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PubMed1990

The effect of four chemical forms of selenium on mammary tumor incidence in BALB/c female mice treated with 7-12-dimethylbenz[a]anthracene.

The study was conducted to determine the effect of four forms of selenium on inhibition of DMBA-induced mammary tumors. BALB/c virgin female mice were fed the AIN-76 diet containing 0.2 or 2.0 ppm Se as selenite, selenate, selenomethionine, or selenocystine prior to and for 6 months post DMBA-treatment. At necropsy, mammary glands were histologically treated for confirmation of adenocarcinomas and the livers were removed for analysis of glutathione-peroxidase (GSHPx) activity and selenium concentrations. Dietary levels or forms of selenium had no effect on body weights. Inorganic selenium fed at 2.0 ppm Se (selenite and selenate) decreased mammary tumor incidence, but organic selenium (selenomethionine and selenocystine) had no effect on mammary tumor incidence. Hepatic GSHPx activity was highest with the 2.0 ppm selenium as selenocystine diet, but hepatic selenium levels were highest with the 2.0 ppm selenium as selenite. This study showed that the dietary form of selenium affects inhibition of mammary tumorigenesis. Furthermore, the study suggested that the pathways for selenium incorporation into GSHPx and for tumor inhibition are different.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1995

Studies on the distribution and characteristics of new mammalian selenium-containing proteins.

It has now been established that the essential effects of selenium in mammals are owing to the presence of several biologically active selenium compounds. Seleno-enzymes identified so far include several glutathione peroxidases and the type 1 iodothyronine de-iodinase. Some other selenoproteins have been sequenced and characterized. After in vivo labelling of rats with 75Se and protein separation using gel electrophoretic methods, more than 25 selenium-containing proteins or protein sub-units were detected. Some of the results of the investigations on these compounds are summarized and discussed here. By determining the pattern in a large number of tissues information on the distribution of the selenium-containing proteins was obtained. Their biological significance is not yet known but several findings indicate that some of these proteins may have important functions, especially in the brain and the endocrine and reproductive organs. More detailed information is already available on a 34 kDa-protein found in the testis and spermatozoa. Studies on the effects of dosage and chemical form of dietary selenium indicated that the tissue levels of the seleno-enzymes are homeostatically controlled and cannot be increased by additional supply. The increase in the tissue selenium observed with high selenium intake was found to be mainly caused by the non-specific incorporation of the element into a large number or proteins. The formation of most of the other selenium-containing proteins has priority over that of the cytosolic and plasma glutathione peroxidases. Thus the selenium requirement, which was calculated for optimum plasma glutathione peroxidase activity, also covers the amounts needed for normal levels of the other biologically important selenium compounds.

Animals↗
PubMed2004

Selenium supplementation for asthma.

BACKGROUND: Selenium deficiency may be important in chronic asthma. Observational studies have demonstrated that patients with chronic asthma may have lower levels of selenium than their control. Nevertheless, selenium supplementation has not been recommended with drug therapy for asthma. This review systematically examines RCTs that evaluated the role of selenium supplementation in chronic asthma. OBJECTIVES: Recognition that chronic asthma can be associated with selenium deficiency has led to the investigation of the role of selenium supplementation in reducing the symptoms and impact of chronic asthma. The objective of this review was to assess the efficacy of selenium supplementation as an adjunct to medication for the treatment of chronic asthma. SEARCH STRATEGY: We searched the Cochrane Airways Group trials register, MEDLINE/PUB MED, and EMBASE. Searches were current as of August 2003. SELECTION CRITERIA: Randomised trials comparing patients with chronic asthma receiving selenium supplementation in conjunction with asthma medication, with patients taking asthma medication only. DATA COLLECTION AND ANALYSIS: Two reviewers applied the study inclusion criteria MAIN RESULTS: One trial with a total of 24 patients suffering from chronic asthma was included. The study reported significant clinical improvement in the selenium-supplemented group, as compared with the placebo group, in terms of a 'clinical evaluation'. However, this improvement could not be validated by significant changes in separate objective parameters of lung function and airway hyper-responsiveness. 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.

Asthma↗
PubMed2004

Selenium supplementation for critically ill adults.

