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. 2020 Mar 24;12(3):865.
doi: 10.3390/nu12030865.

Micronutrients Selenomethionine and Selenocysteine Modulate the Redox Status of MCF-7 Breast Cancer Cells

Daniel Gabriel Pons  1   2 , Carmen Moran  1 , Marina Alorda-Clara  1   2 , Jordi Oliver  1   2   3 , Pilar Roca  1   2   3 , Jorge Sastre-Serra  1   2   3
Affiliations

Micronutrients Selenomethionine and Selenocysteine Modulate the Redox Status of MCF-7 Breast Cancer Cells

Daniel Gabriel Pons et al. Nutrients. .

Abstract

Selenium is a micronutrient which is found in many foods, with redox status modulation activity. Our aim was to evaluate the effects of two chemical forms of selenoamino acids, Seleno-L-methionine and Seleno-L-cystine (a diselenide derived from selenocysteine), at different concentrations on cell viability, hydrogen peroxide production, antioxidant enzymes, UCP2 protein expression, as well as lipid and protein oxidative damage in MCF-7 breast cancer cells. Results showed that Seleno-L-methionine did not cause an increase in hydrogen peroxide production at relatively low concentrations, accompanied by a rise in the antioxidant enzymes catalase and MnSOD, and UCP2 protein expression levels. Furthermore, a decrease in protein and lipid oxidative damage was observed at 10 µM concentration. Otherwise, Seleno-L-cystine increased hydrogen peroxide production from relatively low concentrations (100 nM) to a large increase at high concentrations. Moreover, at 10 µM, Seleno-L-cystine decreased UCP2 and MnSOD protein expression. In conclusion, the chemical form of selenoamino acid and their incorporation to selenoproteins could affect the regulation of the breast cancer cell redox status. Taken together, the results obtained in this study imply that it is important to control the type of selenium-enriched nutrient consumption, taking into consideration their composition and concentration.

Keywords: antioxidant enzymes; oxidative damage; oxidative stress; selenocysteine; selenomethionine; ucp2.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Cell viability and hydrogen peroxide production in MCF-7 breast cancer cells after selenomethionine or selenocystine treatment. (A) The cells were treated with vehicle or with increasing concentrations of selenomethionine (from 1 nM to 1 mM) for 48 h. (B) The cells were treated with vehicle (data not shown) or with increasing concentrations of selenocystine (from 100 pM to 50 µM) for 48 h. Solid line represents the cell viability and pointed line represents hydrogen peroxide production. Points in lines represent means and error bars represent SEM (n = 6). The value of control cells was set at 100% (data not shown) and the rest of values were calculated referenced to the control set at 100%. * Significant differences between selenoamino acid treated and control cells (Student’s t-test; p ≤ 0.05). # Significant differences between selenoamino acid treated and control cells (Student’s t-test; p ≤ 0.1). AU: Arbitrary Units.
Figure 2
Figure 2
Antioxidant enzymes and UCP2 protein levels in MCF-7 breast cancer cell lines after treatment with selenoamino acids at 10 nM and 10 μM. The cells were treated with vehicle (clear grey bars), selenoamino acid at 10 nM (dark grey bars) or selenoamino acid at 10 μM (black bars) for 48 h. (A) Manganese Superoxide Dismutase (MnSOD). (B) Copper-Zinc Superoxide Dismutase (CuZnSOD). (C) Catalase. (D) Uncoupling protein 2 (UCP2). The proteins levels were measured by Western Blot. Bars represent means and error bars represent SEM (n = 6). The value of control cells was set at 100% and the rest of values were calculated referenced to the control set at 100%. * Significant differences between selenoamino acid treated and control cells (Student’s t-test; p ≤ 0.05). # Significant differences between selenoamino acid treated and control cells (Student’s t-test; p ≤ 0.1). AU: Arbitrary Units.
Figure 3
Figure 3
Western blot cropped representative bands of (A) selenomethione-treated and (B) selenocystine-treated MCF-7 breast cancer cell line are shown.
Figure 4
Figure 4
Protein and lipid oxidative damage in MCF-7 breast cancer cell lines after treatment with selenoamino acids at 10 nM and 10 μM. The cells were treated with vehicle (clear grey bars), selenoamino acid at 10 nM (dark grey bars) or selenoamino acid at 10 μM (black bars) for 48h. (A) Protein carbonyl groups formation. (B) 4-Hydroxy-2Nonenal adducts formation (4-HNE). Bars represent means and error bars represent SEM (n = 6). The value of control cells was set at 100% and the rest of values were calculated referenced to the control set at 100%. * Significant differences between selenoamino acid treated and control cells (Student’s t-test; p ≤ 0.05). AU: Arbitrary Units.
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