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Selenium is a trace element that is essential in small amounts, but can be toxic in larger amounts. Humans and animals require selenium for the function of a number of selenium-dependent enzymes, also known as selenoproteins. During selenoprotein synthesis, selenocysteine is incorporated into a very specific location in the amino acid sequence in order to form a functional protein. Unlike animals, plants do not appear to require selenium for survival. However, when selenium is present in the soil, plants incorporate it non-specifically into compounds that usually contain sulfur (1, 2).
Selenium may play a role in the prevention and/or treatment of the following health conditions:
Cervical dysplasia
Colorectal cancer
Esophageal cancer
Infertility (male)
Kashin-Beck's disease
Keshan's disease
Multiple sclerosis
Ovarian cysts
Parkinson's disease
Periodontal disease
Rheumatoid arthritis
Senile cataracts
SIDS (sudden infant death syndrome)
Stomach cancer


At least 11 selenoproteins have been characterized, and there is evidence that additional selenoproteins exist.
Glutathione peroxidases
Four selenium-containing glutathione peroxidases (GPx) have been identified: cellular or classical GPx, plasma or extracellular GPx, phospholipid hydroperoxide GPx, and gastrointestinal GPx (3). Although each GPx is a distinct selenoprotein, they are all antioxidant enzymes that reduce potentially damaging reactive oxygen species (ROS), such as hydrogen peroxide and lipid hydroperoxides, to harmless products like water and alcohols by coupling their reduction with the oxidation of glutathione (diagram). Sperm mitochondrial capsule selenoprotein, an antioxidant enzyme that protects developing sperm from oxidative damage and later forms a structural protein required by mature sperm, was once thought to be a distinct selenoprotein, but now appears to be phospholipid hydroperoxide GPx (4).
Thioredoxin reductase
In conjunction with the compound thioredoxin, thioredoxin reductase participates in the regeneration of several antioxidant systems, possibly including vitamin C. Maintenance of thioredoxin in a reduced form by thioredoxin reductase is important for regulating cell growth and viability (3, 5).
Iodothyronine deiodinases (thyroid hormone deiodinases)
The thyroid gland releases very small amounts of biologically active thyroid hormone (triiodothyronine or T3) and larger amounts of an inactive form of thyroid hormone (thyroxine or T4) into the circulation. Most of the biologically active T3 in the circulation and inside cells is created by the removal of one iodine atom from T4 in a reaction catalyzed by selenium-dependent iodothyronine deiodinase enzymes. Through their actions on T3, T4, and other thyroid hormone metabolites, three different selenium-dependent iodothyronine deiodinases (types I, II, and III) can both activate and inactivate thyroid hormone, making selenium an essential element for normal development, growth, and metabolism through the regulation of thyroid hormones (3, 6).
Selenoprotein P
Selenoprotein P is found in plasma and also associated with vascular endothelial cells (cells that line the inner walls of blood vessels). Although the function of selenoprotein P has not been clearly delineated, it has been suggested to function as a transport protein, as well as an antioxidant capable of protecting endothelial cells from damage by a reactive nitrogen species (RNS) called peroxynitrite
Selenoprotein W
Selenoprotein W is found in muscle. Although its function is presently unknown, it is thought to play a role in muscle metabolism (3).
Selenophosphate synthetase
Incorporation of selenocysteine into selenoproteins is directed by the genetic code and requires the enzyme selenophosphate synthetase. A selenoprotein itself, selenophosphate synthetase catalyzes the synthesis of monoselenium phosphate, a precursor of selenocysteine which is required for the synthesis of selenoproteins.