BACKGROUND: Selenium is a trace mineral essential to human health, which has an important role in the immune response, defence against tissue damage and thyroid function. Improving selenium status could help protect against overwhelming tissue damage and infection in critically ill adults. OBJECTIVES: This review assessed the effects of selenium supplementation including the selenium-containing compound, ebselen, on adults recovering from critical illness. SEARCH STRATEGY: We searched CENTRAL (The Cochrane Library, Issue 2, 2003), MEDLINE, (1966 to July 2003), EMBASE (1980 to Week 30 2003),CAB NAR (1973 to March 2003), BIOSIS (1985 to July 2003), CINAHL (1982 to July 2003), HEALTHSTAR (1975 to September 2002), Current Controlled Trials, and reference lists. We contacted investigators, and handsearched four journals. Date of the most recent search: December 2003. SELECTION CRITERIA: Randomized trials of selenium or ebselen supplementation by any route, in adults with critical illness (including burns, head injury, brain haemorrhage, cerebrovascular accident and surgery). DATA COLLECTION AND ANALYSIS: Two reviewers independently extracted data and assessed trial quality. We sought additional information as required from trialists. We also undertook pooling of data for outcomes and selected exploratory analyses were undertaken. MAIN RESULTS: Seven randomized trials involving813participants were included. The quality of trials, as reported, was poor, particularly for allocation concealment. The availability of outcome data was limited and trials involving selenium supplementation, were small. Thus the results must be interpreted with caution. Because of heterogeneity, results are presented for the random effects models. Four selenium trials showed no statistically significant difference in mortality (relative risk (RR) 0.52, 95% confidence interval (CI) 0.20 to 1.34). Three trials of ebselen also showed no statistically significant difference in mortality (RR 0.83, 95% CI 0.51 to 1.35). One trial of selenium found no statistically significant difference between groups for participants developing infection (RR 1.33, 95% CI 0.55 to 3.24). Three trials of ebselen provided data for participants developing infections (pyrexia, respiratory infections or meningitis), which was not statistically significant (RR 0.60, 95% CI 0.36 to 1.02). No clear evidence emerged for the benefits of selenium or ebselen supplementation for the outcomes of days on a ventilator, length of intensive care unit stay, length of hospital stay or quality of life. REVIEWERS' CONCLUSIONS: There is insufficient evidence to recommend supplementation of critically ill patients with selenium or ebselen. Trials are required which overcome the defects of the reviewed studies, particularly inadequate size and methodology. This review will be updated when four ongoing trials are completed.

Adult↗
PubMed1998

Randomized clinical trial of enteral yeast-selenium supplementation in preterm infants.

There are no data in the literature on effects of supplementing infants with yeast-selenium. We therefore studied the impact of selenium-enriched yeast on the serum selenium concentration of preterm infants living in a selenium-low area (Hungary). Twenty-eight preterm infants with a mean +/- SD birthweight of 962 +/- 129 g and a gestational age of 27 +/- 1 weeks were randomized into two groups at birth with respect to selenium supplementation. In the supplemental group (n = 14) infants received 4.8 mg yeast containing 5 microgram selenium daily with naso-gastric drip during the first 14 postnatal days. The nonsupplemented infants were used as a reference group. In the supplemented group the serum selenium concentration increased from 32.1 +/- 8.5 microgram/l to 41.5 +/- 6.5 microgram/l and in the nonsupplemented group it decreased from 25.9 +/ 6.8 microgram/l to 18.2 +/- 6.4 microgram/l within two weeks. The serum glutathione peroxidase activity increased from 2.97 +/- 0.73 U/20 microliter to 6.42 +/- 3.11 U/20 microliter in the supplemented group, and it did not change significantly (from 3.53 +/- 0.94 U/20 microliter to 3.85 +/- 0.95 U/20 microliter) in the nonsupplemented group. We did not observe any complications or side effects in connection with enteral yeast-selenium supplementation. It is concluded that selenium-enriched yeast is a safe and an effective form of short term enteral selenium supplementation for preterm infants.

Food, Fortified↗
PubMed1990

Inhibitory effect of selenium on hamster pancreatic cancer induction by N'-nitrosobis(2-oxopropyl)amine.

