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PubMed1985

Effect of various amounts of selenium on the metabolism of mercuric chloride in mice.

Male ddY mice were given one injection of (1) mercury (mercuric chloride) simultaneously with various doses of selenium (sodium selenite), (2) mercury alone, or (3) various doses of selenium alone. The interaction between mercury and selenium in the liver and kidneys at 1, 5, 24, 120, and 240 hr after administration was investigated. The concentrations of mercury in the liver of mice receiving mercury and selenium simultaneously were higher than those after administration of mercury alone, while the concentrations of mercury in the kidney decreased markedly over a 1-120 hr period after administration, depending on the dose of selenium administered simultaneously with mercury. Clearly, selenium had a different effect on the accumulation of mercury in the liver and kidneys. Subcellular distribution studies revealed that mercury and selenium which were administered simultaneously were incorporated into the crude nuclear and mitochondrial fractions as stable complexes. The transport of these complexes to the kidneys seems to be limited. In addition, gel filtration of supernatant fractions of liver and kidney through a Sephadex G-75 column indicated that the proportion of mercury bound to metallothionein fraction decreased depending on the dose of selenium administered simultaneously with the mercury. This reduction was attributed to the decreased synthesis of mercury-thionein due to a reduction in the activity of Hg2+ which results from binding between mercury and selenium in the cells.

Animals↗
PubMed1996

Effects of dietary selenium on mood in healthy men living in a metabolic research unit.

Eleven healthy men were confined in a metabolic research unit for 120 days in a double-blind study of the effects of dietary selenium on mood as assessed by the Profile of Mood States-Bipolar Form. At an intake of 2800 kcal/day, the diet of conventional foods provided 80 micrograms/day of selenium for the first 21 days, then either 13 or 356 micrograms/day for the remaining 99 days. There were no significant changes in any of the mood scales due to dietary selenium. However, in the low-selenium group, the changes in the agreeable-hostile and the elated-depressed subscales were correlated with initial erythrocyte selenium concentration; that is, the lower the initial selenium status, the more the mood scores decreased. These results suggest that persons with low selenium status might experience relatively depressed moods and support the idea that selenium plays a special role in the brain. However, these studies do not support the notion that selenium supplementation could promote improvements in mood in persons eating a typical U.S. diet.

Adult↗
PubMed1981

Properties of mercury and selenium in a high-molecular weight substance in rabbit tissues formed by simultaneous administration.

The properties of mercury and selenium existing in high-molecular weight substance(s) (HMWS) obtained from plasma, stroma-free hemolysate, soluble and insoluble fractions of the liver of rabbits dosed with mercuric chloride and selenite were studied. Analytical procedures--gel filtration, ion exchange chromatography, and sucrose density gradient ultracentrifugation--showed that equimolar amounts of mercury and selenium were present in HMWS in the blood and the liver. Dialysis against mercaptoethanol suggested that selenium and mercury were tightly bound to HMWS in the liver soluble fraction. The formation of the HMWS may contribute to reducing the toxicity of both mercury and selenium. Since mercury and selenium in HMWS in the blood and the liver were present in smaller fragments after trypsin digestion, these HMWS appeared to be protein associated with mercury and selenium. However, after exhaustive digestion with Pronase, mercury and selenium in HMWS were rendered insoluble. The above process appears to take in the body of rabbits after simultaneous administration of mercury and selenium, because the livers excised from these rabbits were found to contain iso-molar and sodium dodecyl sulfate-insoluble selenium and mercury which increased in amount with time.

Animals↗
PubMed1985

The genotoxicity of selenium.