Nutrient interactions
Antioxidant nutrients
As an integral part of the glutathione peroxidases and thioredoxin reductase, selenium probably interacts with every nutrient that affects the pro-oxidant/antioxidant balance of the cell. Other minerals that are critical components of antioxidant enzymes include copper, zinc (as superoxide dismutase),  and iron (as catalase). Selenium as gluthathione peroxidase also appears to support the activity of vitamin E (a-tocopherol) in limiting the oxidation of lipids. Animal studies indicate that selenium and vitamin E tend to spare one another and that selenium can prevent some of the damage resulting from vitamin E deficiency in models of oxidative stress (1). Thioredoxin reductase also maintains the antioxidant function of vitamin C by catalyzing its regeneration (5).
Selenium deficiency may exacerbate the effects of iodine deficiency. Iodine is essential for the synthesis of thyroid hormone, but the selenoenzymes, iodothyronine deiodinases, are also required for the conversion of thyroxine (T4) to the biologically active thyroid hormone triiodothyronine (T3). Selenium supplementation in a small group of elderly individuals decreased plasma T4, indicating increased deiodinase activity with increased conversion to T3 (2).
Insufficient selenium intake results in decreased activity of the glutathione peroxidases. Individuals at increased risk of selenium deficiency
Clinical selenium deficiency has been observed in chronically ill patients who were receiving total parenteral nutrition (TPN) without added selenium for prolonged periods of time. Muscular weakness, muscle wasting, and cardiomyopathy (inflammation and damage to the heart muscle) have been observed in these patients. TPN solutions are now supplemented with selenium to prevent such problems. People who have had a large portion of the small intestine surgically removed or those with severe gastrointestinal problems, such as Crohn's disease, are also at risk for selenium deficiency due to impaired absorption. Specialized medical diets used to treat metabolic disorders, such as phenylketonuria (PKU), are often low in selenium.
Both iron deficiency and copper deficiency appear to increase the risk of selenium deficiency.
Glucocorticoids are a widely-used family of anti-inflammatory drugs based on a prototype substance called cortisol. In the United States, cortisol-based anti-inflammatory drugs are available under 70 different brand names. Many of these medications are based on one of the three major cortisol subtypes that consist of prednisolone, dexamethasone, and triamcinolone. All of these medications can reduce the body's supply of selenium.

Keshan disease
Keshan disease is a cardiomyopathy that affects young women and children in a selenium deficient region of China. The acute form of the disease is characterized by the sudden onset of cardiac insufficiency, while the chronic form results in moderate to severe heart enlargement with varying degrees of cardiac insufficiency. The incidence of Keshan disease is closely associated with very low dietary intakes of selenium and poor selenium nutritional status. Selenium supplementation has been found to protect people from developing Keshan disease but cannot reverse heart muscle damage once it occurs (1, 8). Despite the strong evidence that selenium deficiency is a fundamental factor in the etiology of Keshan's disease, the seasonal and annual variation in its occurrence suggests that an infectious agent is involved in addition to selenium deficiency. Coxsackievirus is one of the viruses that has been isolated from Keshan patients, and this virus has been found to be capable of causing an inflammation of the heart called myocarditis in selenium deficient mice.
Kashin-Beck Disease
Kashin-Beck disease is characterized by the degeneration of the articular cartilage between joints (osteoarthritis) and is associated with poor selenium status in areas of northern China, North Korea, and eastern Siberia. The disease affects children between the ages 5 and 13 years. Severe forms of the disease may result in joint deformities and dwarfism, due to degeneration of cartilage forming cells.

The Recommended Dietary Allowance (RDA)
The RDA was revised in 2000 by the Food and Nutrition Board (FNB) of the Institute of Medicine. The most recent RDA is based on the amount of dietary selenium required to maximize the activity of the antioxidant enzyme glutathione peroxidase in blood plasma (11).

