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PubMed1982

Selenium in the testis of the rat: studies on its regulation and its importance for the organism.

In male rats, fed for 10 weeks on a Torula yeast-based, low selenium and low vitamin E diet, the selenium level and the glutathione peroxidase activity in the blood and in several tissues decreased by 50 to 98% compared with animals that received the same basal diet supplemented with 0.25 mg Se/kg sodium selenite. In the testes, however, the selenium content did not differ from that of the control animals. Despite the low selenium levels in the extragonadal tissues and their increased requirement of this element due to the low vitamin E status, the selenium from an intravenously injected dose of sodium selenite was retained above all in the testes. After the removal of the pituitary gland, because of the decrease in the testicular mass and in the selenium content in the remaining testicular tissue, the amount of selenium in the testes was greatly reduced. After administration of pregnant mare's serum gonadotropin (PMS), due to the regeneration of the tissue and the simultaneous restoration of the selenium content, a relatively large amount of this element was shifted to the testes even though the selenium status in the other tissues was low. The results of these studies show that the selenium level in the male gonads is maintained by regulation mechanisms and that the supply of sufficient amounts of selenium to the testes has priority over the supply to other tissues.

Animals↗
PubMed1986

Intestinal absorption of 75Se-labeled sodium selenite and selenomethionine in chicks: effects of time, segment, selenium concentration and method of measurement.

The purpose of the present experiments was to obtain information on the intestinal transport of different selenium compounds in chicks. Absorption of selenium was studied in 3-wk-old white Leghorn cockerels both by introducing the radiolabeled selenium compounds into ligated intestinal loops of the anesthetized birds and after oral or parenteral administration of the isotope to previously fasted animals. Increasing the stable selenite concentration slightly reduced the percentage of [75Se]selenite transferred from the intestinal lumen to the body, while the transport of [75Se]selenomethionine was not similarly affected by the carrier concentration. Selenomethionine was more rapidly removed from the ligated intestinal segment and more efficiently retained after oral or parenteral administration. It was shown that the liver selenium cannot be used as an indicator of the efficiency of selenium absorption in short-term studies, since after dosing the liver accumulates sodium selenite more efficiently than selenomethionine, in spite of the greater percentage absorption of the latter compound. The percentage absorption of both selenium compounds was greatest from the duodenal segment of the small intestine. The transport of these selenium compounds does not appear to depend on the dietary level of selenium since the percentage absorption was not altered by feeding the birds diets supplemented with 0.4 or 4.0 ppm selenium prior to the measurement of absorption. The data imply that there are differences, in the chick, in the processes by which various selenium compounds are transported across the intestinal epithelium and retained in the body. The differences in absorption are not of nutritional importance, since, regardless of the chemical form, selenium is efficiently absorbed.

Administration, Oral↗
PubMed2003

Selenium supplements do not increase plasma total homocysteine concentrations in men and women.

Studies in rats indicate that plasma total homocysteine (tHcy) is decreased in selenium deficiency and increases with selenium supplementation. The aim of this study was to determine the effect of selenium supplements on plasma tHcy concentrations in a population that has suboptimal selenium status. Subjects from Dunedin, New Zealand (n = 189) were randomly assigned to receive a supplement containing 200 micro g selenium or placebo for 20 wk. At baseline, 67% (n = 112) of the participants had plasma selenium concentrations < 1.2 micro mol/L, a concentration believed to be that necessary for full glutathione peroxidase (Gpx) activity. At 20 wk, plasma selenium concentration and Gpx activity increased in the selenium group by 1.2 micro mol/L [95% confidence interval (CI): 1.1, 1.3] and 5.1 nkat/g protein (3.7, 6.5), respectively, changes that were significantly greater than the changes in the placebo group (P < 0.001). At 20 wk, mean changes in plasma tHcy concentrations were 0.1 micro mol/L (95% CI: -0.4, 0.5) and -0.2 micro mol/L (-0.7, 0.3) in the supplemented and placebo groups, respectively, compared to baseline. There was no difference in the mean changes in plasma tHcy between the supplemented and placebo groups (P = 0.54). These results suggest that selenium supplementation does not influence plasma tHcy concentrations in healthy populations in developed countries, whose selenium status is characterized by lower plasma selenium concentrations.