The effect of selenium intake on the development of pancreatic cancer was investigated in female Syrian golden hamsters. Four-week-old hamsters were divided into 2 groups according to the selenium level in their drinking water and were fed a purified diet containing less than 0.05 ppm selenium. Starting 4 weeks later, groups received 10 s.c. injections at weekly intervals of N'-nitrosobis(2-oxopropyl)amine (BOP) dissolved in saline, while controls received saline alone. When the animals were killed 18 weeks after the last injection, palpable tumors were less frequent in the high-selenium group than in animals receiving low-selenium supplement, the numbers of histologically diagnosed cancerous lesions also being significantly reduced by high selenium intake. The selenium level and glutathione peroxidase activity in serum and pancreas were significantly greater in the high-selenium group. Moreover, selenium levels and glutathione peroxidase activity were both significantly higher in tumor-bearing tissue. The results suggest that glutathione peroxidase is involved as an intermediate factor in prevention of carcinogenesis by selenium.

Animals↗
PubMed2003

Skeletal muscle disorders associated with selenium deficiency in humans.

Skeletal muscle disorders manifested by muscle pain, fatigue, proximal weakness, and serum creatine kinase (CK) elevation have been reported in patients with selenium deficiency. The object of this report was to review the conditions in which selenium deficiency is associated with human skeletal muscle disorders and to evaluate the importance of mitochondrial alterations in these disorders. A systematic literature review using the Medline database and Cochrane Library provided 38 relevant articles. The main conditions associated with selenium deficiency fell into three categories: (1) insufficient selenium intake in low soil-selenium areas; (2) parenteral or enteral nutrition, or malabsorption; and (3) chronic conditions associated with oxidative stress, such as chronic alcohol abuse and human immunodeficiency virus (HIV) infection. In low soil-selenium areas, reversibility of muscle symptoms was similar after selenium supplementation and placebo administration, suggesting a role for other factors in the development of disease. In parenteral or enteral nutrition, or malabsorption, muscle symptoms improved after selenium supplementation in 18 of 19 patients (median delay: 4 weeks). The reason that only a minority of selenium-deficient patients present with skeletal muscle disorders is unclear and is possibly related to cofactors, such as viral infections and drugs. Prospective studies of selenium-deficient myopathies would be useful in critically ill patients, alcohol abusers, and HIV-infected patients.

Adult↗
PubMed2004

Evaluation of flushing of a high-selenium backwater channel in the Colorado River.

Concern has been raised that selenium contamination may be adversely affecting endangered fish in the upper Colorado River basin. The objective of the study was to determine if operation of a water control structure (opened in December 1996) that allowed the Colorado River to flow through a channel area at Walter Walker State Wildlife Area (WWSWA) would reduce selenium and other inorganic elements in water, sediment, aquatic invertebrates, and forage fish. Endangered Colorado pikeminnow were collected and muscle plug samples taken for selenium analysis. Selenium concentrations in filtered water were 21.0 microg/L in 1995, 23.5 microg/L in 1996, 2.1 microg/L in 1997, and 2.1 microg/L in 1998. Selenium concentrations in sediment cores and sediment traps were 8.5 microg/g in 1995, 8.2 microg/g in 1996, 4.8 microg/g in 1997, and 1.1 microg/g in 1998. Selenium concentrations in aquatic invertebrates were 27.4 microg/g in 1996, 15.5 microg/g in 1997, and 4.9 microg/g in 1998. Selenium concentrations in forage fish were 27.2 microg/g in 1996, 20.2 microg/g in 1997, and 8.6 microg/g in 1998. Selenium concentrations in muscle plugs of Colorado pikeminnow were 9.8 microg/g in 1995, 9.5 microg/g in 1996, 9.0 microg/g in 1997, and 10.3 microg/g in 1998. Although selenium concentrations in water, sediment, aquatic invertebrates, and forage fish decreased substantially after operation of the water control structure, a corresponding change in Colorado pikeminnow did not seem to occur. Selenium concentrations in muscle plugs decreased with increasing fish total length and weight, did not change between repeat sampling in the same year or recapture in subsequent years, and seemed to be most closely associated with the mean monthly river flow for the March-July period.

Animals↗
PubMed1998

Blood selenium and glutathione peroxidase status in patients with colorectal cancer.