Recommended Dietary Allowance (RDA) for Selenium
Life Stage  Age  Males (mcg/day)  Females (mcg/day)  
Infants  0-6 months  15 (AI)  15 (AI)  
Infants  7-12 months  20 (AI)  20 (AI)  
Children  1-3 years  20  20  
Children  4-8 years  30  30  
Children  9-13 years  40  40  
Adolescents  14-18 years  55  55  
Adults  19 years and older  55  55  
Pregnancy  all ages  -  60  
Breastfeeding  all ages  -  70

Immune function
Selenium deficiency has been associated with impaired function of the immune system. Moreover, selenium supplementation in individuals who are not overtly selenium deficient appears to stimulate the immune response. In two small studies, healthy (12, 13) and immunosuppressed individuals (14) supplemented with 200 mcg/day of selenium as sodium selenite for 8 weeks showed an enhanced immune cell response to foreign antigens compared with those taking a placebo. A considerable amount of basic research also indicates that selenium plays a role in regulating the expression of cell signaling molecules called cytokines, which orchestrate the immune response (15).
Viral infection
Selenium deficiency appears to enhance the virulence or progression of some viral infections. The increased oxidative stress resulting from selenium deficiency may induce mutations or changes in the expression of some viral genes. When selenium deficient mice are inoculated with a relatively harmless strain of coxsackievirus, mutations occur in the viral genome that result in a more virulent form of the virus, which causes an inflammation of the heart muscle known as myocarditis. Once mutated, this form of the virus also causes myocarditis in mice that are not selenium deficient, demonstrating that the increased virulence is due to a change in the virus rather than the effects of selenium deficiency on the host immune system. Recently, a study in mice that lack the cellular glutathione peroxidase enzyme (GPx-1 knockout mice) demonstrated that cellular glutathione peroxidase provides protection against myocarditis resulting from mutations in the genome of a previously benign virus. Selenium deficiency results in decreased activity of glutathione peroxidase, increasing the likelihood of mutations in the viral genome induced by oxidative damage. Coxsackievirus has been isolated from the blood of some sufferers of Keshan disease, suggesting that it may be a cofactor in the development of this cardiomyopathy associated with selenium deficiency in humans (9, 10).
Animal studies
There is a great deal of evidence indicating that selenium supplementation at high levels reduces the incidence of cancer in animals. More than two-thirds of over 100 published studies in 20 different animal models of spontaneous, viral, and chemically induced cancers found that selenium supplementation significantly reduced tumor incidence (16). The evidence indicates that the methylated forms of selenium are the active species against tumors, and these methylated selenium compounds are produced at the greatest amounts with excess selenium intakes. Selenium deficiency does not appear to make animals more susceptible to developing cancerous tumors (17).
Epidemiologic studies
Geographic studies have consistently shown a trend for populations who live in areas with low soil selenium and have relatively low selenium intakes to have higher cancer mortality rates. Results of epidemiologic studies of cancer incidence in groups with less variable selenium intakes have been less consistent, but also show a trend for individuals with lower selenium levels (blood and nails) to have a higher incidence of several different types of cancer. However, this trend is less pronounced in women. For example, a prospective study of more than 60,000 female nurses in the U.S. found no association between toenail selenium levels and total cancer risk (18). Chronic infection with viral hepatitis B or C significantly increases the risk of liver cancer. In a study of Taiwanese men with chronic viral hepatitis B or C infection, decreased plasma selenium concentrations were associated with an even greater risk of liver cancer (19). A case-control study within a prospective study of over 9,000 Finnish men and women examined serum selenium levels in 95 individuals subsequently diagnosed with lung cancer and 190 matched controls (20). Lower serum selenium levels were associated with an increased risk of lung cancer and the association was more pronounced in smokers. In this Finnish population, selenium levels were only about 60% of selenium levels common in generally observed in other western countries. Another case-control study within a prospective study of over 50,000 male health professionals in the U.S. found a significant inverse relationship between toenail selenium content and the risk prostate cancer in 181 men diagnosed with advanced prostate cancer and 181 matched controls (21). In individuals whose toenail selenium content was consistent with an average intake of 159 mcg/day the risk of advanced prostate cancer was only 35% of that of individuals with toenail selenium content consistent with an intake of 86 mcg/day. Within a prospective study of more than 9,000 Japanese-American men, a case-control study that examined 249 confirmed cases of prostate cancer and 249 matched controls found the risk of developing prostate cancer to be 50% less in men with serum selenium levels in the highest quartile compared those in the lowest quartile (22), while another case-control study found that men with prediagnostic plasma selenium levels in the lowest quartile were 4 to 5 times more likely to develop prostate cancer than those in the highest quartile (23). In contrast, one of the largest case-control studies to date found a significant inverse association between toenail selenium and the risk of colon cancer, but no associations between toenail selenium and the risk of breast cancer or prostate cancer (24).
Human intervention trials
Undernourished populations: An intervention trial undertaken among a general population of 130,471 individuals in five townships of Quidong, China, a high-risk area for viral hepatitis B infection and liver cancer, provided table salt enriched with sodium selenite to the population of one township (20,847 people), using the other four townships as controls. During an 8-year follow up period the average incidence of liver cancer was reduced by 35% in the selenium enriched population, while no reduction was found in the control populations. In a clinical trial in the same region, 226 individuals with evidence of chronic hepatitis B infection were supplemented with either 200 mcg of selenium in the form of a selenium-enriched yeast tablet or a placebo yeast tablet daily. During the four-year follow up period 7 out of 113 individuals on the placebo developed primary liver cancer, while none of the 113 subjects supplemented with selenium developed liver cancer (25).

