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Selenium

Selenium is an essential trace mineral named after the Greek goddess of the moon, Selene, (33) as a result of the recent discovery of a similar element, tellurium, that was named after the Earth. (126) Selenium is directly incorporated into more than 25 proteins, which have a variety of functions including antioxidation (glutathione peroxidase, GPx; or thioredoxin reductases, TrxR), regulation of thyroid hormones (iodothyronine deiodinases), immunoregulation (methionine-R-sulfoxide reductase), as well as DNA synthesis, epigenetic modulation, cell signalling, and metabolism (various selenoproteins). (13)(33) Given these important functions, selenium has several therapeutic applications, such as to maintain and improve an individual’s immune and antioxidative profile, thyroid health, and endocrine function, to name a few. Selenium has had particular effectiveness in regions with low selenium intake (e.g., China) for reducing the risk of developing Keshan disease (86%), (139) as well as Kashin-Beck disease (81 to 82%) with 2.2 to 4.4 times better odds of improvement in existing cases. (110)(132)

During the first year of life, adequate selenium intakes range between 15 to 20 μg for infants. For ages one to three, the recommended dietary allowance is 20 μg, and this amount increases incrementally by ~10 mg every four years, up to a maximum of 55 μg after the age of 14. (92) The RDAs are based on optimizing glutathione peroxidase (GPx) activity, (19) which occurs when plasma selenium is approximately 80 ng/ml, though Americans and Canadians often possess levels between 125 ng/ml and 145 ng/ml, respectively. (31)

While selenium deficiencies are relatively rare in North America, lower selenium levels can lead to the development of many chronic conditions, including various forms of cancer, (5)(17)(18)(21)(27)(34)(39)(46)(50)(56)(94)(107)(124)(140) cardiovascular disease, (72)(100)(136) and gestational and type II diabetes. (12)(68)(125) Selenium deficiency may also lead to higher cardiovascular mortality and all-cause mortality. (60)(130) However, being aptly named after the moon, excessive selenium intake also has a dark side. (20)(96) Specifically, excessive selenium intake has been associated with increased risk of type II diabetes. (66)(67)(85)(122)(125)

A number of foods contain relatively high concentrations of selenium, particularly Brazil nuts as well as fish and other seafood, meat, seeds, and grain products. (20)(118) In the majority of cases in North America, supplementation is typically indicated where there is significant suspected or demonstrated deficiency or suspected dysregulation of the physiological functions mentioned above. (49)

Main uses

Antioxidation
Chemoprevention and cancer therapy support
Insulin function (in cardiometabolic conditions)
Thyroid function

Formulations

Form	Characteristics
Selenomethionine (l-selenomethionine)	Organic Equivalent bioavailability at equal doses of selenomethionine content to selenium-enriched yeast (103)(119) ~4.6x higher AUC than methylselenocysteine (40) ~2x more bioavailable than selenite, (129) with up to a 5.2x higher AUC (40) ~33% higher absorption than selenite, raising plasma selenium 72-89% more (26)(30) ~80% higher plasma selenium than selenate (30)
Selenium-enriched yeast	Selenium in brewer’s yeast (Saccharomyces cerevisiae) mainly provides organic forms of selenium (i.e., selenomethionine), but variability in the percentage of selenomethionine can occur between products. (41) ~1.5-2x more bioavailable than inorganic selenium (20) ~30% higher serum selenium than selenite, but produced equivalence in GPx activity (2) ~72% higher plasma selenium, but produced equivalence in Gpx activity (116) Reduced oxidative stress biomarkers (8-iso-PGF2α & 8-OHdG), whereas a matched dose of selenomethionine did not, suggesting that additional properties of the yeast may provide added benefit to antioxidative stress over selenomethionine alone (103)
Methylselenocysteine	Organic ~4.6x lower AUC than selenomethionine, but 14% higher AUC than sodium selenite (40)
Sodium selenite (SeO3(2-))	Inorganic ~40% lower absorption than selenate, but was excreted 67% slower, supporting equivalence in their bioavailability (retention) (119)
Sodium selenate (SeO4(2-))	Inorganic Sodium selenate increased GPx activity in Px with liver cirrhosis, but selenomethionine did not, suggesting that individuals with hepatic impairments, leading to a reduced ability to metabolize selenomethionine to selenide for incorporation into selenoproteins, may require inorganic selenium. (25)
Selenium chelates	Binding of an organic molecule (e.g., glycinate, citrate, apartate, etc.) to selenium to improve its absorption No comparative evidence available for these formulations

