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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 1 deiodinase activity and expression. Sodium selenite does not reverse the inhibitory effect of IL6 on deiodinase type 1 (D1)-catalyzed T4-to-T3 conversion in HepG2 cells, as observed with NAC (A). The IL6-induced increases on DIO1 mRNA levels in HepG2 cells is not reverted by sodium selenite or NAC (B). *P<0.001, difference between control 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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f0020: Effect of sodium selenite on type 1 deiodinase activity and expression. Sodium selenite does not reverse the inhibitory effect of IL6 on deiodinase type 1 (D1)-catalyzed T4-to-T3 conversion in HepG2 cells, as observed with NAC (A). The IL6-induced increases on DIO1 mRNA levels in HepG2 cells is not reverted by sodium selenite or NAC (B). *P<0.001, difference between control 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: Similar experiments were performed using cells expressing endogenous D1 (HepG2 cells, 30). The addition of sodium selenite to the culture media slightly increase the conversion of T4-to-T3, but failed to prevent IL6 induced D1 inhibition (P<0.0001; Fig. 4A), which was restored in the presence of NAC. As observed with DIO2, sodium selenite or NAC did not reverse the IL6 -induced increase in DIO1 mRNA levels (Fig. 4B).


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 1 deiodinase activity and expression. Sodium selenite does not reverse the inhibitory effect of IL6 on deiodinase type 1 (D1)-catalyzed T4-to-T3 conversion in HepG2 cells, as observed with NAC (A). The IL6-induced increases on DIO1 mRNA levels in HepG2 cells is not reverted by sodium selenite or NAC (B). *P<0.001, difference between control 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

f0020: Effect of sodium selenite on type 1 deiodinase activity and expression. Sodium selenite does not reverse the inhibitory effect of IL6 on deiodinase type 1 (D1)-catalyzed T4-to-T3 conversion in HepG2 cells, as observed with NAC (A). The IL6-induced increases on DIO1 mRNA levels in HepG2 cells is not reverted by sodium selenite or NAC (B). *P<0.001, difference between control 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: Similar experiments were performed using cells expressing endogenous D1 (HepG2 cells, 30). The addition of sodium selenite to the culture media slightly increase the conversion of T4-to-T3, but failed to prevent IL6 induced D1 inhibition (P<0.0001; Fig. 4A), which was restored in the presence of NAC. As observed with DIO2, sodium selenite or NAC did not reverse the IL6 -induced increase in DIO1 mRNA levels (Fig. 4B).

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