PURPOSE: It is still controversial whether a low selenium level and a reduced activity of the selenium-dependent enzyme, glutathione peroxidase, in blood are associated with an increased risk and poor prognosis of cancer in humans. This study evaluates whether colorectal cancer patients have lower serum selenium and glutathione peroxidase levels than a gender-matched and age-matched control group and whether there is a correlation to clinical data and prognosis. METHODS: In a retrospective study, serum selenium and glutathione peroxidase activity of 106 patients with colorectal cancer were determined. Clinical data were provided by our long-term follow-up program for colorectal cancer patients. RESULTS: Patients with a selenium level <70 microg/l had a significantly lower mean survival time and a lower cumulative cancer-related survival rate than patients with a selenium level >70 microg/l (P = 0.0009). When considering the different tumor stages, a decline of the mean selenium level in the T4 carcinoma group was found in the analysis of variance (P < 0.05). The lowest selenium level was found for patients with advanced tumor disease and in a preoperative situation, ie., high tumor burden. In comparison with the control group, the cancer group showed a significant reduction of serum glutathione peroxidase activity (P < 0.01) but no significant difference in selenium level. CONCLUSIONS: These results support the hypothesis of an association between low selenium level and advanced tumor disease. From our data, it cannot be decided whether this phenomenon is more likely to be a consequence or a causative factor for development and course of the disease.

Adult↗
PubMedDate not supplied

The selenium content of selected meats, seafoods, and vegetables from Lubbock, Texas.

The selenium content of some frequently consumed foods from a commercial beef packer, a road-side vendor, and local stores in Lubbock, Texas was determined and compared to selenium data for the same or similar foods in the United States and from other countries. The comparative content of selenium in foods covered the period of time between 1970 and 1993. Our selenium analyses of foods show that on a fresh weight basis, the selenium content of seafoods > commercial beef > pork > ground beef > chicken. Cooking, air- or freeze-drying increased the selenium content of all foods significantly. When the selenium content of local foods is compared to similar foods in the United States and other countries, with few exceptions, there exists great uniformity in the selenium content in the major food groups, meats, fish, milk, and vegetables. New Zealand, known for its low soil selenium, had the lowest comparative food selenium content.

Biological Availability↗
PubMed1990

Selenium concentrations in the human thyroid gland.

Recently, we found that prediagnostic serum selenium concentration was significantly lower for cases developing thyroid cancer (n = 43) than for controls. We assumed that redistribution of serum selenium into the affected tissue took place in the prediagnostic period. The present study was carried out to determine the physiological concentration of selenium in the thyroid, since very few data are available in the literature. The concentrations of selenium in the thyroid (n = 45) and liver samples from Norwegians who had died because of acute illness or accidents were determined by hydride generation atomic absorption spectrometry. The mean selenium concentration was found to be 0.72 +/- 0.44 microgram/g in the thyroid and 0.45 +/- 0.11 microgram/g in the liver tissue. The surprisingly high concentration of selenium in apparently normal thyroids indicates that selenium has important functions in this organ. The remarkably broad range, together with the observation that no significant correlation exists between thyroid and liver concentrations, suggest that factors other than the selenium status are important determinants for the selenium concentration in the thyroid gland. This observation is consistent with our hypothesis that in carcinogenesis, prediagnostic processes influence the serum-/thyroid-ratio of selenium.

Adult↗
PubMedDate not supplied

Selenium in animal nutrition: the Oregon and San Joaquin Valley (California) experiences--examples of correctable deficiencies in livestock.

White muscle disease and other selenium deficiency syndromes, once extremely common in young calves and lambs in Oregon, especially in the areas of volcanic origin east of the Cascade mountain range, prompted extensive investigations in the Oregon Agricultural Experiment Station that resulted in the implementation of large-scale selenium supplementation programs. Although selenium deficiency in livestock is consequently now rare in Oregon, selenium-deficient soils and attendant selenium deficiency conditions have been reported near the Kesterson Wildlife Refuge in the Northern part of the San Joaquin Valley, California, where, paradoxically, selenium toxicity in wildfowl, nesting near evaporation ponds, occurred and attracted wide attention. This review cites studies which explain why there is no evidence of selenium toxicity in livestock, but some selenium deficiency on the east side of the San Joaquin Valley. They also show that there is no threat to the food supply owing to excessive selenium in this area and that the consumption of meat and milk from the herds would not exceed the safe range of selenium for humans.