Dosing & administration

Antioxidation
General outcomes from A-level evidence	↑ (small to moderate effect, SMD= 0.36-0.56) & total antioxidative capacity (small effect, SMD= 0.39) ↓ MDA (moderate effect, SMD= 0.54) & lipid hydroperoxide (45)(52)(61)(62) Note: No effect was observed for GSH, TBARS, or adiponectin; (52) improvements in exercise-induced oxidative stress did not translate to improved athletic performance. (45)
Dosing & administration	100-285 μg (as selenomethionine or selenium-enriched yeast) per day for 3-9 months to healthy volunteers
Outcomes	↑ GPx activity (9%) compared to baseline in three months (115) & GSH (19%) than placebo by nine months (32% increase from baseline, but associated changes in GSH may be more pronounced in caucasians) (37)(104) ↓ 8-isoprostane (28%) and 8-OHdG (34%) compared to baseline by nine months using higher dose selenium-enriched yeast (and not selenomethionine) (103)
Class of evidence	B
Dosing & administration	100-200 μg (as selenomethionine, selenium-enriched yeast, or sodium selenite) per day for 8-12 weeks to Px with various cardiometabolic conditions
Outcomes	↑ total antioxidative capacity (246.2-428.5 mmol/L difference), GPx (30 U/ml difference), & glutathione (228.7 µmol/l difference) compared to placebo ↓ nitric oxide (5.4 µmol/l) & MMP-2 (688.3 ng/ml difference) compared to placebo in Px with diabetes (14)(15)(44) ↑ total antioxidative capacity (218.8 mmol/L difference), GSH (72.9 µmol/l difference), & GPx activity (4.1-5 U/gHb difference) compared to placebo in Px with coronary artery disease or congestive heart failure (87)(95)(108) ↓ MDA (10%) & DNA damage (2.6x) compared to placebo in Px receiving hemodialysis (106)(134)
Class of evidence	B
Dosing & administration	400 μg (as sodium selenite) per day for six months to Px with oral cancer
Outcomes	↑ GSH levels (44-52%), and GPx (16-22%), SOD (19-23%), CAT (27-34%), GRx (22-28%), & G6PDH activities (16-22%) compared to Px undergoing radiotherapy or who are untreated (38)
Class of evidence	C

Cancer
General outcomes from A-level evidence	↓ overall cancer incidence (28%) and mortality (24%) in observational studies, but no effect of selenium on overall cancer incidence or mortality was observed in RCTs; (122) Intakes higher than the RDA of 55 μg/day reduced relative risk of cancer (6%), with additional benefit from supplementation (11%) (72) Older analyses show that selenium supplementation reduced the relative risk of cancer mortality (22%) (16) and cancer incidence (24%) in RCTs, particularly in populations at higher risk for cancer or with lower baseline selenium (<125.6 µg/L) (76)
Dosing & administration	200 μg (as selenium-enriched yeast) per day, ongoing to Px with history of skin cell carcinomas
Outcomes	↓ total cancer incidence (25-37%) with 45% fewer carcinomas, 49-76% less prostate cancer (greater effects may be observed in Px with <4 ng/ml prostate-specific antigen), 33-64% less colorectal cancer, and 46% less lung cancer, & total cancer mortality (50%) and lung cancer mortality (53%) compared to placebo over 8-10 years Note: There may be stronger associations for Px with low initial selenium levels. No reduction in skin cancers were observed. (28)(29)(31)(36)(101)(102)
Class of evidence	B
Dosing & administration	200 μg (as selenium-enriched yeast) or 500 μg (as sodium selenite) per day for 3-4 years to Px at high risk for liver cancer
Outcomes	↓ incidence of liver cancer (49%) compared to placebo (78) Note: Continued use is required to provide an ongoing preventative effect. (133)
Class of evidence	B

