, Volume 41, Issue 3, pp 532–538 | Cite as

Positive correlation between type 1 and 2 iodothyronine deiodinases activities in human goiters

  • Valmara S. Pereira
  • Michelle P. Marassi
  • Doris Rosenthal
  • Mário Vaisman
  • Vânia M. Corrêa da Costa
Original Article


Type 1 (D1) and 2 (D2) iodothyronine deiodinases are selenocysteine-containing enzymes that catalyze the deiodination of T4 to T3 in the thyroid and in peripheral tissues. Despite their importance to the plasma T3 pool in human beings, there are few studies about their behavior in human thyroids. In order to better understand iodothyronine deiodinase regulation in the thyroid gland, we studied thyroid tissue samples from follicular adenoma (AD, n = 5), toxic diffuse goiter (TDG, n = 6), nontoxic multinodular goiter (NMG, n = 40), papillary thyroid carcinoma (PTC, n = 8), and surrounding normal tissues (NT, n = 7) from 36 patients submitted to elective thyroidectomy. D1 and D2 activities were determined by quantification of the radioiodine released by 125I-rT3 or 125I-T4 under standardized conditions, and expressed as pmol rT3 deiodinated per minute and mg protein (pmol rT3 min−1 mg−1 ptn) and fmol T4 deiodinated per minute and mg protein (fmol T4 min−1 mg−1 ptn), respectively. D1 activity detected in TDG and AD tissues were significantly higher than in NT, PTC or NMG samples. D2 activity was also significantly higher in TDG and AD samples than in PTC, NMG, or NT. There was great variability in D1 and D2 enzymatic activities from distinct patients as well as from different areas from the same goiter. There was a positive correlation (P < 0,0001, r = 0.4942) between D1 and D2 activities when all samples were taken into account, suggesting that—in the thyroid—these two iodothyronine deiodinases may have related regulatory mechanisms, even if conditioned by other as yet unknown factors.


Human goiters Type 1 iodothyronine deiodinase Type 2 iodothyronine deiodinase Positive correlation 



We are grateful for the technical assistance of Advaldo Nunes Bezerra, Norma Lima de Araújo Faria, and Wagner Nunes Bezerra. This study was supported by grants from Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ) and Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq).

Supplementary material

12020_2011_9587_MOESM1_ESM.docx (23 kb)
Supplementary Table 1: *TSH reference: 0.4–4.0 μUI/ml. **FT4 reference: 0.8–1.9 ng/dl. NA not available. Supplementary material 1 (DOCX 23 kb)


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Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  • Valmara S. Pereira
    • 1
  • Michelle P. Marassi
    • 1
  • Doris Rosenthal
    • 1
  • Mário Vaisman
    • 2
  • Vânia M. Corrêa da Costa
    • 1
  1. 1.Laboratório de Fisiologia Endócrina Doris Rosenthal, Instituto de Biofísica Carlos Chagas FilhoUniversidade Federal do Rio de JaneiroRio de JaneiroBrazil
  2. 2.Serviço de Endocrinologia, Hospital Universitário Clementino Fraga FilhoUniversidade l do Rio de JaneiroRio de JaneiroBrazil

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