Adult↗
PubMed2006

Iodine deficiency mitigates growth retardation and osteopenia in selenium-deficient rats.

Selenium deficiency is associated with impaired bone metabolism and osteopenia in rats. However, it is not known how combined selenium and iodine deficiency affects bone metabolism. Therefore, we investigated the effect of selenium and iodine deficiency on bone metabolism in 2nd-generation selenium- and iodine-deficient rats. Selenium-deficient (Se-), iodine-deficient (I-), selenium- and iodine-deficient (Se-/I-), and control rats (Se+/I+), were pair-fed their respective diets until they were 74 d old. Each pair-fed rat was fed a selenium-adequate diet in the same amount as that consumed the day before by its selenium-deficient counterpart, taking food spillage into account. The skeletal phenotype was analyzed by dual energy X-ray absorptiometry, histomorphometry, and bone metabolism markers. Erythrocyte glutathione peroxidase activity (Gpx) and plasma thyroid hormones were measured to assess selenium and iodine status, respectively. In both Se-/I+ and Se-/I- rats, Gpx was reduced by 99% compared with pair-fed Se+/I+ and Se+/I- rats (P < 0.001). Iodine deficiency reduced plasma thyroxine by 64% in the 2 iodine-deficient groups (P < 0.001). Body weight, tail length, plasma insulin-like growth factor, pituitary growth hormone concentration, and femur and tibia bone mineral density were significantly greater in the Se-/I- rats than in the Se-/I+ rats. This study shows that iodine deficiency mitigated growth retardation and osteopenia in 2nd-generation selenium-deficient rats and suggests that adequate selenium status should be ensured before measures are taken to correct iodine deficiency.

Animal Feed↗
PubMed1995

Prospective study of toenail selenium levels and cancer among women.

BACKGROUND: Inverse associations between selenium status and cancer risk have been observed in animal studies, ecologic studies, and some case-control and prospective studies. Whereas results of some prospective studies have suggested an overall inverse relationship between selenium levels and cancer, other prospective studies have failed to confirm this finding. Prospective data on women are particularly limited because fewer women than men have been studied prospectively. PURPOSE: The aim of this study was to prospectively examine the relationship between selenium levels in toenails (previously shown to reflect selenium intake) and incidence of cancer among women. METHODS: The Nurses' Health Study cohort began in 1976 with 121,700 female nurses aged 30-55 years living in 11 U.S. states. In 1982, we requested toenail clippings from the members of the cohort, and 62,641 participants with no history of cancer returned these clippings. During 41 months of follow-up, 503 cases of cancer other than breast cancer (results previously reported) or nonmelanoma skin cancer were analyzed. For each case patient, a control subject was chosen from women who remained free of diagnosed cancer, matched by age and by date of nail return. RESULTS: No inverse association was observed between selenium levels in toenails and cancer risk. The age- and smoking-adjusted relative risk (RR), comparing the highest with the lowest quintile of toenail selenium level, was 1.44 (95% confidence interval [CI] = 0.97-2.13), and the trend across quintiles was marginally significant (two-sided P = .06). Comparing the highest with the lowest decile, the RR (age- and smoking-adjusted) was 1.77 (95% CI = 1.04-3.02). When these data were combined with the data from 434 breast cancer case patients and their matched control subjects identified in parallel from this same cohort, the RR comparing the highest with the lowest quintile was 1.24 (95% CI = 0.93-1.65). Toenail selenium level was not inversely associated with cancer at any major site, including uterine cancer, colorectal cancer, melanoma, ovarian cancer, or lung cancer (after adjusting for smoking); in fact, nonsignificant positive associations were observed at several sites. CONCLUSIONS: Toenail selenium levels were not inversely associated with cancer risk in this study. IMPLICATIONS: These data, in conjunction with previous findings of no association between toenail selenium status and breast cancer risk, strongly suggest that higher selenium intake within the range consumed by most U.S. women (as reflected by toenail selenium levels) is not protective against overall cancer incidence in women.

Adult↗
PubMed1990

Selenium in diet, blood, and toenails in relation to breast cancer: a case-control study.