Cardiometabolic conditions
General outcomes from A-level evidence	↓ insulin levels (3.6 μIU/ml, small effect, SMD= 0.42), (113) insulin resistance (1 point), HOMA-B (13.6 points), (112) TGs (small effect, SMD= 0.19), total cholesterol (small effect, SMD= 0.13), VLDL (small effect, SMD= 0.34), (53) & CRP (small effect, SMD= 0.48) (62) ↑ insulin sensitivity (large effect, SMD= 0.83) (113) Note: Individual analyses also showed that no effects were observed on mortality, diabetes complications, FBG, insulin resistance, TGs, total cholesterol, HDL, LDL, VLDL, blood pressure, or QoL in Px with metabolic diseases (53)(112)(113)
Dosing & administration	200 μg per day for 6-12 weeks in Px with metabolic diseases
Outcomes	↓ insulin levels (small effect, SMD= 0.42) ↑ insulin sensitivity (large effect, SMD= 0.83) (113)
Class of evidence	A
Dosing & administration	200 μg (as selenium-enriched yeast) per day for 8-12 weeks to Px with diabetes
Outcomes	↓ insulin (3.6-5.8 μIU/ml difference), insulin resistance (1.0-1.6 point difference), HOMA-B (13.6-22.6 point difference), & hs-CRP (1272.5-1472.1 ng/ml difference) compared to placebo ↑ insulin sensitivity (0.02 point difference) compared to placebo (14)(44)
Class of evidence	B
Dosing & administration	200 μg (as selenium-enriched yeast) per day for six weeks to pregnant women with gestational diabetes mellitus
Outcomes	↓ FBG (15 mg/dl difference), insulin (7.24 μIU/mL difference), insulin resistance (2.3 point difference), hs-CRP (1292.3 ng/ml difference), & MDA (0.67 μmol/L difference) ↑ insulin sensitivity (0.01 point difference) and glutathione (92.07 μmol/L difference) levels (8) & PPAR-y and GLUT-1 expression (involved in lipid and insulin metabolism) Note: Selenium also reduced the incidence of newborn hyperbilirubinemia & hospitalization (27.7% difference) (64)
Class of evidence	B
Dosing & administration	200 μg (as selenium-enriched yeast) per day for 12 weeks to Px with congestive heart failure
Outcomes	↓ insulin (4.23 µIU/mL), insulin resistance (1.56 point difference), LDL (6.95 mg/dl difference), total cholesterol to HDL-C ratio (0.41 point difference), & hs-CRP (2296.1 ng/ml difference) ↑ insulin sensitivity (0.01 point difference) & HDL (6.19 mg/dl difference) (95)
Class of evidence	B

Chemo- and radiotherapy support
General outcomes from A-level evidence	No data currently available.
Dosing & administration	200 μg twice per day for two weeks to Px with leukemia undergoing chemotherapy
Outcomes	↓ incidence of grade 1-2 mucositis (24% difference) & duration of grade 2-4 mucositis (1.7 days) compared to placebo (58)
Class of evidence	B
Dosing & administration	200 μg/kg (as intravenous sodium selenite) per day for 5-7 days and up to 30 days to Px with non-Hodgkin’s lymphoma adjunct to chemotherapy
Outcomes	↓ percentage of apoptotic lymphoma cells (20% difference) CD4/CD8 ratio (32%), a complete response rate (20% higher), & survival time (~2 month difference) compared to chemotherapy alone (10)(11) ↑ neutrophil apoptosis (50%) with an associated reduction in post-chemotherapy infection (47%) compared to chemotherapy alone (9)
Class of evidence	C
Dosing & administration	300-500 μg (as sodium selenite) per day to Px with various cancers undergoing radiotherapy
Outcomes	↓ saliva gland damage caused by radiation in thyroid cancer (111) ↓ loss of taste and dysphasia (trends for improvement) in head and neck cancer (23) ↓ incidence of diarrhea (24% difference) in cervical and uterine cancer (90)
Class of evidence	C