Selenium at nutritional levels has been shown to have numerous anticarcinogenic or preventative effects against carcinogen-induced breast, colon, liver and skin cancer in animals. Many of these anticarcinogenic effects have been summarized. In addition, numerous mutagenic and antimutagenic effects of selenium compounds have been reported. Some of the selenium compounds frequently tested for mutagenicity are listed in Table 1. Because of the numerous reported anticarcinogenic and preventative effects of selenium, many individuals are supplementing their diets with amounts of selenium that are greater than the recommended daily requirement. Selenium is also used widely in industrial products such as selenium rectifiers, photoelectric batteries, alloys and paints. Because selenium at higher levels is known to be toxic, there should be a greater understanding about its genotoxic as well as its beneficial effect. The object of this review is to summarize experimental evidence both for the antimutagenic and the mutagenic effect of selenium.

Alkylation↗
PubMed1984

Effect of dietary selenium on the metabolism of aflatoxin B1 in turkeys.

To investigate the biochemical mechanism of the previously reported protective effect of dietary selenium against aflatoxin toxicity, the hepatic metabolism of aflatoxin B1 in turkey poults was examined at various dietary selenium concentrations. Diets were supplemented with 0.2, 2.0 or 4.0 ppm selenium (as sodium selenite) and 500 ng aflatoxin B1/g diet in an 18-day trial. Free and conjugated aflatoxin and metabolites were quantified using high-performance liquid chromatography. The proportion of liver aflatoxins in conjugated forms increased and the ratio of free aflatoxin B1/M1 decreased with increasing dietary selenium concentrations. These in vivo results provide evidence of selenium-induced enhancement of aflatoxin detoxification processes. In a similar experiment using 2.0 ppm selenium and 750 ng aflatoxin B1/g diet, the concentration of hepatic reduced glutathione, cytochrome P-450 and the activity of enzymes involved in the metabolism of aflatoxin B1 and glutathione were determined. Although the selenium supplement increased glutathione peroxidase activity, dietary selenium had no effect on reduced glutathione or cytochrome P-450 concentrations or on the activities of glutathione transferase E, glucuronyl transferase and cytochrome c reductase. These data indicate that the protective action of selenium is not mediated by an increase in glutathione availability for aflatoxin conjugation or by effects on the activities of these enzymes as measured in vitro.

Aflatoxin B1↗
PubMed2006

Oxidative stress on domestic ducks (Shaoxing duck) chronically exposed in a Mercury-Selenium coexisting mining area in China.

The Wanshan mercury mine is the largest mercury deposit in Guizhou Province, China. Few attempts have been made to study the toxic effects of mercury on biota in this mining area. This study was the first to investigate the oxidative stress on domestic ducks (Shaoxing duck) chronically exposed to mercury in the Wanshan mining area. Chemical analyses revealed higher concentrations of both, mercury and selenium in samples from the Wanshan area. Total mercury and selenium concentrations in duck tissues varied from 0.073 to 4.465 mg/kg and from 1.073 to 6.35 mg/kg, respectively. Analysis of covariance revealed that there were significant effects of zone on accumulation of mercury and selenium in all duck tissues (P<0.01). Moreover, analysis of covariance indicated that mercury content significantly affected the accumulation of selenium in duck muscle, brain, and liver (P<0.01). Mercury and selenium were also highly correlated in Wanshan duck liver, muscle, brain, and lung. The statistical analysis suggested that selenium might be an interactive factor in mercury toxicity. As for the biochemical analyses, it was observed that selenium-dependent glutathione peroxidase and superoxide dismutase activities and glutathione (GSH) content were significantly increased in the livers and brains of Wanshan ducks (P<0.01, 0.05). However, no significant changes were observed in malondialdehyde content (P>0.05). Although the results indicated that adaptive responses of the redox-defense system are associated with the increased enzyme activities and GSH content, the most likely explanation is that selenium plays a critical role. Therefore, the effects of the interaction environmentally occurring selenium and mercury on public health in the Wanshan area should be examined in further studies.

Animals↗
PubMed2005

Alterations in human trabecular meshwork cell homeostasis by selenium.