Well-nourished populations: In the U.S., a double blind, placebo-controlled study of more than 1300 older adults with a history of nonmelanoma skin cancer found that supplementation with 200 mcg/day of selenium-enriched yeast for an average of 7.4 years was associated with a 51% decrease in prostate cancer incidence in men (26). The protective effect of selenium supplementation was greatest in those men with lower baseline plasma selenium and prostate-specific antigen (PSA) levels. Surprisingly, the most recent results from this study indicate that selenium supplementation increased the risk of one type of skin cancer (squamous cell carcinoma) by 25% (27). Although selenium supplementation shows promise for the prevention of prostate cancer, its effects on the risk for other types of cancer is unclear. In response to the need to confirm these findings, several large placebo-controlled trials designed to further investigate the role of selenium supplementation in prostate cancer prevention are presently under way (28, 29).

Mutat Res. 2004 Jul 13;551(1-2):181-97.
Mechanisms of mammary cancer chemoprevention by organoselenium compounds.
El-Bayoumy K, Sinha R.
Institute for Cancer Prevention, American Health Foundation Cancer Center, 1 Dana Road, Valhalla, NY 10595, USA.

Cardiovascular diseases

Theoretically, optimizing selenoenzyme activity could decrease the risk of cardiovascular diseases by decreasing lipid peroxidation and influencing the metabolism of cell signaling molecules known as prostaglandins. However, prospective studies in humans have not demonstrated strong support for the cardioprotective effects of selenium. While one study found a significant increase in illness and death from cardiovascular disease in individuals with serum selenium levels below 45 mcg/liter compared to matched pairs above 45 mcg/liter (30), another study, using the same cutoff points for serum selenium, found a significant difference only in deaths from stroke (31). A study of middle aged and elderly Danish men found an increased risk of cardiovascular disease in men with serum selenium levels below 79 mcg/liter (32), but several other studies found no clear inverse association between selenium nutritional status and cardiovascular disease risk (33). In a multi-center study in Europe, toenail selenium levels and risk of myocardial infarction (heart attack) were only associated in the center where selenium levels were the lowest (34). While some epidemiologic evidence suggests that low levels of selenium (lower than those commonly found in the U.S.) may increase the risk of cardiovascular diseases, definitive evidence regarding the role of selenium in preventing cardiovascular diseases will require controlled clinical trials.