Critical care
General outcomes from A-level evidence	↓ risk of 28-day mortality by 16% and mortality by 17-27% in Px with sepsis, (3)(4)(55)(75)(137) the number of acute renal failures (45-76%), (89) & the relative risk development of sepsis among preterm neonates by 26-33% using parenteral therapy (35)(47) Note: No effect on rate of six-month mortality, pulmonary infections, and renal failure, (75) on 28-day mortality and 90-day mortality when using intravenous selenium, (4)(77)(84)(137) or on rates of mortality and other conditions associated with prematurity in neonates was noted (35)(47)
Dosing & administration	1,000-2,000 μg (as intravenous sodium selenite) bolus injection, followed by a 10-14 day period of 1,000-1,600 μg continuous infusions to Px with severe systemic inflammatory response syndrome and sepsis
Outcomes	↓ 28-day mortality odds (44%) (7), sequential organ failure assessment score (72%), rate of ventilator-associated pneumonia infection (31% difference), & hospital-acquired pneumonia post-discharge (83)
Class of evidence	B
Dosing & administration	10 μg per day for one month to preterm very low-birthweight neonates
Outcomes	↓ incidence of sepsis (13.3% difference), incidence of probable sepsis (20%), & total incidence of any late-onset sepsis (33%) compared to placebo (1)
Class of evidence	B
Dosing & administration	500-535 μg (as intravenous) sodium selenite for three days, followed by 250-285 μg for three days, followed by 125-155 μg for three days, and followed by 35 mg thereafter to Px with systemic inflammatory response syndrome
Outcomes	↓ Acute Physiology and Chronic Health Evaluation II score Normalized selenium and glutathione peroxidase levels, required fewer initiations of hemodialysis due to acute renal failure, (6 & reduced mortality by 40% in Px with higher initial APACHE-II scores compared to low-dose selenium (35 μg/day) (48)
Class of evidence	C

Human immunodeficiency virus (HIV)
General outcomes from A-level evidence	↓ the decline in CD4 count, potentially prolonging the onset of AIDS (91) and may reduce the risk of HIV-related diarrhea mortality and hospital admissions (65)
Dosing & administration	200 μg per day for up to 24 months in Px with HIV
Outcomes	↓ the decline in CD4 count, potentially prolonging the onset of AIDS (91)
Class of evidence	A
Dosing & administration	200 μg (as selenium-enriched yeast) per day for 9-24 months adjunct to antiretroviral therapy to Px with HIV
Outcomes	↓ CD4 count with a possible reduction in viral load (57) ↑ the decline in CD4 count by 43.8% per month (63)
Class of evidence	C
Dosing & administration	200 μg (as selenomethionine) per day from 12-27 weeks gestation to six months postpartum to pregnant women with HIV
Outcomes	↓ HIV-associated diarrhea (40%) compared to placebo (71)
Class of evidence	B

Male infertility
General outcomes from A-level evidence	Improved semen parameters with a moderate effect in oligospermia (SMD= 0.64) & large effect in asthenozoospermia (SMD= 1.39) (22)
Dosing & administration	200 μg per day for 26 weeks to men with oligospermia, asthenospermia, or teratospermia
Outcomes	↓ sperm count (25%), concentration (23%), motility (18%), normal morphology (28%), ejaculate volume (19%), testosterone (16%), & inhibin B (18%) ↑ luteinizing hormone (12%) & FSH (25%) compared to baseline, but no change in placebo (105)
Class of evidence	B
Dosing & administration	100 μg (as selenomethionine) per day for three months to men with asthenozoospermia
Outcomes	↑ motility (37%) with 11% more Px achieving paternity (109)
Class of evidence	B

Pregnancy-related outcomes
General outcomes from A-level evidence	↓ relative risk of preeclampsia by 72% (131)
Dosing & administration	100 μg (selenium-enriched yeast) per day for ~six months until delivery to pregnant women
Outcomes	↓ postpartum depression score (18%) & incidence of premature rupture of membranes (21%) compared to placebo (88)(114)
Class of evidence	B
Dosing & administration	60 μg (selenium-enriched yeast) per day from 12-14 weeks gestation until delivery to pregnant women
Outcomes	↓ odds of preeclampsia and pregnancy-induced hypertension by 65% with a reduction in soluble vascular endothelial growth factor receptor-1 (a biomarker for preeclampsia) in Px with the lowest selenium status (97)
Class of evidence	B