Epidemiological evidence indicates that selenium supplementation may increase risk for glaucoma and ocular hypertension. The purpose of this study was to determine the effects of selenium on trabecular meshwork cells, a likely site of pathology for glaucoma. Human trabecular meshwork (HTM) cells and human umbilical vein endothelial cells (HUVECs) were treated with selenium (MSeA) at or near physiologically relevant concentrations. Selenium uptake by cells was monitored using mass spectrometry. Alterations in protein secretion, intracellular signaling, and cell morphology were monitored; and the role of integrin signaling in MSeA-induced morphological alterations was investigated using divalent cation treatments. Radiolabeling was used to assess protein synthesis and secretion, while luciferase and MTT assays monitored total cellular ATP and cell viability, respectively. Whereas detectible changes in intracellular selenium were observed after exposure to 1-10 microM MSeA for 24hr, the majority remained in the conditioned medium. Selenium-induced morphological changes (< or =3 hr) occurred before alterations in protein secretion and intracellular signaling (3-6 hr). Zinc treatment prevented selenium-mediated alterations in protein secretion and changes in cell-matrix adhesion. MSeA treatment (5 microM) led to a 60% decrease in protein synthesis after 3 hr and a 30% reduction in secretion, although significant alterations in cell viability and total ATP were not observed after MSeA treatment. Selenium altered several indicators of HTM cell homeostasis, but did not affect viability at physiologically relevant doses. Similar results with HUVECs have implications for understanding selenium's mechanisms of action as an anti-angiogenic agent.

Adult↗
PubMed2005

Gestational hyperglycemia, zinc, selenium, and antioxidant vitamins.

OBJECTIVE: Lower levels of selenium and vitamin E have been described in gestational diabetes, a condition similar to type 2 diabetes, but few data are available about zinc (known to be associated with diabetes) and gestational hyperglycemia. This study evaluated the dietary intake of antioxidant vitamins, zinc, selenium, and serum levels of zinc and selenium in women with gestational hyperglycemia and normoglycemia. METHODS: A food-frequency questionnaire was administered to 504 pregnant women (210 with hyperglycemia and 294 with normoglycemia). Serum levels of zinc and selenium were analyzed during pregnancy in a second cohort of 71 hyperglycemic and 123 normoglycemic women, with a mean age and body mass index similar to those in the first cohort. RESULTS: Dietary intakes of zinc and selenium were significantly lower in hyperglycemic patients. In multiple logistic regression analysis, intakes were negatively associated with gestational hyperglycemia (odds ratios of 0.89 for zinc and 0.97 for selenium) after multiple adjustments. There were no significant differences in vitamin intakes. In the second cohort of 194 patients, serum levels of zinc and selenium were significantly lower in patients who had impaired glucose tolerance and negatively associated with gestational hyperglycemia in a multiple logistic regression model (odds ratios of 0.93 for serum zinc and 0.92 for serum selenium). CONCLUSIONS: Our data suggested a significant inverse association of dietary intakes and serum levels of zinc and selenium with gestational hyperglycemia. If future studies confirm these results, it might be a useful interventional approach to appropriate dietary counseling in order to evaluate the possible decrease in gestational metabolic abnormalities and their adverse consequences.

Adult↗
PubMed2004

Review of selenium toxicity in the aquatic food chain.

In many environmental contaminant situations selenium has become the primary element of concern because of its bioaccumulative nature in food webs. Initial concerns about selenium were related to fish kills at Belews Lake, NC, Martin Lake, TX, and Kesterson Reservoir, CA, and to bird deformities at Kesterson Reservoir. Additional concerns were identified under the National Irrigation Water Quality Program at Salton Sea, CA, Kendrick, WY, Stewart Lake, UT, and Grand Valley and Uncompahgre Valley, CO. Recent studies have raised concerns about selenium impacts on aquatic resources in Southeastern Idaho and British Columbia. The growing discomfort among the scientific community with a waterborne criterion has lead the US Environment Protection Agency to consider a tissue-based criterion for selenium. Some aquatic ecosystems have been slow to recover from selenium contamination episodes. In recent years, non-governmental researchers have been proposing relatively high selenium thresholds in diet and tissue relative to those proposed by governmental researchers. This difference in opinions is due in part to the selection of datasets and caveats in selecting scientific literature. In spite of the growing selenium literature, there are needs for additional research on neglected organisms. This review also discusses the interaction of selenium with other elements, inconsistent effects of selenium on survival and growth of fish, and differences in depuration rates and sensitivity among species.

