Toxicity of nutritionally available selenium compounds in primary and transformed hepatocytes

Weiller, Markus; Latta, Markus; Kresse, Matthias; Lucas, Rudolf; Wendel, Albrecht

doi:10.1016/j.tox.2004.03.026

Cited by 58 publications

(27 citation statements)

References 34 publications

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“…Previous studies have suggested that high doses of sodium selenite were able to induce apoptosis in primary hepatocytes and normal keratinocytes [20,21]. Our study shows that apoptotic splenocytes increase with increasing the Se content of the feed.…”

Section: Discussionsupporting

confidence: 65%

Excess Dietary Sodium Selenite Alters Apoptotic Population and Oxidative Stress Markers of Spleens in Broilers

Peng

Cui

et al. 2011

Biol Trace Elem Res

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Three hundred 1-day-old avian broilers were fed on a basic diet (0.2 mg/kg selenium) or the same diet amended to contain 1, 5, 10, and 15 mg/kg selenium supplied as sodium selenite (n = 60/group). In comparison with those of 0.2 mg/kg selenium group, the percentages of annexin V-positive splenocytes were increased in 5, 10, and 15 mg/kg selenium groups. TUNEL assay revealed that apoptotic cells with brown-stained nuclei distributed within the red pulp and white pulp of the spleens with increased frequency of occurrence in 10 and 15 mg/kg selenium groups in comparison with that of 0.2 mg/kg Se group. Sodium selenite-induced oxidative stress in spleens of chickens was evidenced by decrease in glutathione peroxidase, superoxide dismutase, and catalase activities and increase in malondialdehyde contents. The results indicate that excess dietary selenium in the range of 5-15 mg/kg of feed causes oxidative stress, which may be mainly responsible for the increased apoptosis of splenocytes in chickens.

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Section: Discussionsupporting

confidence: 65%

Excess Dietary Sodium Selenite Alters Apoptotic Population and Oxidative Stress Markers of Spleens in Broilers

Peng

Cui

et al. 2011

Biol Trace Elem Res

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“…A great variability of results were reported on the SeMet dose necessary to elicit toxicity in cultured cells, with IC 50 values ranging from a few μm to tenths of mm, depending on the cell type, culture conditions and type of assay (129,130). Such a disparity may be partly explained by the strong inverse dependency of SeMet toxicity on the methionine concentration in the growth medium of yeast or mammalian cell cultures (113,131).…”

Section: Selenomethionine Toxicitymentioning

confidence: 99%

Recent advances in the mechanism of selenoamino acids toxicity in eukaryotic cells

Lazard

Dauplais

Blanquet

et al. 2017

Biomolecular Concepts

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Selenium is an essential trace element due to its incorporation into selenoproteins with important biological functions. However, at high doses it is toxic. Selenium toxicity is generally attributed to the induction of oxidative stress. However, it has become apparent that the mode of action of seleno-compounds varies, depending on its chemical form and speciation. Recent studies in various eukaryotic systems, in particular the model organism Saccharomyces cerevisiae, provide new insights on the cytotoxic mechanisms of selenomethionine and selenocysteine. This review first summarizes current knowledge on reactive oxygen species (ROS)-induced genotoxicity of inorganic selenium species. Then, we discuss recent advances on our understanding of the molecular mechanisms of selenocysteine and selenomethionine cytotoxicity. We present evidences indicating that both oxidative stress and ROSindependent mechanisms contribute to selenoamino acids cytotoxicity. These latter mechanisms include disruption of protein homeostasis by selenocysteine misincorporation in proteins and/or reaction of selenols with protein thiols.

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“…[89][90][91][92] Indeed, the cytotoxic effects of both inorganic and organic Se compounds were more potent in normal hepatocytes as compared with hepatic carcinoma cells, and nontumorigenic prostate cells are highly sensitive to Se toxicity as compared with prostate cancer cells at physiologically relevant concentrations. 93,94 For Se-induced cytotoxicity to be able to operate as a chemopreventive mechanism, Se toxicity would appear to be unavoidable. Therefore, Se-dependent selenoproteins and Se-induced phase II enzyme mechanisms, which are not associated with evoked toxicity, become more attractive to explain the cancerpreventive effects of Se, whereas the "enhanced cytotoxicity" mechanism ought to be limited to Se-sensitive cancer cells whose proliferation can be effectively suppressed by Se at safe doses.…”

Section: Se-mediated Cytotoxicity and Cancer Preventionmentioning

confidence: 99%

Encapsulated nanoepigallocatechin-3-gallate and elemental selenium nanoparticles as paradigms for nanochemoprevention

Zhang¹

2012

IJN

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Chemoprevention that impedes one or more steps in carcinogenesis, via long-term administration of naturally occurring or synthetic compounds, is widely considered to be a crucial strategy for cancer control. Selenium (Se) has chemopreventive effects, but its application is limited due to a low therapeutic index as shown in numerous animal experiments. In contrast to Se, which was known for its toxicity prior to the discovery of its beneficial effects, the natural compound epigallocatechin-3-gallate (EGCG) was originally considered to be nontoxic. Due to its preventive effects on many types of cancer in various animal models, EGCG has been regarded as a prime example of a promising chemopreventive agent without major toxicity concerns. However, very recently, evidence has accumulated showing that efficacious doses of EGCG used in health promotion may not be far from its toxic dose level. Therefore, both Se and EGCG need to be modified by novel pharmaceutical technologies to attain enhanced efficacy and/or reduced toxicity. Nanotechnology may be one of these technologies. In support of this hypothesis, the characteristics of polylactic acid and polyethylene glycol-encapsulated nano-EGCG and elemental Se nanoparticles dispersed by bovine serum albumin are reviewed in this article. Encapsulation of EGCG to form nano-EGCG leads to its enhanced stability in plasma and remarkably superior chemopreventive effects, with more than tenfold dose advantages in inducing apoptosis and inhibition of both angiogenesis and tumor growth. Se at nanoparticle size ("Nano-Se"), compared with Se compounds commonly used in dietary supplements, has significantly lower toxicity, without compromising its ability to upregulate selenoenzymes at nutritional levels and induce phase II enzymes at supranutritional levels.

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Toxicity of nutritionally available selenium compounds in primary and transformed hepatocytes

Cited by 58 publications

References 34 publications

Excess Dietary Sodium Selenite Alters Apoptotic Population and Oxidative Stress Markers of Spleens in Broilers

Excess Dietary Sodium Selenite Alters Apoptotic Population and Oxidative Stress Markers of Spleens in Broilers

Recent advances in the mechanism of selenoamino acids toxicity in eukaryotic cells

Encapsulated nanoepigallocatechin-3-gallate and elemental selenium nanoparticles as paradigms for nanochemoprevention

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