The association between breast cancer and selenium, measured in the diet, plasma, erythrocytes, and toenails, was investigated in a case-control study in the Netherlands during 1985-1987. Dietary selenium intake was assessed by a structured dietary history technique among 133 breast cancer cases and 238 population controls. Absolute and energy-adjusted selenium intake and selenium concentrations in plasma, erythrocytes, and toenails were similar in cases and controls. The multivariate adjusted odds ratios of breast cancer for subjects in the lowest quartile compared with the highest quartile were 1.6 (95% confidence interval (CI) 0.8-3.4) for dietary selenium, 2.0 (95% CI 0.9-4.4) for plasma selenium, 0.9 (95% CI 0.4-1.9) for erythrocyte selenium, and 1.1 (95% CI 0.6-2.1) for toenail selenium. No statistically significant trend was observed in the odds ratios for any of the four indicators of selenium. These results do not suggest a substantial association between selenium and breast cancer for both short- and long-term markers of selenium status.

Adult↗
PubMed1998

Selenium deficiency in tissue culture: implications for oxidative metabolism.

BACKGROUND: Selenium is located at the catalytic site of the enzyme glutathione peroxidase, and with selenium deficiency the activity of glutathione peroxidase is decreased. Cell culture is an important tool for studying oxidative processes-that is generation and metabolism of oxygen-derived metabolites in the gastrointestinal system. Cell culture is also used to understand the mechanisms of cell injury by oxygen-derived metabolites. METHODS: To assess the importance of the selenium content of cell culture media, Caco-2 cells and the hepatoma-derived cell lines, Hep3B and HepG2, were grown to confluence and placed in media with various concentrations of selenium. After 7 to 14 days, cells were harvested and assayed for glutathione peroxidase, lactate dehydrogenase, and protein content. RESULTS: Cells maintained in media unsupplemented with selenium demonstrated a progressive decrease in glutathione peroxidase activity. Cells maintained in media supplemented with various concentrations of selenium demonstrated a dose-dependent increase in glutathione peroxidase until a plateau was reached. The plateau was reached at approximately 400 times the selenium concentration routinely used in cell culture. In the Caco-2 and hepatoma cells, no toxicity was observed at selenium supplementation five times the lowest concentration needed to reach a plateau. CONCLUSIONS: Cell culture media are routinely deficient in selenium, and cells that are cultured in this medium are deficient in glutathione peroxidase activity. Studies of oxidative metabolism based on cultures deficient in selenium may yield results that could be falsely interpreted. The addition of 1 nM selenium is sufficient for these cell lines to reach a plateau for intracellular glutathione peroxidase activity. These observations may have important ramifications for the study of reactive oxygen metabolite injury in cell culture.

Caco-2 Cells↗
PubMed1981

Metabolic and functional defects in selenium deficiency.

This paper is concerned with present-day knowledge of the biological role of selenium, of its interaction with other nutrients including trace elements, and with the importance of selenium in human nutrition and health. Selenium has been shown to be an integral part of glutathione peroxidase, which catalyses the reduction of a large range of lipid hydroperoxides and hydrogen peroxide. The interrelation between vitamin E, selenium and polyunsaturated fatty acids is complex. First, selenium in glutathione peroxidase may control intracellular levels of hydrogen peroxide, which affect the formation of active oxygen metabolites that may serve as initiators of lipid peroxidation; this role of selenium is closely related to that of superoxide dismutases, which control intracellular levels of the superoxide anion. Secondly, vitamin E may control the formation of lipid hydroperoxides through its antioxidant function, as well as possibly entering into a structural relation with membrane phospholipids. Thirdly, glutathione peroxidase may catalyse the reduction of lipid hydroperoxides, formed from membrane lipids, to hydroxyacids without detriment to the cellular economy. In the field of human nutrition, the lack of selenium has been shown to be the cause of a cardiomyopathy known as Keshan disease, occurring in the People's Republic of China. Blood selenium levels in patients from this area are compared with blood selenium levels in three other parts of the world and the conclusion is reached that the blood selenium level of populations in Keshan disease regions are exceptionally low and that Keshan disease is the first demonstration that selenium is an essential trace element for man.