Animals↗
PubMed1998

Enhancement of selenium excretion in bile by sulfobromophthalein: elucidation of the mechanism.

This work was intended to explore the mechanism whereby sulfobromophthalein (BSP), an electrophilic and cholephilic organic acid, increases the biliary excretion of selenium in rats injected with sodium [75Se]selenite. In such animals, neither BSP-glutathione conjugate nor dibromosulfophthalein, nonelectrophilic congeners of BSP, enhanced the hepatobiliary transport of selenium, suggesting that reaction of nucleophilic selenite metabolites formed in vivo with the injected BSP may be involved. Indeed, HPLC analysis of bile from rats receiving [75Se]selenite and BSP revealed two peaks (X and Y) that were simultaneously detected both by absorbance as BSP metabolites and by radioactivity as [75Se] metabolites, indicating that these represent selenium-containing BSP metabolites. Pretreatment of rats with inhibitors of selenium methylation, such as periodate-oxidized adenosine (PAD) and ethionine, drastically diminished the size of peak X, while increasing (PAD) or not influencing (ethionine) the size of peak Y. This finding indicates that production of metabolite X, but not Y, is dependent on formation of methylated selenium metabolites. A compound chromatographically indistinguishable from that in peak X was formed in vitro during incubation of BSP with methylselenol, suggesting that biliary metabolite X is identical to the reaction product of BSP and selenite-derived methylselenol. Incubation of BSP with selenite in the presence of a thiol, namely glutathione, cysteine or N-acetylcysteine (which convert selenite into nucleophilic products, i.e. the respective selenopersulfides and hydrogen selenide) resulted in product(s) chromatographically identical to the biliary selenium-containing BSP metabolite(s) of peak Y, irrespective of the nature of the thiol used. Thus, biliary metabolite(s) Y may be reaction products of BSP and hydrogen selenide. Finally, BSP significantly diminished exhalation of dimethyl selenide in selenite-injected rats, purportedly because it reacted with precursors of dimethyl selenide, that include hydrogen selenide and methylselenol. In summary, BSP increases biliary excretion of selenium in rats receiving selenite because it forms selenium-containing BSP metabolites that are readily transported into bile. It is suggested that the in vivo reaction of nucleophilic selenite metabolites with electrophilic compounds may influence the fate of selenium and may contribute to some of the effects of this essential and anticarcinogenic metalloid.

Animals↗
PubMed1978

Selenium in human nutrition: dietary intakes and effects of supplementation.

The dietary selenium intakes of a young couple residing in Southern California were determined to be 107 and 99 micrograms/day for the husband and the wife, respectively, on the basis of a 30 day study. For other young adult Californians, the selenium intakes were estimated from 90 to 168 micrograms/day. The highest intakes were observed in individuals subsisting on diets rich in whole wheat grain cereal products and seafoods. The selenium concentrations in whole blood of the subjects under study correlated with the dietary selenium intakes directly (P less than 0.001). The administration of 150 micrograms of selenium/day in the form of commercially available supplements increases the blood selenium concentrations. After 3 weeks of supplementation, the selenium concentrations in whole blood of our subjects reached 0.21 micrograms/ml. Prolonged supplementation at higher Se dosage levels causes further increases of the blood concentrations: Two individuals who had been ingesting 350 and 600 micrograms/day for 18 months exhibited blood selenium levels of 0.35 and 0.62 micrograms/ml. The blood selenium concentration of all subjects declined slowly after cessation of supplementation. Selenium uptake from the supplements was not affected by the joint administration of zinc supplements at 15 mg zinc/day. Glutathione peroxidase blood levels did not correlate with blood Se concentrations.

