2-iodohexadecanal induces autophagy during goiter involution.

2-iodohexadecanal goiter iodine iodolopids thyroid

Journal

Prostaglandins & other lipid mediators
ISSN: 1098-8823
Titre abrégé: Prostaglandins Other Lipid Mediat
Pays: United States
ID NLM: 9808648

Informations de publication

Date de publication:
10 Feb 2024
Historique:
received: 24 08 2023
revised: 03 11 2023
accepted: 09 02 2024
medline: 13 2 2024
pubmed: 13 2 2024
entrez: 12 2 2024
Statut: aheadofprint

Résumé

Iodine plays an important role in thyroid physiology and biochemistry. The thyroid is capable of producing different iodolipids such as 2-iodohexadecanal (2-IHDA). Data from different laboratories have shown that 2-IHDA inhibits several thyroid parameters and it has been postulated as intermediary on the action of iodide function. To explore different mechanisms involved during the involution of the hyperplastic thyroid gland of Wistar rats towards normality induced by 2-IHDA. Goiter was induced by the administration of MMI for 10 days, then the treatment was discontinued and Wistar rats were injected with 2-IHDA or KI. During involution, 2-IHDA treatment reduced PCNA expression compared to spontaneous involution. KI treatment caused an increase of Caspase-3 activity and TUNEL-positive cells. In contrast, 2-IHDA failed to alter this value but induced an increase of LC3B expression. KI but not 2-IHDA led to an increase in peroxides levels, catalase and glutathione peroxidase activity. We demonstrated that 2-IHDA, in contrast to iodide, did not lead to an increase in oxidative stress or apoptosis induction, indicating that the involution triggered by 2-IHDA in Wistar rats, is primarily due to the inhibition of cell proliferation and the induction of autophagy.

Sections du résumé

BACKGROUND BACKGROUND
Iodine plays an important role in thyroid physiology and biochemistry. The thyroid is capable of producing different iodolipids such as 2-iodohexadecanal (2-IHDA). Data from different laboratories have shown that 2-IHDA inhibits several thyroid parameters and it has been postulated as intermediary on the action of iodide function.
OBJECTIVE OBJECTIVE
To explore different mechanisms involved during the involution of the hyperplastic thyroid gland of Wistar rats towards normality induced by 2-IHDA.
METHODS METHODS
Goiter was induced by the administration of MMI for 10 days, then the treatment was discontinued and Wistar rats were injected with 2-IHDA or KI.
RESULTS RESULTS
During involution, 2-IHDA treatment reduced PCNA expression compared to spontaneous involution. KI treatment caused an increase of Caspase-3 activity and TUNEL-positive cells. In contrast, 2-IHDA failed to alter this value but induced an increase of LC3B expression. KI but not 2-IHDA led to an increase in peroxides levels, catalase and glutathione peroxidase activity.
CONCLUSIONS CONCLUSIONS
We demonstrated that 2-IHDA, in contrast to iodide, did not lead to an increase in oxidative stress or apoptosis induction, indicating that the involution triggered by 2-IHDA in Wistar rats, is primarily due to the inhibition of cell proliferation and the induction of autophagy.

Identifiants

pubmed: 38346574
pii: S1098-8823(24)00013-3
doi: 10.1016/j.prostaglandins.2024.106819
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

106819

Informations de copyright

Copyright © 2024. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Conflicts of Interest The authors declare that there are no conflicts of interest.

Auteurs

Leonardo Salvarredi (L)

Nuclear Medicine School Foundation (FUESMEN), National Commission of Atomic Energy (CNEA), Mendoza, Argentina.

Romina A Oglio (RA)

Instituto Balseiro, National Comission of Atomic Energy & National University of Cuyo, Mendoza, Argentina.

Carla Rodriguez (C)

Department of Radiobiology (CAC), National Commission of Atomic Energy (CNEA), Buenos Aires, Argentina.

Daniela Navarro (D)

Universidad Miguel Hernández de Elche d'Alacant, Spain.

Marina Perona (M)

Department of Radiobiology (CAC), National Commission of Atomic Energy (CNEA), Buenos Aires, Argentina; National Council of Scientific and Technical Research (CONICET), CABA, Argentina.

María A Dagrosa (MA)

Department of Radiobiology (CAC), National Commission of Atomic Energy (CNEA), Buenos Aires, Argentina; National Council of Scientific and Technical Research (CONICET), CABA, Argentina.

Guillermo J Juvenal (GJ)

Department of Radiobiology (CAC), National Commission of Atomic Energy (CNEA), Buenos Aires, Argentina; National Council of Scientific and Technical Research (CONICET), CABA, Argentina.

Lisa Thomasz (L)

Department of Radiobiology (CAC), National Commission of Atomic Energy (CNEA), Buenos Aires, Argentina; National Council of Scientific and Technical Research (CONICET), CABA, Argentina. Electronic address: lisa75ar@yahoo.com.ar.

Classifications MeSH