Disease Treatment

There appears to be a unique interaction between selenium and the human immunodeficiency viruses (HIV) that cause acquired immunodeficiency syndrome (AIDS). Declining selenium levels in HIV-infected individuals are sensitive markers of disease progression and severity, even before malnutrition becomes a factor. Low levels of plasma selenium have also been associated with a significantly increased risk of death from HIV. Adequate selenium nutritional status may increase resistance to HIV infection by enhancing the function of important immune system cells known as T cells and modifying their production of intracellular messengers known as cytokines (15)....
Only a few trials of selenium supplementation in HIV-infected individuals have been published and reported subjective improvement, but did not demonstrate any improvement in biological parameters related to AIDS progression

Cochrane Database Syst Rev. 2004;(2):CD003538.
Selenium supplementation for asthma.
Allam MF, Lucane RA.
Preventive Medicine and Public Health Department, Faculty of Medicine, University of Cordoba, Avda. Menendez Pidal, s/n, Cordoba, Spain, 14004.
..........REVIEWERS' CONCLUSIONS: There is some indication that selenium supplementation may be a useful adjunct to medication for patients with chronic asthma. This conclusion is limited because of insufficient studies and lack of improvement in the clinical parameters of lung function.

Food sources
The richest food sources of selenium are organ meats and seafood, followed by muscle meats. In general, there is wide variation in the selenium content of plants and grains because plants do not appear to require selenium. Thus, the incorporation of selenium into plant proteins is dependent only on soil selenium content. Brazil nuts grown in areas of Brazil with selenium-rich soil may provide more than 100 mcg of selenium in one nut, while those grown in selenium-poor soil may provide 10 times less

Food Serving Selenium (mcg)
Brazil nuts (from selenium-rich soil) 1 ounce (6-8 kernels) 839*
Shrimp 3 ounces (10-12) 34
Crab meat 3 ounces  40
Salmon 3 ounces 40
Halibut 3 ounces 40
Noodles, enriched 1 cup, cooked 35
Rice, brown 1 cup, cooked 19
Chicken (light meat) 3 ounces 20
Pork 3 ounces 33
Beef 3 ounces 17
Whole wheat bread 2 slices 15
Milk  8 ounces (1 cup) 5
Walnuts, black 1 ounce, shelled 5
*Above the tolerable upper intake level (UL) of 400 mcg/day.

Mushrooms, Crimini, Raw 5 oz-wt  36.85  excellent
Cod, Pacific, Fillet, Baked, Broiled 4 oz-wt  53.07  excellent
Mushrooms, Shiitake, Raw 8 oz-wt  37.07  excellent
Shrimp, MixedSpecies, Steamed, Boiled 4 oz-wt  44.91  excellent
Snapper, Baked 4 oz-wt  55.57  excellent
Tuna, Yellowfin, Baked/Broiled 4 oz-wt  53.07 excellent
Halibut, Baked/Broiled 4 oz-wt  53.07 excellent
Liver, Calf 4 oz-wt  57.84  excellent
Seeds, Mustard 2 tsp  9.96  excellent
Chinook Salmon Fillet-Baked/Broiled 4 oz-wt  53.07  excellent
Egg, Hen, Whole, Boiled 1 each  13.55 very good
Turkey Breast, Roasted 4 oz-wt  33.00  very good
Lamb, Loin, Roasted 4 oz-wt 34.36 very good
Barley 1 cup36.40 very good
Oats, Whole Grain 1 cup 18.95 very good
Chicken Breast, Roasted 4 oz-wt4 28.01 very good
Tofu, Raw 4 oz-wt 10.09 very good
Beef Tenderloin, Lean Broiled 4 oz-wt  27.67 very good
Broccoli, Raw 1 cup  2.13 very good
Sunflower Seeds, Dried 0.25 cup  21.42 very good
Garlic 1 oz-wt  4.03 very good