Polycystic ovary syndrome (PCOS)
General outcomes from A-level evidence	↓ inflammatory, oxidative, and lipid profiles, possibly leading to reduced insulin resistance and hyperandrogenism, but data is too scarce to draw conclusions on these mechanisms (51)
Dosing & administration	200 μg (selenium-enriched yeast) per day for eight weeks to women with PCOS using metformin
Outcomes	Improved pregnancy rate (15.7% difference), alopecia (31.2% difference), acne (34.4% difference), & hirsutism (19%) compared to placebo ↓ DHEA (18%), hs-CRP (33%), & MDA (3%) compared to baseline with no change in placebo (except for rising MDA) (99) ↓ insulin (5.6 μIU/ml difference), insulin resistance (1.57 point difference), B-cell dysfunction score (23.61 point difference), TGs (22.14 mg/dl difference), & VLDL (1.93 mg/dl difference) compared to placebo ↓ insulin sensitivity (10%) compared to placebo (59) ↓ LDL-R, IL-1, & TNF-ɑ gene expression compared to placebo ↓ PPAR-y, VEGF, GLUT-1 gene expression compared to placebo (54)(135)
Class of evidence	B

Thyroid health
General outcomes from A-level evidence	Hashimoto’s thyroiditis: ↓ thyroid peroxidase autoantibody (TPOAb, 512 IU/ml) and thyroglobulin autoantibody (TgAb, 215 IU/ml) at three months when used alone, and effects extend with adjunct use of levothyroxine where TPOAb is reduced (271-469 IU/ml) over 3-6 months and TgAb (176 IU/ml) at 12 months (but not 3-6 months) (117)(120)(121)(127) ↑ relative chance of improved well-being and mood by three months (43)(117) Note: A consistent effect on TgAb is less prevalent than for TPOAb, (43) which is considered large by six months (large effect, SMD= 1.51) and 12 months (large effect, SMD= 4.94) (43) One analysis showed no support for the use of selenium to improve TSH, QoL, or thyroid ultrasound in Px using or not using levothyroxine for autoimmune thyroiditis (128) Graves’ disease: ↓ free thyroxine at 3-6 months (large effect, SMD= 0.86-1.01), free triiodothyronine at 3-6 months (small-moderate effect, SMD= 0.34-0.67), & TRAb at six months (large effect, SMD=2.31), but no difference observed by nine months compared to methylimidazole alone in Px with Graves’ disease ↑ TSH at six months (large effect, SMD = 3.12), but no difference at three or nine months compared to methylimidazole alone in Px with Graves’ disease (138)
Dosing & administration	200 μg (as selenomethionine) per day for a minimum of three months to Px with Hashimoto’s thyroiditis
Outcomes	↓ TPOAb (267-512 IU/ml) & TgAb (215 IU/ml) by three months when used alone, with effects extending with adjunct use of levothyroxine for up to 12 months for TPOAb (271-469 IU/ml, providing large effects for months 6-12, SMD= 1.51-4.94) and TgAb (176 IU/ml) ↑ likelihood of improved well-being and mood by third month Note: Sodium selenite was not effective (43)(117)(127)
Class of evidence	A
Dosing & administration	100-300 μg per day for 3-6 months to Px with Graves’ disease using methylimidazole
Outcomes	↓ free thyroxine at 3-6 months (large effect, SMD= 0.86-1.01), free triiodothyronine at 3-6 months (small-moderate effect, SMD= 0.34-0.67), & TRAb at six months (large effect, SMD=2.31), but no difference observed by nine months compared to methylimidazole alone in Px with Graves’ disease ↑ TSH at six months (large effect, SMD = 3.12), but no difference at three or nine months compared to methylimidazole alone in Px with Graves’ disease (138)
Class of evidence	A
Dosing & administration	200 μg (as selenomethionine) per day for six months to children and adolescents with autoimmune thyroiditis using levothyroxine
Outcomes	↓ TgAb (64.2 IU/ml difference) compared to placebo (74)
Class of evidence	B
Dosing & administration	100 μg (as sodium selenite) twice per day for six months to Px with Grave’s orbitopathy
Outcomes	↑ Grave’s orbitopathy QoL score for visual function and appearance (~10%) & rate of improvement (25% difference) compared to placebo ↓ disease activity score (~35%) & rate of worsening (19% difference) compared to placebo (86)
Class of evidence	B
Dosing & administration	200 μg (as selenium enriched-yeast) per day for 12 weeks to women who are overweight or obese and live with hypothyroidism
Outcomes	↓ total T3 (0.23 nmol/L) & total T4 (7.46 nmol/L) compared to baseline, but no change in placebo (80)
Class of evidence	B
Dosing & administration	80-200 μg (as selenomethionine) per day throughout pregnancy and for 6-12 months post-pregnancy to euthyroid pregnant women
Outcomes	↓ TPOAb (255 IU/ml) & TgAb (19.86 IU/ml) which are maintained six months postpartum, whereas placebo group rebounded after an initial decrease during pregnancy (82) ↓ incidence of postpartum thyroid dysfunction (20% difference) & permanent hypothyroidism (8.6% difference) compared to placebo incidence of postpartum thyroid dysfunction (20% difference) & permanent hypothyroidism (8.6% difference) compared to placebo (93)
Class of evidence	B
Dosing & administration	200 μg (as selenomethionine) per day for six months to euthyroid women with Hashimoto’s thyroiditis adjunct to levothyroxine
Outcomes	↓ TPOAb (44%), lymphocytic hsCRP, TNF-ɑ, IL-2, & interferon-γ when using selenium alone, but with greater efficacy adjunct to levothyroxine compared to placebo (69)(70)
Class of evidence	B

