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Unité de Morphologie Expérimentale, Université Catholique de Louvain, UCL-5251, 52 Avenue E. Mounier, B-1200 Bruxelles, Belgium

(Correspondence should be addressed to A-C Gérard; Email: anne-catherine.gerard{at}uclouvain.be)

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, peroxiredoxin (PRDX) five expression was reduced by NAC, whereas peroxiredoxin three increased and catalase remained unchanged. In vivo, the expression of both dual oxidases and peroxiredoxin five 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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				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]