Selenium (sodium selenite) causes cytotoxicity and apoptotic mediated cell death in PLHC-1 fish cell line through DNA and mitochondrial membrane potential damage

Selvaraj, Vellaisamy; Tomblin, Justin; Armistead, Mindy Yeager; Murray, Elizabeth E.

doi:10.1016/j.ecoenv.2012.09.028

Cited by 50 publications

(24 citation statements)

References 36 publications

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“…Specifically, Se and/or converted forms of Se induce oxidative stress and apoptosis (Palace et al, 2004;Selvaraj et al, 2013). Regarding Se-induced apoptosis, Se has been shown to significantly upregulate ROS production and the activity of caspase 3 in vitro in the fish cell line PLHC-1 (Selvaraj et al, 2013).…”

Section: Case Study 3: Selenium-induced Fish Embryo Toxicitymentioning

confidence: 99%

Significance of adverse outcome pathways in biomarker-based environmental risk assessment in aquatic organisms

Lee

Won

Raisuddin

et al. 2015

Journal of Environmental Sciences

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Section: Case Study 3: Selenium-induced Fish Embryo Toxicitymentioning

confidence: 99%

Significance of adverse outcome pathways in biomarker-based environmental risk assessment in aquatic organisms

Lee

Won

Raisuddin

et al. 2015

Journal of Environmental Sciences

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“…In the present study, Se toxicity is manifested in ROS overproduction, with apoptosis acting to eliminate the critically damaged cells. Similarly, Selvaraj et al (2013) have demonstrated that high level of Se exposure induces mitochondrial membrane potential damage, DNA damage and Fish Physiol Biochem elevated production of ROS-induced Poeciliopsis lucida hepatoma cell death. The peroxidation of membrane lipids due to ROS insult also increased with increasing selenomethionine (SeMet) exposure in isolated hepatocytes of rainbow trout (Misra et al 2012), and the peak of activity for generating superoxide from SeMet occurs after early liver development in the embryos of this fish (Palace et al 2004).…”

Section: Discussionmentioning

confidence: 97%

“…Not only can Se itself trigger a generation of ROS, but ROS are also generated intracellularly via the mitochondrial pathway of apoptosis when mitochondrial membranes are damaged (Selvaraj et al 2013). There are three main ways in which Se results in toxicity: the excess amount of Se can form CH 3 Se-, which enters a redox cycle, generates superoxide and oxidative stress, or forms free radicals (Spallholz and Hoffman 2002); selenocysteine as a result of excess Se inhibits the Se methylation metabolism and may cause other Serelated adverse effects (Spallholz and Hoffman 2002); in particular, Se can disrupt proteins via substituting as sulphur in sulphur bonds, resulting in incorrect protein shape, dysfunctional enzymes and impairment of normal cellular biochemistry (Lemly 2002;Spallholz and Hoffman 2002).…”

Section: Discussionmentioning

confidence: 99%

“…Heavy metals such as cadmium, copper, arsenic, silver and zinc are known inducers of apoptosis (Faverney et al 2001;Gao et al 2013;. Although Seinduced apoptosis has been described in poeciliopsis lucida and rainbow trout (Misra and Niyogi 2009;Misra et al 2012;Selvaraj et al 2013), there is little information on Se-induced apoptosis in aquatic animals. Oxidative stress has been linked to apoptosis in various systems.…”

Section: Introductionmentioning

confidence: 96%

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Deficient and excess dietary selenium levels affect growth performance, blood cells apoptosis and liver HSP70 expression in juvenile yellow catfish Pelteobagrus fulvidraco

Huang

Wang

et al. 2015

Fish Physiol Biochem

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We investigated the effects of deficient and excess dietary selenium (Se) on growth, blood cells apoptosis and liver heat shock protein 70 (HSP70) expression in juvenile yellow catfish (Pelteobagrus fulvidraco). After 8 weeks, yellow catfish (initial weight: 2.12 ± 0.01 g) fed isonitrogenous and isolipid diets containing <0.05 (deficient dietary Se) or 6.5 (excess dietary Se) mg Se/kg displayed a significantly lower weight gain ratio (WGR) than those fed a diet containing 0.23 (normal dietary Se) mg Se/kg. As dietary Se levels increased, liver Se concentration, glutathione peroxidase activity and the hepatosomatic index increased significantly. Plasma glucose concentration was highest in the normal treatment compared with the excess dietary Se treatment. Both deficient and excess dietary Se lead to increased reactive oxygen species (ROS) production and apoptosis ratio in blood cells, whereas only excess dietary Se increased their cytoplasmic free-Ca(2+) (CF-Ca(2+)) concentration. Excess dietary Se also resulted in the highest level of HSP70 expression, thereby possibly providing a protective mechanism against oxidative stress. These results indicate that both deficient and excess dietary Se restrained the growth of juvenile yellow catfish and caused oxidative stress. The overproduction of ROS may act as a signal molecule mediate apoptosis when dietary Se deficiency. Both ROS and CF-Ca(2+) were recorded when dietary Se excess, suggesting that Ca(2+) may be activated by Se and play a major role during Se-induced oxidative stress and cell apoptosis.

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“…In animal and yeast cells, selenite has been shown to induce ROS-dependent DNA strand breaks and/or base oxidation that lead to cell death by apoptosis or necrosis (30,(79)(80)(81)(82)(83)(84). It is likely that reduction of selenite into hydrogen selenide in vivo ( Figure 2D) (85)(86)(87), followed by redox cycling of selenide in the presence of oxygen and thiols (Figure 2A), accounts for selenite-induced DNA damage.…”

Section: Selenite/selenide 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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Selenium (sodium selenite) causes cytotoxicity and apoptotic mediated cell death in PLHC-1 fish cell line through DNA and mitochondrial membrane potential damage

Cited by 50 publications

References 36 publications

Significance of adverse outcome pathways in biomarker-based environmental risk assessment in aquatic organisms

Significance of adverse outcome pathways in biomarker-based environmental risk assessment in aquatic organisms

Deficient and excess dietary selenium levels affect growth performance, blood cells apoptosis and liver HSP70 expression in juvenile yellow catfish Pelteobagrus fulvidraco

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

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