Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/24191
Type: Artigo de periódico
Title: Effect of iodide on Fas, Fas-ligand and Bcl-w mRNA expression in thyroid of NOD mice pretreated with methimazole
Author: Boechat, L.H.B.
Vilella, C.A.
Zollner, R.L.
Abstract: Nonobese diabetic (NOD) mice and a derived strain, NOD.H.2h4, have been used as a model for experimental spontaneous thyroiditis and thyroiditis induced by iodide excess after a goiter-inducing period. Some authors have proposed that iodide, given after methimazole or propylthiouracil, is capable of inducing apoptosis in thyroid cells and that anti-thyroid drugs can modulate the expression of apoptosis components such as Fas and its ligand (Fas-L). Here we evaluated the effect of potassium iodide (20 µg/animal for 4 days, ip) given to NOD mice at the 10th week of life after exposure to methimazole (1 mg/ml) in drinking water from the 4th to the 10th week of life. Fas, Fas-L and Bcl-w expression were analyzed semiquantitatively by RT-PCR immediately after potassium iodide administration (group MI44D) or at week 32 (MI32S). Control groups were added at 10 (C10) and 32 weeks (C32), as well as a group that received only methimazole (CM10). An increase in the expression of Fas-L and Bcl-w (P<0.01, ANOVA) was observed in animals of group MI44D, while Fas was expressed at higher levels (P = 0.02) in group C32 (72.89 ± 47.09 arbitrary units) when compared to group C10 (10.8 ± 8.55 arbitrary units). Thus, the analysis of Fas-L and Bcl-w expression in the MI44D group and Fas in group C32 allowed us to detect two different patterns of expression of these apoptosis components in thyroid tissue of NOD mice.
Subject: Thyroiditis
Nonobese diabetic mice
Apoptosis
Methimazole
Iodide
Fas mRNA
Fas-L mRNA
Bcl-w mRNA
Editor: Associação Brasileira de Divulgação Científica
Citation: Brazilian Journal of Medical and Biological Research. Associação Brasileira de Divulgação Científica, v. 35, n. 3, p. 289-295, 2002.
Rights: aberto
Identifier DOI: 10.1590/S0100-879X2002000300003
Address: http://dx.doi.org/10.1590/S0100-879X2002000300003
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2002000300003
Date Issue: 1-Mar-2002
Appears in Collections:Unicamp - Artigos e Outros Documentos

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