Animal Nutritional Physiological Phenomena↗
PubMed1986

Selenium and other trace elements in lung tissue in smelter workers relationship to the occurrence of lung cancer.

In summary lower selenium concentrations were found in the lung cancer group compared to other smelter workers and controls. The two lowest selenium values in the total material were found in two of the lung cancer workers. This is in agreement with earlier reports of lower blood selenium levels in cancer patients (Willett et al 1983, Salonen et al 1984). An increased cancer incidence has also been found in geographical areas with low selenium contents in forage crops (Shamberger et al 1976). Numerous animal experiments have demonstrated an anticarcinogenic effect of selenium. Our conclusion is that selenium might have a protective effect in occupational exposure against at least certain carcinogens causing lung cancer. Looking at the dominant worksites the workers have obviously been exposed to different concentrations of selenium over the years. As selenium has not been particularly under observation, few dust analyses are available, and so the dust load in exposed workers cannot be directly calculated. The excretion rates show individual differences. In three of the seven lung cancer cases we noted that, despite a considerable and continuous exposure to selenium in the course of their work, they had low selenium concentrations in their lung tissue at the time of death. Two other workers in the lung cancer group had also been working at worksites with considerable exposure to selenium. Raised cadmium levels were noted in the lung cancer group.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Isolation and characterization of a selenium metabolism mutant of Salmonella typhimurium.

Selenium is a constituent in Escherichia coli of the anaerobic enzyme formate dehydrogenase in the form of selenocysteine. Selenium is also present in the tRNA of E. coli in the modified base 5-methylaminomethyl-2-selenouracil (mnm5Se2U). The pathways of bacterial selenium metabolism are largely uncharacterized, and it is unclear whether nonspecific reactions in the sulfur metabolic pathways may be involved. We demonstrated that sulfur metabolic pathway mutants retain a wild-type pattern of selenium incorporation, indicating that selenite (SeO32-) is metabolized entirely via selenium-specific pathways. To investigate the function of mnm5Se2U, we isolated a mutant which is unable to incorporate selenium into tRNA. This strain was obtained by isolating mutants lacking formate dehydrogenase activity and then screening for the inability to metabolize selenium. This phenotype is the result of a recessive mutation which appears to map in the general region of 21 min on the Salmonella typhimurium chromosome. A mutation in this gene, selA, thus has a pleiotropic effect of eliminating selenium incorporation into both protein and tRNA. The selA mutant appears to be blocked in a step of selenium metabolism after reduction, such as in the actual selenium insertion process. We showed that the absence of selenium incorporation into suppressor tRNA reduces the efficiency of suppression of nonsense codons in certain contexts and when wobble base pairing is required. Thus, one function of mnm5Se2U in tRNA may be in codon-anticodon interactions.

Chromatography, High Pressure Liquid↗
PubMed2006

Selenium, apoptosis, and colorectal adenomas.

BACKGROUND: Selenium is an essential trace element found in cereals, wheat, dairy products, meat, and fish. This micronutrient may prevent carcinogenesis through several biochemical pathways; one suggested pathway is enhanced apoptosis. OBJECTIVES: The relation between selenium and colorectal adenomas was evaluated because the colorectal adenoma is the established precursor lesion of most colorectal cancers. Apoptosis was a pathway of interest because decreased apoptosis has been associated with an increased prevalence of adenomas. Our objectives were as follows: to investigate the association between (a) selenium and colorectal adenomas and (b) selenium and apoptosis. METHODS: The study population was assembled for the Diet and Health Study III (n = 803), a cross-sectional study conducted at the University of North Carolina Hospital (Chapel Hill, NC). There were 451 participants in the analysis of selenium and adenoma prevalence and 351 participants in the analysis of selenium and apoptosis. Selenium was measured from serum collected at the time of colonoscopy. Apoptosis was measured in biopsies from normal rectal epithelium obtained during the colonoscopy procedure. RESULTS: Participants in the highest fifth of serum selenium were less likely to have adenomas in comparison with those in the lowest fifth (prevalence ratio, 0.6; 95% confidence interval, 0.4-1.1). Selenium and apoptosis (>2.76 cells per crypt) were not strongly related, but results collectively suggested a roughly inverse association. CONCLUSIONS: High selenium was associated with a reduced prevalence of colorectal adenomas. Apoptosis, however, did not seem to be the mechanism by which selenium was related to adenoma prevalence in our data.

