Early changes during goiter induction and involution in the rat

LISA THOMASZ; R OGLIO; ANDREA RANDI; MN FERNáNDEZ; RL CABRINI; GJ JUVENAL; MARIO PISAREV

THYROID

MARY ANN LIEBERT INC

Año: 2010 vol. 20 p. 1003 - 1013

1050-7256

In previous studies we have demonstrated that administration of 5-iodo-delta lactone of arachidonic acid (IL-ä), a mediator in thyroid autoregulation, prevents goiter induction in rats. Other studies have shown that TGF-â1 mimics some of the actions of excess iodine, and its possible participation in autoregulation is disputed. The present studies were performed to analyze the biochemical changes which occur during goiter induction and involution after 3, 7 and 14 days of treatment. MMI caused a progressive increase in thyroid weight accompanied by an increase in cell number, PCNA, c-fos and c-myc expression. In addition MMI increased the asymmetry of the ploidy histograms and the nuclear area. Besides, an early increase in caspase-3 activity and by the TUNEL assay, as an index of apoptotic markers. Peroxides as well glutathione peroxidase and catalase activities.were also elevated in goitrous animals. The goiter inhibitory action of IL-ä is due to the inhibition of cell proliferation evidenced by a significant decrease in cell number, PCNA expression and a decreased in the asymmetry of the ploidy histograms accompanied by a transient stimulation of apoptosis, as evidenced by the significant increase of both caspase-3 and TUNEL values after 7 days of treatment. MMI administration stimulated TGF-â1 synthesis but not TGF-â3. IL-ä alone caused a slight increase of TGF-â3 but not of TGF-â1, while KI stimulated both isoforms and MMI reversed KI effect on TGF-â1 expression but not on TGF-â3. Therefore it may be  concluded that the TGF-â1 does not play a role in the autoregulatory pathway mediated by IL-ä and that iodide stimulates TGFB3 without the need of being organified (autoregulatory-independent effect).