Animal Nutritional Physiological Phenomena↗
PubMedDate not supplied

Selenium status of Irish adults: evidence of insufficiency.

BACKGROUND: Sub-optimal selenium status may have a role in the aetiology of various pathologies. Selenium status depends on adequate selenium in the diet. A relatively high proportion of Irish adults (17% men; 46% women) have an inadequate dietary intake. AIM: A study was designed to examine the selenium status of healthy Irish adults. METHODS: Ninety-one healthy Irish adults, aged 18-67 years, were recruited from the Cork City area. A fasting blood sample was collected from each subject and each was assayed for serum selenium an index of serum selenium. RESULTS: Mean (+/- SD) serum selenium concentration in healthy Irish adults was 76 (+/- 21)microg/l. There was no significant difference in values between males and females or between postmenopausal and premenopausal women or between the three main age categories. CONCLUSION: Current serum selenium values of Irish adults would not appear to be sufficient to achieve optimal activity of glutathione peroxidase, which occurs at serum selenium concentration around 95microg/l. Sub-optimal selenium status may increase susceptibility to various chronic disorders.

Adolescent↗
PubMed1999

Selenium bioaccumulation by the water boatman Trichocorixa reticulata (Guerin-Meneville).

The input of selenium from subsurface agricultural drainage into surface water systems can result in the accumulation of toxic concentrations of selenium in aquatic food chains. Elevated selenium concentrations in aquatic systems is a significant environmental problem in many areas of the United States. A laboratory investigation was conducted to determine the dominant route of selenium bioaccumulation by the corixid Trichocorixa reticulata, an important food chain organism. The roles of waterborne and foodborne exposure in selenium bioaccumulation were examined using 48-h bioassays. Waterborne selenium concentrations ranged from 0 to 1,000 microgram Se/L as selenate. A mixture of two species of blue-green algae cultured in media with selenium concentrations ranging from 0 to 1,000 microgram Se/L as selenate was used as a corixid diet in the foodborne treatments. Corixids exposed to waterborne selenate did not accumulate selenium above control concentrations. Corixids fed algae exposed to >/=100 microgram Se/L as selenate had significantly higher selenium concentrations than control organisms. These data suggest that corixids may be effectively isolated from the water and selenium accumulation is solely through dietary exposure.

Agrochemicals↗
PubMed1985

Effect of selenium deficiency on the disposition of plasma glutathione.

Selenium deficiency causes increased hepatic synthesis and release of GSH into the blood. The purpose of this study was to examine the effect of selenium deficiency on the disposition of plasma glutathione. Plasma glutathione concentration was 40 +/- 3.4 nmol GSH equivalents/ml in selenium-deficient rats and 17 +/- 5.4 nmol GSH equivalents/ml in control rats. The half-life and systemic clearance of plasma glutathione were found to be the same in selenium-deficient and control rats (t1/2 = 3.4 +/- 0.7 min). Because selenium-deficient plasma glutathione concentration was twice that of control, the determination that selenium deficiency did not affect glutathione plasma systemic clearance indicated that the flux of glutathione through the plasma was doubled by selenium deficiency. It has been proposed that the kidney is responsible for the removal of a major fraction of plasma glutathione. In these studies, renal clearance accounted for 24% of plasma systemic glutathione clearance in controls and 44% in selenium-deficient rats. This indicates that a significant amount of glutathione is metabolized at extrarenal sites, especially in control animals. More than half of the increased plasma glutathione produced in selenium deficiency was removed by the kidney. Thus, selenium deficiency results in a doubling of cysteine transport in the form of glutathione from the liver to the periphery as well as a doubling of plasma glutathione concentration.

Animals↗
PubMed1989

Selenium deficiency inhibits prostacyclin release and enhances production of platelet activating factor by human endothelial cells.

