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2-iodohexadecanal induces autophagy during goiter involution.

Leonardo Salvarredi1, Romina A Oglio2, Carla Rodriguez2

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2-iodohexadecanal (2-IHDA) promotes thyroid involution in rats by inhibiting cell proliferation and inducing autophagy, unlike iodide which increases oxidative stress and apoptosis.

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Biology

Background:

  • Iodine is crucial for thyroid function, with iodolipids like 2-iodohexadecanal (2-IHDA) potentially mediating iodide's effects.
  • 2-IHDA has been shown to inhibit various thyroid parameters.

Purpose of the Study:

  • To investigate the mechanisms by which 2-IHDA induces involution of hyperplastic rat thyroid glands.
  • To compare the effects of 2-IHDA with iodide (KI) during thyroid involution.

Main Methods:

  • Goiter was induced in Wistar rats using methimazole (MMI).
  • Following MMI discontinuation, rats received either 2-IHDA or KI injections.
  • Thyroid tissue was analyzed for cell proliferation (PCNA), apoptosis (Caspase-3, TUNEL), autophagy (LC3B), and oxidative stress markers.

Main Results:

  • 2-IHDA reduced PCNA expression, indicating inhibited cell proliferation.
  • Unlike KI, 2-IHDA did not increase Caspase-3 activity or TUNEL-positive cells, suggesting no apoptosis induction.
  • 2-IHDA increased LC3B expression, indicative of autophagy induction, while KI increased oxidative stress markers.

Conclusions:

  • 2-IHDA-induced thyroid involution in rats is primarily driven by the inhibition of cell proliferation and the induction of autophagy.
  • In contrast to iodide, 2-IHDA does not elevate oxidative stress or trigger apoptosis.
  • These findings highlight distinct mechanisms of action for 2-IHDA and iodide in thyroid regulation.