Adverse effects

Similar rates of adverse events have been reported between selenium and control groups across various systematic reviews; (43)(75)(91)(120)(121) however, one analysis indicated that there was a five times higher relative risk of an adverse event (i.e., gastric discomfort, headache, or skin rash) compared to control groups in Hashimoto’s thyroiditis. (127)

One large trial showed that the daily use of 200 μg over seven to 12 years increased the likelihood of alopecia (28%) and dermatitis (17%), (79) while the use of 800 μg for 16 weeks did not lead to brittle hair or nails. This may suggest that selenium toxicity might only be observed as a result of extremely long and high intakes. (119) For example, the use of 300 μg per day as selenium-enriched yeast over five years increased the likelihood of all-cause mortality after ten years as compared to placebo by 59%, while doses between 100-200 μg did not increase the risk. (98)

It should be noted that various analyses have also shown that long-term selenium use may increase the risk of developing type II diabetes. Analyses of randomized controlled trials using >200 μg over three to 13 years showed that selenium increased the relative risk of type II diabetes by 9 to 11%, (85)(123) though findings may be inconsistent. (67) Analyses of observational studies show even greater associations with up to two times greater odds of developing type II diabetes. (66)(125) There the may only be a small window of optimized benefit for selenium blood levels (100 to 130 µg/L) to avoid an increased risk of type II diabetes, as this association is observed at both relatively lower (<100 µg/L) and higher blood levels (>130 µg/L). (125) It should also be noted that despite selenium’s benefits on insulin metabolism (as noted in the “cardiometabolic profile” section above), selenium can potentially increase blood glucose or HbA1c in type II diabetes. (42)

Pharmacokinetics

Absorption

Selenium is well absorbed with more than 95% of the organic form selenomethionine, up to 90% of inorganic selenate, and up to 50% of inorganic selenite being absorbed. (81)(119)
Selenomethionine is absorbed by intestinal methionine transporters. (24)

Distribution

With adequate intake, selenium is primarily used for the synthesis of selenoproteins.
The majority of selenium is stored in the liver, but it can be redistributed to other tissues and organs, including the kidneys, brain, reproductive organs, and muscles, when selenium levels are reduced.
An individual weighing 70 kg likely stores between 10 to 15 mg of selenium. (24)

Metabolism

In the liver, selenomethionine is metabolized to selenocysteine via the transsulfuration pathway, and subsequently to selenide via selenocysteine lyase.
Alternatively, it can be metabolized to methylselenol via cystathionine γ-lyase and subsequently demethylated to selenide.
Selenite and selenate are also metabolized to selenide by thioredoxin reductases (selenoproteins) or in a reaction with glutathione.
Selenide may either produce smaller metabolites for excretion or can help re-synthesize selenoproteins as needed. (24)

Excretion

Regulation of selenium stores is mainly determined by its rate of excretion and not its absorption. After intake is sufficient to optimize selenoprotein content, further intake is almost completely counteracted by increased excretion. (24)
Selenium is primarily excreted in the urine, though it can also be excreted via stool, lost skin cells, or respiration. (24)(26)(119)
Approximately 55 μg is lost each day when consuming placebo, but this increases dose-dependently when selenium is introduced. (119)
Approximately 90% of selenium was excreted in 40 hours for selenate and in 121 hours for selenite. (119)