Although selenium is required for health, high doses can be toxic. Acute and fatal toxicities have occurred with accidental or suicidal ingestion of gram quantities of selenium. Clinically significant selenium toxicity was reported in 13 individuals after taking supplements that contained 27.3 milligrams (27,300 mcg) per tablet due to a manufacturing error. Chronic selenium toxicity (selenosis) may occur with smaller doses of selenium over long periods of time. The most frequently reported symptoms of selenosis are hair and nail brittleness and loss. Other symptoms may include gastrointestinal disturbances, skin rashes, a garlic breath odor, fatigue, irritability, and nervous system abnormalities.
Nausea, vomiting, hair loss, skin lesions, abnormalities in the beds of the fingernails, and fingernail loss can all be symptomatic of selenium toxicity. Levels of selenium necessary to trigger these toxicity symptoms cannot be obtained from food, however, but only from selenium supplementation.
Overexposure of selenium fumes may produce accumulation of fluid in the lungs, garlic breath, bronchitis, pneumonitis, bronchial asthma, nausea, chills, fever, headache, sore throat, shortness of breath, conjunctivitis, vomiting, abdominal pain, diarrhea and enlarged liver. Selenium is an eye and upper respiratory irritant and a sensitizer. Overexposure may result in red/yellow staining of the nails, teeth and hair. Selenium dioxide reacts with moisture to form selenious acid, which is corrosive to the skin and eyes.

Drug Interactions

At present, few interactions between selenium and medications are known (44). The anticonvulsant medication, valproic acid, has been found to decrease plasma selenium levels. Supplemental sodium selenite has been found to decrease toxicity from the antibiotic nitrofurantoin and the herbicide paraquat in animals (45).

Antioxidant Supplements and HMG-CoA Reductase Inhibitors (Statins)
A 3-year randomized controlled trial in 160 patients with documented coronary heart disease (CHD) and low HDL levels found that a combination of simvastatin (Zocor) and niacin increased HDL2 levels, inhibited the progression of coronary artery stenosis (narrowing), and decreased the frequency of cardiovascular events, such as myocardial infarction (heart attack) and stroke (46). Surprisingly, when an antioxidant combination (1,000 mg vitamin C, 800 IU alpha-tocopherol, 100 mcg selenium, and 25 mg beta-carotene daily) was taken with the simvastatin-niacin combination, the protective effects were diminished. Although the individual contribution of selenium to this effect cannot be determined, these findings highlight the need for further research on potential interactions between antioxidant supplements and cholesterol-lowering agents, such as HMG-CoA reductase inhibitors (statins).

The only controlled trial to examine the effect of selenium supplementation on cancer risk in a well-nourished population found that 200 mcg/day of supplemental selenium significantly decreased the risk of prostate cancer in men by 51% (26). However, the risk of one type of skin cancer was increased by 25% . Although mortality from prostate cancer is considerably higher than mortality from squamous cell cancer of the skin, these findings suggest that the overall effects of selenium supplementation on cancer risk are not yet clear enough to support a general recommendation for an extra selenium supplement. Men taking supplemental selenium in order to reduce the risk of prostate cancer should not exceed 200 mcg/day and should take precautions to reduce the risk of squamous cell carcinoma, such as using sunscreen and avoiding prolonged sun exposure.

Integr Cancer Ther. 2004 Mar;3(1):5-12.  
Cruciferous vegetables: cancer protective mechanisms of glucosinolate hydrolysis products and selenium.
Keck AS, Finley JW.
United States Department of Agriculture, Agricultural Research Service, Grand Forks Human Nutrition Research Center, Grand Forks, North Dakota 58202-9034, USA.