Adenoma↗
PubMed2004

Selective modulation of the therapeutic efficacy of anticancer drugs by selenium containing compounds against human tumor xenografts.

PURPOSE: Studies were carried out in athymic nude mice bearing human squamous cell carcinoma of the head and neck (FaDu and A253) and colon carcinoma (HCT-8 and HT-29) xenografts to evaluate the potential role of selenium-containing compounds as selective modulators of the toxicity and antitumor activity of selected anticancer drugs with particular emphasis on irinotecan, a topoisomerase I poison. EXPERIMENTAL DESIGN: Antitumor activity and toxicity were evaluated using nontoxic doses (0.2 mg/mouse/day) and schedule (14-28 days) of the selenium-containing compounds, 5-methylselenocysteine and seleno-L-methionine, administered orally to nude mice daily for 7 days before i.v. administration of anticancer drugs, with continued selenium treatment for 7-21 days, depending on anticancer drugs under evaluation. Several doses of anticancer drugs were used, including the maximum tolerated dose (MTD) and toxic doses. Although many chemotherapeutic agents were evaluated for toxicity protection by selenium, data on antitumor activity were primarily obtained using the MTD, 2 x MTD, and 3 x MTD of weekly x4 schedule of irinotecan. RESULTS: Selenium was highly protective against toxicity induced by a variety of chemotherapeutic agents. Furthermore, selenium increased significantly the cure rate of xenografts bearing human tumors that are sensitive (HCT-8 and FaDu) and resistant (HT-29 and A253) to irinotecan. The high cure rate (100%) was achieved in nude mice bearing HCT-8 and FaDu xenografts treated with the MTD of irinotecan (100 mg/kg/week x 4) when combined with selenium. Administration of higher doses of irinotecan (200 and 300 mg/kg/week x 4) was required to achieve high cure rate for HT-29 and A253 xenografts. Administration of these higher doses was possible due to selective protection of normal tissues by selenium. Thus, the use of selenium as selective modulator of the therapeutic efficacy of anticancer drugs is new and novel. CONCLUSIONS: We demonstrated that selenium is a highly effective modulator of the therapeutic efficacy and selectivity of anticancer drugs in nude mice bearing human tumor xenografts of colon carcinoma and squamous cell carcinoma of the head and neck. The observed in vivo synergic interaction is highly dependent on the schedule of selenium.

Administration, Oral↗
PubMed2006

Differential effects of dietary selenium (se) and folate on methyl metabolism in liver and colon of rats.

A previous study compared the effects of folate on methyl metabolism in colon and liver of rats fed a selenium-deficient diet (< 3 microg Se/kg) to those of rats fed a diet containing supranutritional Se (2 mg selenite/kg). The purpose of this study was to investigate the effects of folate and adequate Se (0.2 mg/kg) on methyl metabolism in colon and liver. Weanling, Fischer-344 rats (n = 8/diet) were fed diets containing 0 or 0.2 mg selenium (as selenite)/kg and 0 or 2 mg folic acid/kg in a 2 x 2 design. After 70 d, plasma homocysteine was increased (p < 0.0001) by folate deficiency; this increase was markedly attenuated (p < 0.0001) in rats fed the selenium-deficient diet compared to those fed 0.2 mg Se/kg. The activity of hepatic glycine N-methyltransferase (GNMT), an enzyme involved in the regulation of tissue S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH), was increased by folate deficiency (p < 0.006) and decreased by selenium deprivation (p < 0.0003). Colon and liver SAH were highest (p < 0.006) in rats fed deficient folate and adequate selenium. Although folate deficiency decreased liver SAM (p < 0.001), it had no effect on colon SAM. Global DNA methylation was decreased (p<0.04) by selenium deficiency in colon but not liver; folate had no effect. Selenium deficiency did not affect DNA methyltransferase (Dnmt) activity in liver but tended to decrease (p < 0.06) the activity of the enzyme in the colon. Dietary folate did not affect liver or colon Dnmt. These results in rats fed adequate selenium are similar to previous results found in rats fed supranutritional selenium. This suggests that selenium deficiency appears to be a more important modifier of methyl metabolism than either adequate or supplemental selenium.

