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Sodium selenite supplementation does not fully restore oxidative stress-induced deiodinase dysfunction: Implications for the nonthyroidal illness syndrome.

Wajner SM, Rohenkohl HC, Serrano T, Maia AL - Redox Biol (2015)

Bottom Line: Increased ROS was paralleled by D1 and D2-decreased T3-production (P<0.01) and increased D3-catalyzed T3-inactivation (P<0.001).Selenite decreases the IL6-induced ROS and carbonyl content, while enhances Gpx and Trx activities.In conclusion, although sodium selenite reduces IL6-induced redox imbalance it does not fully repair deiodinase function.

View Article: PubMed Central - PubMed

Affiliation: Thyroid Section, Endocrine Division, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.

No MeSH data available.


Related in: MedlinePlus

Effect of sodium selenite on type 2 deiodinase activity and expression. Sodium selenite does not reverse the inhibitory effect of interleukin IL6 on deiodinase type 2 (D2)-catalyzed T4-to-T3 conversion in endogenous D2 expressing MSTO-211 cells, as observed in the presence of N-acetylcysteine (NAC) (A). The IL6-induced increases on DIO2 mRNA levels in MSTO-211 cells is not reverted by sodium selenite or NAC (B). *P<0.001, difference between controls and IL6 treated cells; §P<0.001, difference between controls in the presence or not of sodium selenite. Data are mean±SD of at least three independent experiments. The net iodide release in this system is specific and equivalent to T3 production.
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f0015: Effect of sodium selenite on type 2 deiodinase activity and expression. Sodium selenite does not reverse the inhibitory effect of interleukin IL6 on deiodinase type 2 (D2)-catalyzed T4-to-T3 conversion in endogenous D2 expressing MSTO-211 cells, as observed in the presence of N-acetylcysteine (NAC) (A). The IL6-induced increases on DIO2 mRNA levels in MSTO-211 cells is not reverted by sodium selenite or NAC (B). *P<0.001, difference between controls and IL6 treated cells; §P<0.001, difference between controls in the presence or not of sodium selenite. Data are mean±SD of at least three independent experiments. The net iodide release in this system is specific and equivalent to T3 production.

Mentions: The conversion of T4-to-T3 by D2 decreases in the presence of increased levels of IL6 (Fig. 3A). The addition of sodium selenite to the culture media slightly increased T4-to-T3 conversion in control cells but failed to prevent the IL6 induced dose-dependent D2 inhibition, as observed with NAC addition (P<0.001; Fig. 3A). Pretreatment with sodium selenite or NAC did not prevent the IL6-induced increase in the levels of DIO2 mRNA (Fig. 3B).


Sodium selenite supplementation does not fully restore oxidative stress-induced deiodinase dysfunction: Implications for the nonthyroidal illness syndrome.

Wajner SM, Rohenkohl HC, Serrano T, Maia AL - Redox Biol (2015)

Effect of sodium selenite on type 2 deiodinase activity and expression. Sodium selenite does not reverse the inhibitory effect of interleukin IL6 on deiodinase type 2 (D2)-catalyzed T4-to-T3 conversion in endogenous D2 expressing MSTO-211 cells, as observed in the presence of N-acetylcysteine (NAC) (A). The IL6-induced increases on DIO2 mRNA levels in MSTO-211 cells is not reverted by sodium selenite or NAC (B). *P<0.001, difference between controls and IL6 treated cells; §P<0.001, difference between controls in the presence or not of sodium selenite. Data are mean±SD of at least three independent experiments. The net iodide release in this system is specific and equivalent to T3 production.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4588414&req=5

f0015: Effect of sodium selenite on type 2 deiodinase activity and expression. Sodium selenite does not reverse the inhibitory effect of interleukin IL6 on deiodinase type 2 (D2)-catalyzed T4-to-T3 conversion in endogenous D2 expressing MSTO-211 cells, as observed in the presence of N-acetylcysteine (NAC) (A). The IL6-induced increases on DIO2 mRNA levels in MSTO-211 cells is not reverted by sodium selenite or NAC (B). *P<0.001, difference between controls and IL6 treated cells; §P<0.001, difference between controls in the presence or not of sodium selenite. Data are mean±SD of at least three independent experiments. The net iodide release in this system is specific and equivalent to T3 production.
Mentions: The conversion of T4-to-T3 by D2 decreases in the presence of increased levels of IL6 (Fig. 3A). The addition of sodium selenite to the culture media slightly increased T4-to-T3 conversion in control cells but failed to prevent the IL6 induced dose-dependent D2 inhibition, as observed with NAC addition (P<0.001; Fig. 3A). Pretreatment with sodium selenite or NAC did not prevent the IL6-induced increase in the levels of DIO2 mRNA (Fig. 3B).

Bottom Line: Increased ROS was paralleled by D1 and D2-decreased T3-production (P<0.01) and increased D3-catalyzed T3-inactivation (P<0.001).Selenite decreases the IL6-induced ROS and carbonyl content, while enhances Gpx and Trx activities.In conclusion, although sodium selenite reduces IL6-induced redox imbalance it does not fully repair deiodinase function.

View Article: PubMed Central - PubMed

Affiliation: Thyroid Section, Endocrine Division, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.

No MeSH data available.


Related in: MedlinePlus