Effect of iodide on Fas, Fas-ligand and Bcl-w mRNA expression in thyroid of NOD mice pretreated with methimazole

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 Bclw (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. Correspondence

Role of iodine in pathogenesis of thyroid disease - is induction of apoptosis consequence of iodine cytotoxicity?

“…This effect is very rapid and possibly connected with inhibition of polyamine synthesis, which are potent inhibitors of oligonucleosomal DNA fragmentation [41]. In line with this results, Boechat et al [42] found higher levels of FasL expression, in NOD mice with methimazole-induced goiter after the administration of KI in animals sacrificed four days after the administration [42]. Some authors consider that follicular cell injury, apoptosis, and necrosis precede lymphocytic infiltration in the thyroid gland and they are considered the initial events in, and prerequisites for, the development of iodine-induced AIT [7].…”

Diacerhein downregulate proinflammatory cytokines expression and decrease the autoimmune diabetes frequency in nonobese diabetic (NOD) mice

“…Total cells from pancreatic islets were submitted to RNA extraction by a modified protocol of acid guanidium thiocyanate/phenol/ chloroform extraction [11,30,31]. The RNA was first reversetranscribed into cDNA (Superscript™ II -Life Sciences).…”

Phenotype of blood lymphocytes in correlation with histological picture in thyroid gland of rats treated with potassium iodide

“…Also some authors have found that in autoimmune-prone mice, excessive iodine administration might induce goiter, thyroiditis, worsen lymphocytic infiltration, as well as damage the thyroid follicular structure in a dose-dependent manner (Teng et al, 2009). Also, experimental thyroiditis induced by administration of supraphysiologic doses of iodine has been described in nonobese diabetic (NOD) mice or their derived strains such as NOD.H.2h4 (Boechat et al, 2002;Damotte et al, 1997), and in other models of thyroid autoimmunity, such as BB/W rats (Li and Boyages, 1994), and obese strain chickens (Sundick et al, 1996).…”