Animals↗
PubMed2001

The effects of dietary selenium on the immune system in healthy men.

Eleven men were fed foods naturally high or low in selenium for 120 d. Selenium intake was stabilized at 47 microg/d for 21 d, then changed to either 13 or 297 microg/d for 99 d, leading to significantly different blood selenium and glutathione peroxidase concentrations. Serum immunoglobulins, complement components, and primary antibody responses to influenza vaccine were unchanged. Antibody titers against diphtheria vaccine were 2.5-fold greater after reinoculation in the high selenium group. White blood cell counts decreased in the high-selenium group and increased in the low-selenium group, resulting primarily from changes in granulocytes. Apparent increases in cytotoxic T-lymphocytes and activated T-cells in the high-selenium group only approached statistical significance. Lymphocyte counts increased on d 45 in the high-selenium group. In vitro proliferation of peripheral lymphocytes in autologous serum in response to pokeweed mitogen was stimulated in the high-selenium group by d 45 and remained elevated throughout the study, whereas proliferation in the low selenium group did not increase until d 100. This study indicates that the immune-enhancing properties of selenium in humans are the result, at least in part, of improved activation and proliferation of B-lymphocytes and perhaps enhanced T-cell function.

Cell Division↗
PubMed2004

Derivation of a chronic site-specific water quality standard for selenium in the Great Salt Lake, Utah, USA.

The purpose of this study was to develop a site-specific water quality standard for selenium in the Great Salt Lake, Utah, USA. The study examined the bioavailability and toxicity of selenium, as selenate, to biota resident to the Great Salt Lake and the potential for dietary selenium exposure to aquatic dependent birds that might consume resident biota. Because of its high salinity, the lake has limited biological diversity with bacteria, algae, diatoms, brine shrimp, and brine flies being the only organisms present in the main (hypersaline) portions of the lake. To evaluate their sensitivity to selenium, a series of acute and chronic toxicity studies were conducted on brine shrimp (Artemia franiciscana), brine fly (Ephydra cinerea), and a hypersaline alga (Dunaliella viridis). The resulting acute and chronic toxicity data indicated that resident species are more selenium tolerant than many freshwater species. Because sulfate is known to reduce selenate bioavailability, this selenium tolerance is thought to result in part from the lake's high ambient sulfate concentrations (>5,800 mg/L). The acute and chronic test results were compared to selenium concentrations expected to occur in a mining effluent discharge located at the south end of the lake. Based on these comparisons, no appreciable risks to resident aquatic biota were projected. Field and laboratory data collected on selenium bioaccumulation in brine shrimp demonstrated a linear relationship between water and tissue selenium concentrations. Applying a dietary selenium threshold of 5 mg/kg dry weight for aquatic birds to this relationship resulted in an estimate of 27 microg/L Se in water as a safe concentration for this exposure pathway and an appropriate chronic site-specific water quality standard. Consequently, protection of aquatic birds represents the driving factor in determining a site-specific water quality standard for selenium.

Animals↗
PubMed2005

Evaluation of the respiratory elimination kinetics of selenium after oral administration in sheep.

OBJECTIVE: To evaluate the respiratory excretion and elimination kinetics of organic and inorganic selenium after oral administration in sheep. ANIMALS: 38 crossbred sheep. PROCEDURES: Selenium was administered PO to sheep as a single dose of 0, 1, 2, 3, or 4 mg/kg as sodium selenite or selenomethionine. Expired air was collected and analyzed from all sheep at 4, 8, and 16 hours after administration. RESULTS: Clinical signs consistent with selenium intoxication were seen in treatment groups given sodium selenite but not in treatment groups given the equivalent amount of selenium as selenomethionine. However, a distinct garlic-like odor was evident in the breath of all sheep receiving 2 to 4 mg of selenium/kg. The intensity of odor in the breath did not correlate with clinical signs in affected animals receiving sodium selenite treatment. CONCLUSIONS AND CLINICAL RELEVANCE: The concentration of selenium in expired air was greater in sheep receiving selenium as selenomethionine than sodium selenite. The concentration of selenium in expired air from sheep receiving high doses of selenium (3 and 4 mg of selenium/kg) was larger and selenium was expired for a longer duration than the concentration of selenium in expired air from sheep receiving low doses of selenium (1 and 2 mg of selenium/kg).

