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Accepted Preprint first posted online on 23 January 2009

Journal of Endocrinology 2009;201:161.

Journal of Endocrinology (2009) In press
DOI: 10.1677/JOE-08-0470
© 2009 Society for Endocrinology
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RESEARCH

Minimal oxidative load: a prerequisite for thyroid cell function.

Sylvie Poncin, Ides Colin and Anne-Catherine Gerard

S Poncin, Morphologie Experimentale (MOEX), Universite catholique de Louvain (UCL), Brussel, Belgium
I Colin, Morphologie Experimentale (MOEX), Universite catholique de Louvain (UCL), Brussel, Belgium
A Gerard, Morphologie Experimentale (MOEX), Universite catholique de Louvain (UCL), Brussel, 1200, Belgium

Correspondence: Anne-Catherine Gerard, Email: anne-catherine.gerard{at}uclouvain.be

Abstract

In addition to reactive oxygen species (ROS) produced by mitochondria during aerobic respiration, thyrocytes are continuously producing H2O2, a key element for hormonogenesis. Because nothing is known about ROS implication in normal non stimulated cells, we studied their possible involvement in thyrocytes incubated with a potent antioxidant, N-acetylcysteine (NAC). NAC, which blocked the production of intracellular ROS, also decreased dual oxidases, thyroperoxidase, pendrin and thyroglobulin protein and/or gene expression. By contrast, Na+/I- symporter mRNA expression was unaffected. Among antioxidant systems, peroxiredoxin5 expression was reduced by NAC, whereas peroxiredoxin3 increased and catalase remained unchanged. In vivo, the expression of both dual oxidases and peroxiredoxin5 proteins was also decreased by NAC. In conclusion, when intracellular ROS levels drop below a basal threshold, the expression of proteins involved in thyroid cell function is hampered. This suggests that keeping ROS at a minimal level is required for safeguarding thyrocyte function.




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Am. J. Physiol. Endocrinol. Metab.Home page
A.-C. Gerard, S. Poncin, J.-N. Audinot, J.-F. Denef, and I. M. Colin
Iodide deficiency-induced angiogenic stimulus in the thyroid occurs via HIF- and ROS-dependent VEGF-A secretion from thyrocytes
Am J Physiol Endocrinol Metab, June 1, 2009; 296(6): E1414 - E1422.
[Abstract] [Full Text] [PDF]




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