Adult↗
PubMed1997

Prevention by selenium supplementation of cyclosporin-A-induced vascular toxicity.

OBJECTIVE: The aim was to determine whether selenium supplementation, an important component of glutathione peroxidase, might attenuate cyclosporin (Cx)-induced vascular toxicity. METHODS: Four groups of rats were treated in parallel: the first group was supplemented with selenium (sodium selenite, 0.5 mg.kg-1) orally (p.o.) for 5 weeks and the same dose of selenium plus Cx 20 mg.kg-1 (i.m.) during the 6th week; group 2 received Cx only (20 mg.kg-1 i.m. for 1 week); group 3 was supplemented with selenium (0.5 mg.kg-1 p.o., for 6 weeks) and group 4 served as control. Thoracic aortas isolated from these various groups were studied in organ baths. RESULTS: In comparison with the control group, selenium supplementation did not modify acetylcholine (Ach)- and nitroprusside-induced relaxations. In group 2, endothelium-dependent relaxations (Ach) were markedly impaired and endothelium-independent relaxations (nitroprusside) were shifted to the right; with selenium supplementation (group 1), the responses to Ach were partially restored whereas the rightward shift of the concentration-response curves to nitroprusside persisted. Incubation with superoxide dismutase (SOD, 150 IU.ml-1) or selenium (1 microgram.ml-1) (but not with selenium plus an inhibitor of the glutathione redox cycle) improved the relaxations to Ach in group 2. CONCLUSIONS: The vascular toxicity of Cx seems related to generation of oxygen-derived radicals promoting EDRF destruction and is attenuated by selenium supplementation.

Acetylcholine↗
PubMed1988

Protective effects of selenium on acetaminophen-induced hepatotoxicity in the rat.

Experiments were undertaken to examine the ability of selenium to protect against acetaminophen-induced hepatotoxicity and to examine possible mechanisms for this protective effect. Pretreatment of male, Sprague-Dawley rats with sodium selenite (12.5 mumol Se/kg, ip) 24 hr prior to acetaminophen administration produced a significant protection against the hepatotoxic effects of acetaminophen as assessed by a decrease in the plasma appearance of alanine aminotransferase and aspartate aminotransferase activities following acetaminophen. This was accompanied by an increase in the hepatic glutathione levels in selenium-treated animals and an inhibition in the decrease in hepatic glutathione content observed in animals receiving hepatotoxic doses of acetaminophen. Selenium pretreatment decreased the in vivo covalent binding of acetaminophen metabolites to hepatic protein, but did not alter hepatic microsomal cytochrome P-450 content or NADPH cytochrome c reductase activity, suggesting that selenium does not significantly alter the metabolism of acetaminophen to reactive electrophilic metabolites by the cytochrome P-450-dependent mixed-function oxidase enzyme system. Selenium produced an increase in the activity of gamma-glutamylcysteine synthetase which may account for the increased glutathione availability in selenium-treated animals and increased the activities of glutathione S-transferase and glucose-6-phosphate dehydrogenase. Examination of the urinary metabolite profile in selenium-treated animals revealed that the urinary excretion of acetaminophen and its metabolites was significantly increased over a 72-hr period. The increase occurred in the AAP-glucuronide metabolite while parent AAP and AAP-sulfate were actually decreased in selenium-treated rats. No change in recovery was observed in the AAP-glutathione or AAP-mercapturate urinary metabolites. While the glutathione conjugating system is enhanced by selenium treatment, amelioration of acetaminophen toxicity is most likely the result of enhanced glucuronidation which effectively diverts the amount of acetaminophen to be converted by the cytochrome P-450 system to the toxic metabolite.