Administration, Oral↗
PubMedDate not supplied

Effect of selenium in combination with Adriamycin or Taxol on several different cancer cells.

The anti-neoplastic properties of an Selenium compound were studied in vitro on several tumor cell lines: Breast (MCF-7, MCF-10, SKBR-3, BCAP37), Lung (RH2), Prostate (LNCap and PC-3), Colon (T84, Caco-2), Small Intestine (HCF8), and Liver (HepG2). We also examined additive or synergistic effect of Selenium in combination with standard anti-cancer drugs, Adriamycin (Doxorubicin) and Taxol. The effect of Selenium was assessed by apoptosis; DNA synthesis; growth rate by MTT assay; uptake of amino acid MeAIB by System A; and morphological changes. Our results demonstrate that MCF-7 and SKBR-3 showed increase in apoptosis as measured by DNA fragmentation and increase in "rounded" cells and membrane "blebbing", decrease in MeAIB uptake, and decrease in DNA synthesis. These changes were Selenium dose dependent with optimal inhibition at Selenium concentration between 4 and 40 ng/ml after 72 hrs of treatment. Similar observations were made with RH2, HCF8, Caco-2, and HepG2 cells. In contrast, LNCap, PC-3, and T-84 were not significantly affected by Selenium. However, addition of Adriamycin or Taxol in combination with Selenium caused small but significant inhibition of prostate cancer cells LNCap and PC-3. Addition of chemotherapeutic agents either Taxol or Doxorubicin with Selenium caused further inhibition of MCF-7, SKBR-3, RH2, HCF8, and HepG2 cells. In conclusion, Selenium has a significant anti-neoplastic effect on breast, lung, liver, and small intestinal tumor cells. Supplementation of Selenium enhanced chemotherapeutic effect of Taxol and Doxorubicin in these cells beyond that seen with the chemotherapeutic drugs used alone. These in vitro studies on several cancer cell lines suggest a potential benefit of Selenium-enhancement of anticancer effects other systems, and therefore offer further relevance to clinical trials efforts.

Amino Acids↗
PubMed2003

Acquired tolerance of hepatocellular carcinoma cells to selenium deficiency: a selective survival mechanism?

Selenium is essential to human health, and its deficiency is associated with different diseases including liver necrosis. Selenium is protective against viral hepatitis and hepatocellular carcinoma (HCC). The underlying molecular mechanisms of selenium effects are not well known. In this study, in vitro response of HCC-derived cell lines to selenium deficiency is examined alone or in conjunction with Vitamin E and copper/zinc. Here, we show that in vitro selenium deficiency in a subset of HCC-derived cell lines causes oxidative stress and cytochrome c release with subsequent cell death by apoptosis. The oxidative stress and consequent cell death induced by selenium deficiency on these cells are reverted by the antioxidant effect of Vitamin E. However, most HCC cell lines (10 of 13) tolerate selenium deficiency. Consequently, they escape apoptosis. Moreover, nine of these tolerant cell lines have integrated hepatitis B Virus (HBV) DNA in their genomes, and some display p53-249 mutation, indicating past exposure to HBV or aflatoxins, established factors for oxidative stress and cancer risk in liver. An HBV-transfected clone (2.2.15) of the sensitive HepG2 cell line has gained tolerance to selenium deficiency. Our findings indicate that selenium deficiency induces apoptosis in some "hepatocyte-like" cells. However, most HCC cells, particularly HBV-related ones, tolerate selenium deficiency and escape its deadly consequences. Thus, as demonstrated by the gain of survival capacity of apoptosis-sensitive cell lines with Vitamin E, such malignant cells have acquired a selective survival advantage that is prominent under selenium-deficient and oxidative-stress conditions.

Adaptation, Physiological↗