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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

Reactive oxygen species (ROS) generation in cells endogenous expressing type 2 (MSTO; A), type 1 (HepG2; B) or type 3 (MCF-7; C) deiodinases. *P<0.001 refers to the difference between control and IL6 treated (1000 ng/L) while **P<0.001 refers to the difference between sodium selenite supplementation in controls as compared with IL6 treated cells. Data are mean±SD of at least three independent experiments. NAC, N-acetylcysteine.
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f0005: Reactive oxygen species (ROS) generation in cells endogenous expressing type 2 (MSTO; A), type 1 (HepG2; B) or type 3 (MCF-7; C) deiodinases. *P<0.001 refers to the difference between control and IL6 treated (1000 ng/L) while **P<0.001 refers to the difference between sodium selenite supplementation in controls as compared with IL6 treated cells. Data are mean±SD of at least three independent experiments. NAC, N-acetylcysteine.

Mentions: IL6 induced ROS in all 3 cell lines (P<0.001; Fig. 1A–C). Pretreatment with sodium selenite slightly attenuated IL6-induced reactive species detection in MSTO-211, HepG2 and MCF-7 cells (approximately 25%, 12% and 15%, respectively, all P<0.05; Fig. 1A–C, respectively) while NAC completely abolished it (P<0.001; Fig. 1A–C).


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)

Reactive oxygen species (ROS) generation in cells endogenous expressing type 2 (MSTO; A), type 1 (HepG2; B) or type 3 (MCF-7; C) deiodinases. *P<0.001 refers to the difference between control and IL6 treated (1000 ng/L) while **P<0.001 refers to the difference between sodium selenite supplementation in controls as compared with IL6 treated cells. Data are mean±SD of at least three independent experiments. NAC, N-acetylcysteine.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

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

f0005: Reactive oxygen species (ROS) generation in cells endogenous expressing type 2 (MSTO; A), type 1 (HepG2; B) or type 3 (MCF-7; C) deiodinases. *P<0.001 refers to the difference between control and IL6 treated (1000 ng/L) while **P<0.001 refers to the difference between sodium selenite supplementation in controls as compared with IL6 treated cells. Data are mean±SD of at least three independent experiments. NAC, N-acetylcysteine.
Mentions: IL6 induced ROS in all 3 cell lines (P<0.001; Fig. 1A–C). Pretreatment with sodium selenite slightly attenuated IL6-induced reactive species detection in MSTO-211, HepG2 and MCF-7 cells (approximately 25%, 12% and 15%, respectively, all P<0.05; Fig. 1A–C, respectively) while NAC completely abolished it (P<0.001; Fig. 1A–C).

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