzyme function. Deiodinases are able to extract electrons from iodides, and iodides from iodothyronines; so, they are involved in thyroid-hormone regulation, participating in the protection of thyrocytes from damage by H2O2 produced for thyroid-hormone biosynthesis.[61][62] About 200 Mya, new selenoproteins were developed as mammalian GSH-Px enzymes.[68][69][70][71]

See also: Category:Selenium compounds and organoselenium chemistry
Chalcogen compounds

Selenium forms two oxides: selenium dioxide (SeO2) and selenium trioxide (SeO3). Selenium dioxide is formed by the reaction of elemental selenium with oxygen:[12]

Se8 + 8 O2 → 8 SeO2

It is a polymeric solid that forms monomeric SeO2 molecules in the gas phase. It dissolves in water to form selenous acid, H2SeO3. Selenous acid can also be made directly by oxidising elemental selenium with nitric acid:[72]

3 Se + 4 HNO3 → 3 H2SeO3 + 4 NO

Salts of selenous acid are called selenites. These include silver selenite (Ag2SeO3) and sodium selenite (Na2SeO3).

Hydrogen sulfide reacts with aqueous selenous acid to produce selenium disulfide:

H2SeO3 + 2 H2S → SeS2 + 3 H2O

Selenium disulfide consists of 8-membered rings of sulfur atoms with selenium replacing some of the sulfur atoms. It has an approximate composition of SeS2, with individual rings varying in composition, such as Se4S4 and Se2S6. It has various applications, including use in shampoo as an anti-dandruff agent, an inhibitor in polymer chemistry, a glass dye, and a reducing agent in fireworks.[72]

Unlike sulfur, which forms a stable trioxide, selenium trioxide is unstable and decomposes to the dioxide above 185 °C:[12][72]

2 SeO3 → 2 SeO2 + O2 (ΔH = −54 kJ/mol)

Selenium trioxide may be synthesized by dehydrating selenic acid, H2SeO4, which is itself produced by the oxidation of selenium dioxide with hydrogen peroxide:[73]

SeO2 + H2O2 → H2SeO4

Hot, concentrated selenic acid is capable of dissolving gold, forming gold(III) selenate.[74]
Halogen compounds

Selenium reacts with fluorine to form selenium hexafluoride:

Se8 + 24 F2 → 8 SeF6

Unlike its sulfur counterpart, sulfur hexafluoride, however, SeF6 is more reactive and is a toxic pulmonary irritant.[75] It can cause frostbite and severe irritation on contact with skin.[76]

Other selenium halides include SeF4, Se2Cl2, SeCl4, and Se2Br2. Selenium dichloride (SeCl2), an important reagent in the study of selenium chemistry, may be prepared in pure form by reacting elemental selenium with SO2Cl2 in THF solution.[77] Some of the selenium oxyhalides, such as SeOF2, are useful as nonaqueous solvents.[12]

Like oxygen and sulfur, selenium forms selenides with metals. For example, reaction with aluminum forms aluminum selenide:[12]

3 Se8 + 16 Al → 8 Al2Se3

Other selenides include mercury selenide (HgSe), lead selenide (PbSe), and zinc selenide (ZnSe). An important selenide is copper indium gallium selenide (Cu(Ga,In)Se2), a semiconductor.

Selenium does not react directly with hydrogen; so hydrogen selenide, the analogue of hydrogen sulfide and water, is prepared by first reacting selenium with a metal to produce a selenide, and then protonating the selenide anion with an acid to produce H2Se.[12]
Other compounds

Tetraselenium tetranitride, Se4N4, is an explosive orange compound analogous to S4N4.[12][78][79] It can be synthesized by the reaction of SeCl4 with [((CH3)3Si)2N]2Se in dichloromethane solution at −78 °C.[80]

Selenium reacts with cyanides to yield selenocyanates.[12] For example:

8 KCN + Se8 → 8 KSeCN

Selenium: its molecular biology and role in human health, Dolph L. Hatfield

Selenium in food and health, Conor Reilly

Chemical thermodynamics of selenium, Åke Olin, Nuclear Energy Agency

See also

* ACES (nutritional supplement)


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External links

* - Selenium
* National Institutes of Health page on Selenium
* Assay
* ATSDR - Toxicological Profile: Selenium
* Peter van der Krogt elements site

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