Selenium is an essential component of glutathione peroxidase, an enzyme which protects cells against peroxidation and controls concentrations of intracellular peroxides. Since selenium deficiency is clinically associated with an increased degree of atherosclerosis, the effects of selenium deficiency on prostacyclin (PGI2) and platelet activating factor (PAF) production by cultured human umbilical vein endothelial cells (HUVEC) were investigated. In selenium-deficient HUVEC, histamine-induced PGI2 synthesis was significantly decreased when compared to selenium-supplemented HUVEC; in contrast, histamine-induced PAF production was increased by selenium deficiency. Histamine-induced inositol trisphosphate and [Ca2+]i responses and the conversion of PGG2 and PGH2 to PGI2 were not altered by selenium deficiency. However, selenium deficiency decreased the conversion of exogenous arachidonate to PGI2 and markedly suppressed glutathione peroxidase activity. These results suggest that selenium deficiency, by decreasing glutathione peroxidase activity, makes HUVEC susceptible to peroxide-induced inhibition of the cyclooxygenase activity of PGH2 synthase, resulting in decreased PGI2 production. These changes may alter platelet function in vivo and thus play a role in the increased incidence of atherosclerosis reported in selenium-deficient individuals.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Impaired ketone body metabolism in the selenium deficient rat. Possible implications.

Male rats were fed a selenium-deficient Torula yeast diet with or without 0.2 ppm selenium (as sodium selenite) in the drinking water. Selenium deficiency caused a significant increase of urinary acetoacetate excretion in fed rats, and 24 or 48 hours of starvation enhanced this effect. Two days of selenium supplementation decreased the amount of urinary acetoacetate and 3-hydroxybutyrate to 50% of the deficiency value, indicating an enzymatic impairment in the selenium-deficient rat. No selenium-dependent effect was found for the following: (1) urinary pH, amount of nitrite, glucose (negative), hemoglobin or protein, and the urine was negative for phenylketones; (2) blood content of glucose, acetoacetate, or 3-hydroxybutyrate; or (3) liver content of glycogen, glucose, acetoacetate, or 3-hydroxybutyrate. On the other hand, the liver content of triglycerides was significantly lower in selenium deficiency. Indications for a higher content of ketone bodies (acetoacetate plus 3-hydroxybutyrate) in the kidneys from selenium-deficient rats were found. The increased urinary excretion of ketone bodies on selenium deficiency may indicate an impairment of lipid and ketone body turnover (in the kidney), or a decreased kidney reabsorption rate. Possible implications of these results in connection with protective roles of selenium in atherosclerosis and carcinogenesis are suggested.

Acetoacetates↗
PubMed1984

Toxicity studies in isolated hepatocytes from selenium-deficient rats and vitamin E-deficient rats.

Isolated hepatocytes from selenium-deficient, vitamin E-deficient, and control rats were treated with cumene hydroperoxide (CuOOH), phorone (diisopropylene acetone), acetaminophen, and diquat. The effect of these chemicals on cell viability, glutathione synthesis and release, and lipid peroxidation as measured by thiobarbituric acid (TBA)-reactive substances was determined during a 4-hr incubation in a complete medium under 95% O2:5% CO2 at 37 degrees C. CuOOH-treated (0.5 mM) selenium-deficient and vitamin E-deficient hepatocytes lost viability sooner than control hepatocytes. Thus, loss of selenium or vitamin E from the hepatocyte resulted in a cell more susceptible to damage by CuOOH. Phorone treatment (1.65 mM) resulted in depletion of intracellular glutathione in all three groups to approximately 20% of that in untreated hepatocytes. Cell viability and TBA-reactive substances were the same in treated and untreated hepatocytes. Thus, lowering of intracellular glutathione did not result in the spontaneous loss of cell viability or increased lipid peroxidation in selenium-deficient or in vitamin E-deficient hepatocytes. Acetaminophen appeared to be less toxic to selenium-deficient hepatocytes than to controls. This finding is in agreement with whole animal studies reported previously showing that selenium deficiency protects rats against acetaminophen hepatotoxicity. A potential explanation of this result is stimulation of glutathione synthesis by selenium deficiency. Severely vitamin E-deficient hepatocytes were protected from cell death by 12.5 and 25.0 mM acetaminophen, apparently by its antioxidant properties, while 50.0 mM acetaminophen was toxic to them. At all concentrations used, acetaminophen decreased the TBA-reactive substances present in the hepatocyte suspensions. Diquat (0.1 mM) caused more rapid cell death and higher levels of TBA-reactive substances in selenium-deficient hepatocytes than in control hepatocytes. Diquat toxicity in selenium-deficient isolated hepatocytes was not as severe as its toxicity in selenium-deficient whole animals, however.

Acetaminophen↗