Dietetic professionals urge Americans to increase fruit and vegetable intakes. The American Institute of Cancer Research estimates that if the only dietary change made was to increase the daily intake of fruits and vegetables to 5 servings per day, cancer rates could decline by as much as 20%. Among the reasons cited for this health benefit are that fruits and vegetables are excellent sources of fiber, vitamins, and minerals. They also contain nonnutritive components that may provide substantial health benefits beyond basic nutrition. Examples of the latter are the glucosinolate hydrolysis products, sulforaphane, and indole-3-carbinol. Epidemiological studies provide evidence that the consumption of cruciferous vegetables protects against cancer more effectively than the total intake of fruits and vegetables. This review describes the anticarcinogenic bioactivities of glucosinolate hydrolysis products, the mineral selenium derived from crucifers, and the mechanisms by which they protect against cancer. These mechanisms include altered estrogen metabolism, protection against reactive oxygen species, altered detoxification by induction of phase II enzymes, decreased carcinogen activation by inhibition of phase I enzymes, and slowed tumor growth and induction of apoptosis.

Eur J Endocrinol. 2004 May;150(5):605-18.  Related Articles, Links  
The environment and autoimmune thyroid diseases.
Prummel MF, Strieder T, Wiersinga WM.
Department of Endocrinology and Metabolism, F5-171, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.

Genetic factors play an important role in the pathogenesis of autoimmune thyroid disease (AITD) and it has been calculated that 80% of the susceptibility to develop Graves' disease is attributable to genes. The concordance rate for AITD among monozygotic twins is, however, well below 1 and environmental factors thus must play an important role. We have attempted to carry out a comprehensive review of all the environmental and hormonal risk factors thought to bring about AITD in genetically predisposed individuals. Low birth weight, iodine excess and deficiency, selenium deficiency, parity, oral contraceptive use, reproductive span, fetal microchimerism, stress, seasonal variation, allergy, smoking, radiation damage to the thyroid gland, viral and bacterial infections all play a role in the development of autoimmune thyroid disorders. The use of certain drugs (lithium, interferon-alpha, Campath-1H) also increases the risk of the development of autoimmunity against the thyroid gland.

Free Radic Biol Med. 2004 Jun 15;36(12):1481-95.  Related Articles, Links  
Role of Se-dependent glutathione peroxidases in gastrointestinal inflammation and cancer.
Chu FF, Esworthy RS, Doroshow JH.
Department of Medical Oncology and Therapeutics Research, Beckman Research Institute of City of Hope, Duarte, CA 91010-3000, USA.

Increase in reactive oxygen species plays an integral part in the inflammatory response, and chronic inflammation increases cancer risk. Selenium-dependent glutathione peroxidase (GPX) is well recognized for its antioxidant, and thus anti-inflammatory, activity. However, due to the multiple antioxidant families present in the gastrointestinal tract, it has been difficult to demonstrate the importance of individual antioxidant enzymes. Using genetically altered mice deficient in individual Gpx genes has provided insight into the physiological functions of these genes. Insufficient GPX activity in the mucosal epithelium can trigger acute and chronic inflammation. The presence of certain microflora, such as Helicobacter species, may affect cancer risk significantly. However, when damaged cells have progressed into a precancerous status, increased GPX activity may become procarcinogenic, presumably due to inhibition of hydroperoxide-mediated apoptosis. This review summarizes the current view of GPX in inflammation and cancer with emphasis on the GI tract.

selenium and plant

Environ Sci Technol. 2004 Jul 1;38(13):3581-6. Related Articles, Links  
Selenium biotransformations in an insect ecosystem: effects of insects on phytoremediation.
Vickerman DB, Trumble JT, George GN, Pickering II, Nichol H.
Department of Entomology, University of California at Riverside, Riverside, California 92521, USA.