Acetaminophen↗
PubMed2002

Hazard assessment of selenium to endangered razorback suckers (Xyrauchen texanus).

A hazard assessment was conducted based on information derived from two reproduction studies conducted with endangered razorback suckers (Xyrauchen texanus) at three sites near Grand Junction, CO, USA. Selenium contamination of the upper and lower Colorado River basin has been documented in water, sediment, and biota in studies by US Department of the Interior agencies and academia. Concern has been raised that this selenium contamination may be adversely affecting endangered fish in the upper Colorado River basin. The reproduction studies with razorback suckers revealed that adults readily accumulated selenium in various tissues including eggs, and that 4.6 microg/g of selenium in food organisms caused increased mortality of larvae. The selenium hazard assessment protocol resulted in a moderate hazard at the Horsethief site and high hazards at the Adobe Creek and North Pond sites. The selenium hazard assessment was considered conservative because an on-site toxicity test with razorback sucker larvae using 4.6 microg/g selenium in zooplankton caused nearly complete mortality, in spite of the moderate hazard at Horsethief. Using the margin of uncertainty ratio also suggested a high hazard for effects on razorback suckers from selenium exposure. Both assessment approaches suggested that selenium in the upper Colorado River basin adversely affects the reproductive success of razorback suckers.

Animals↗
PubMed2002

Toxicity of selenium and other elements in food organisms to razorback sucker larvae.

Elevated selenium concentrations documented in water, sediment, and biota in irrigation drain water studies by U.S. Department of the Interior agencies and academia have raised concerns that selenium may be adversely affecting endangered fish in the upper Colorado River basin. The objective of the study was to determine the effects on endangered razorback sucker (Xyrauchen texanus) larvae from exposure to selenium and other trace elements in water and zooplankton collected from sites adjacent to the Colorado River near Grand Junction, CO. A 30-day study was initiated with 5-day-old larvae exposed in a 4 x 4 factor experiment with four food and four water treatments, and the biological endpoints measured were survival, growth, development, and whole-body residues of selenium. Mean selenium concentration in reference water (24-Road) was <0.7 microg/l, in reference food (brine shrimp) was 3.2 microg/g, at Horsethief was 1.6 microg/l in water and 6.0 microg/g in zooplankton, at Adobe Creek was 3.4 microg/l in water and 32 microg/g in zooplankton, and at Walter Walker was 13 microg/l in water and 52 microg/g in zooplankton. Although there were differences in concentrations of inorganic elements in water and biota among the three sites, selenium was apparently the only element elevated to concentrations of concern. Effects on survival were more prominent from dietary exposure compared to waterborne exposure. Selenium concentrations of >or=4.6 microg/g in food organisms adversely affected the survival of razorback sucker larvae. The onset of mortality in larvae exposed to food and water from Walter Walker seemed delayed compared to mortality in larvae exposed to food and water from Horsethief, which has been observed in two other studies. Elevated arsenic in one food source seemed to interact with selenium to reduce the toxic effects of selenium.

Animals↗
PubMed2002

Symptoms and implications of selenium toxicity in fish: the Belews Lake case example.