Phytoremediation of selenium-contaminated soils may be influenced by higher trophic levels including insects. We examined how selenium affects the behavior, survival, and development of the wasp parasitoid Cotesia marginiventris, parasitizing its natural host, the beet armyworm Spodoptera exigua, feeding on alfalfa, Medicago sativa, irrigated with water containing selenate. X-ray absorption spectroscopy was used to quantify the selenium chemical forms in each trophic level. Alfalfa partially transformed selenate to organoselenium. S. exigua contained only organoselenium, both directly absorbed from M. sativa and transformed from selenate. C. marginiventris cocoons collected shortly after larval emergence contained only organoselenium derived from the host. The surprising finding of trimethylselenonium-like species in adult parasitoids and the cocoons from which they emerged suggests that adults and pharates can detoxify excess selenium through methylation and volatilization. Adult parasitoids do not discriminate against selenium-containing alfalfa, even though alfalfa generates selenium volatiles. Parasitoids raised on selenium-fed larvae emerged later and pupae weighed less than their selenium-free counterparts. We conclude therefore that C. marginiventris can be used to control S. exigua damage to M. sativa being used to remove selenium from soils. Moreover, the presence of such insects may improve phytoremediation by increasing biotransformation of inorganic selenium and release of volatile selenium species.

Selenium is accumulated by a number of plants in sufficient amounts to be toxic if consumed by livestock. Plants that accumulate high amounts of selenium and may require selenium for growth are often found in selenium rich areas. Historically these plants have been called indicator plants. The indicator plants include certain species of Astragalus, prince's plume, and some woody asters. The indicator plants may accumulate up to 3000 parts per million (ppm) selenium.

Plants that will accumulate selenium but do not have a requirement for it are called facultative or secondary selenium absorbers. These plants can accumulate up to 50 ppm. The secondary selenium accumulators include some native range plants, and crop plants such as western wheatgrass, barley, wheat, and alfalfa. Plants containing more than 5 ppm selenium are potentially toxic in cattle.

Where Selenium-Accumulating Plants Grow
The major seleniferous areas of the West can be found in North and South Dakota, Montana, Wyoming, Colorado, and Utah. Selenium poisoning occurs in the areas that have soils high in selenium. Both indicator and secondary selenium-accumulating plants grow in these areas.

Astragalus bisulcatus, two-grooved milkvetch, is a selenium-accumulating plant. Though it is not palatable to most livestock, it has been implicated in some cases of selenium toxicosis. It has been suggested that even though selenium accumulating plants are not readily eaten, they contribute to selenium toxicosis by making selenium in the soil available  to neighboring, palatable, secondary selenium-accumulating plants.

How It Affects Livestock
Selenium is required in the diet of most animals. Concentrations of 0.3 ppm are recommended for most food producing livestock. Acute selenosis has been associated with ingesting large amounts of selenium such as would happen if animals eat indicator plants (>400 ppm). Oral selenium doses of between 1 and 5 mg/kg body weight are considered toxic. Lower doses of between 5 and 40 ppm in the diet for several weeks or months result in chronic poisoning, oftentimes called alkali disease. The mechanism of toxicity is not completely understood, but the clinical and morphologic lesions suggest glutathione depletion and secondary lipid peroxidation are important in pathogenesis.

Signs and Lesions of Poisoning

Acute Poisoning:  Lethargy, nonresponsiveness
 Dyspnea with abnormal posture
 Unsteady gait
 Abdominal pain (teeth grinding)
 Increased pulse, respiration rate and body temperature.
 Death (Sheep may not show signs and are found dead)
 Necropsy and histologic lesions include pulmonary edema, hydrothorax, and pale myocardium. Additionally there may be mild enteritis and passive congestion of the liver

Chronic Poisoning:

 Rough hair coat
 Lack of vitality, anemia
 Lameness, joint stiffness
 Hooves may become overgrown or deformed (circular bumps or breaks below coronary band)
 Loss of long hair (horses commonly lose their mane and tail)
 Histologic lesions variable but often include cardiomyopathy and liver cirrhosis
 Reproductive losses in cattle

How to Reduce Losses
The only practical method of reducing losses in livestock due to selenium poisoning is to prevent animals from eating excessive amounts of selenium-containing plants. Affected animals that are removed from seleniferous forages may recover without apparent permanent effects. The rate of recovery is dependent upon the severity of intoxication