Belews Lake, North Carolina was contaminated by selenium in wastewater from a coal-fired power plant during the mid-1970s, and toxic impacts to the resident fish community (20 species) were studied for over two decades. Symptoms of chronic selenium poisoning in Belews Lake fish included, (1) telangiectasia (swelling) of gill lamellae; (2) elevated lymphocytes; (3) reduced hematocrit and hemoglobin (anemia); (4) corneal cataracts; (5) exopthalmus (popeye); (6) pathological alterations in liver, kidney, heart, and ovary (e.g. vacuolization of parenchymal hepatocytes, intracapillary proliferative glomerulonephritis, severe pericarditis and myocarditis, necrotic and ruptured mature egg follicles); (7) reproductive failure (reduced production of viable eggs due to ovarian pathology, and post-hatch mortality due to bioaccumulation of selenium in eggs); and (8) teratogenic deformities of the spine, head, mouth, and fins. Important principles of selenium cycling and toxicity were documented in the Belews Lake studies. Selenium poisoning in fish can be 'invisible', because, the primary point of impact is the egg, which receives selenium from the female's diet (whether consumed in organic or inorganic forms), and stores it until hatching, whereupon it is metabolized by the developing fish. If concentrations in eggs are great enough (about 10 microg/g or greater) biochemical functions may be disrupted, and teratogenic deformity and death may occur. Adult fish can survive and appear healthy despite the fact that extensive reproductive failure is occurring--19 of the 20 species in Belews Lake were eliminated as a result of this insidious mode of toxicity. Bioaccumulation in aquatic food chains causes otherwise harmless concentrations of selenium to reach toxic levels, and the selenium in contaminated sediments can be cycled into food chains for decades. The lessons learned from Belews Lake provide information useful for protecting aquatic ecosystems as new selenium issues emerge.

Abnormalities, Drug-Induced↗
PubMedDate not supplied

Selenium interactions with carcinogens.

Although selenium was once considered to be a toxic, undesirable and carcinogenic element, it is now recognized as an essential element with anticarcinogenic properties. Epidemiological studies in the United States have shown an inverse relationship between selenium intake and certain forms of cancer in humans, but other factors must be considered since cancer is not higher in people living in selenium-deficient areas of the world (Finland, New Zealand, and Keshan disease area, China). Under most dietary conditions, selenium has been shown to reduce the spontaneous mammary tumor incidence in an inbred strain of mice. In general, selenium will counteract to various degrees, the chemical carcinogens used to produce lesions of the skin [coal tar, 3-methylcholanthrene, alpha-pyrene, and 7,12 dimethylbenz(a) anthracene (DMBA)], liver (3-methyl-4-dimethyl-aminoazobenzene, aflatoxin B1, and 2-acetylaminofluorene), mammary gland (DMBA and N-methyl-N-nitrosurea), and intestinal tract [1,2-dimethylhydrazine, bis(2-oxopropyl)nitrosamine, and azoxymethane]. Dietary factors, such as fat, will modify the protective effects of selenium. High dietary unsaturated fats, for example, markedly increase the mammary tumors in rats treated with DMBA, and selenium will reduce the tumor incidence but not to the level of rats fed a low fat diet. Other factors known to affect the anticarcinogenic effects of selenium include synthetic antioxidants, vitamin E, vitamin A and ascorbic acid. The mechanisms of selenium counteraction of carcinogens remain unknown.

9,10-Dimethyl-1,2-benzanthracene↗
PubMedDate not supplied

Modification of chemical toxicity by selenium deficiency.

Selenium deficiency causes a number of hepatic metabolic alterations in the rat which could lead to changes in chemical toxicity. It causes a decrease in glutathione peroxidase activity, an increase in glutathione S-transferase activity, and an increase in the rate of glutathione synthesis. The hepatotoxicities of three compounds which bind to glutathione S-transferase; iodipamide, acetaminophen, and aflatoxin B1, are decreased by selenium deficiency. The toxicity of redox cycling compounds is generally increased by selenium deficiency and is accompanied by evidence of lipid peroxidation. Thus, nitrofurantoin (100 mg/kg) causes renal tubular necrosis in selenium-deficient rats but not in controls. Selenium-deficient rats are much more sensitive to diquat toxicity than are controls. Lethality of diquat in selenium-deficient rats appears to be causally linked to lipid peroxidation. Lethality of diquat in control rats is not linked to lipid peroxidation. The effect of selenium does not appear to be mediated by glutathione peroxidase, however, indicating that selenium has another oxidant defense function. Another interesting observation made was that increases in inspired O2 tension decreased ethane production (lipid peroxidation) in selenium-deficient and in control rats given diquat. Thus, O2 appears to prevent diquat-induced lipid peroxidation.

Acetaminophen↗