Evidence map›Paper›PMID 39174753›Full record

ArticleEndocrine2025

Polychlorinated Biphenyls (PCBS)-induced oxidative stress and inflammation in human thyrocytes: involvement of AhR and NRF-2/HO-1 pathway.

Rosaria M Ruggeri, Aurelio Minuti, Fiorenza Gianì, Roberta Masto, Davide Romano, Federica Aliquò, Alfredo Campennì, Salvatore Campo, Salvatore Cannavò, Angela D'Ascola

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Article in Endocrine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Rosaria M RuggeriDepartment of Human Pathology of Adulthood and Childhood DETEV, Endocrine Unit, University of Messina, Messina, Italy. rmruggeri@unime.it.
Aurelio MinutiDepartment of Human Pathology of Adulthood and Childhood DETEV, Endocrine Unit, University of Messina, Messina, Italy.
Fiorenza GianìDepartment of Clinical and Experimental Medicine, University of Catania, Catania, Italy.
Roberta MastoDepartment of Clinical and Experimental Medicine, University of Catania, Catania, Italy.
Davide RomanoDepartment of Biomedical and Dental Sciences, and Morpho-functional Images, University of Messina, Messina, Italy.
Federica AliquòDepartment of Biomedical and Dental Sciences, and Morpho-functional Images, University of Messina, Messina, Italy.
Alfredo CampennìDepartment of Biomedical and Dental Sciences, and Morpho-functional Images, University of Messina, Messina, Italy.
Salvatore CampoDepartment of Biomedical and Dental Sciences, and Morpho-functional Images, University of Messina, Messina, Italy.
Salvatore CannavòDepartment of Human Pathology of Adulthood and Childhood DETEV, Endocrine Unit, University of Messina, Messina, Italy.
Angela D'AscolaDepartment of Clinical and Experimental Medicine, University of Messina, Messina, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeIn this in vitro study, we investigated the effects of polychlorinated biphenyls (PCBs) on human thyrocytes, with a focus on the involvement of AhR, a key player in xenobiotic response, and the anti-oxidant Nrf-2/HO-1 pathway.

methodsPrimary cultured thyrocytes were exposed to the dioxin-like congeners PCB118 and PCB126 at 2.5 and 5 µM concentrations. mRNA expression was assessed by real-time PCR, and protein expression by Western Blot and ELISA, while protein quantification was assessed by densitometric analysis.

resultsIn cultured thyrocytes, PCB118 and PCB126 induced a significant (P < 0.01) increase of mRNA and protein levels of the pro-inflammatory cytokines IL-1beta and IL-6, while reducing those of thyroglobulin (TG) and NIS (p < 0.05), indicating down-regulation of these thyroid-specific genes in PCB-induced inflammation. ROS production also increased (p < 0.001). mRNA levels of AhR and the downstream molecules cytochrome P4501A, Nrf-2/HO-1 increased (p < 0.001), as well as related protein levels (p < 0.01), suggesting the activation of AhR and Nrf-2 pathways in response to PCBs exposure. AhR silencing decreased AhR-related gene expression and restored NIS and TG expression, while reducing inflammatory cytokines and oxidative stress markers (p < 0.05).

conclusionsDioxin-like PCBs (PCB118 and PCB126) may promote inflammation and oxidative stress in thyrocytes, impairing the expression of genes that are key players of thyroid function. These effects can be partially attributed to the activation of the AhR and Nrf-2 pathways. These data may contribute to explain the mechanisms underlying thyroid toxicity of PCBs, highlighting the potential role of these pollutants as a trigger of autoimmune thyroid inflammation and damage.

Indexed as

InflammationNF-E2-Related Factor 2Oxidative StressPolychlorinated BiphenylsReceptors, Aryl HydrocarbonThyroid Epithelial CellsBasic Helix-Loop-Helix ProteinsCells, CulturedHeme Oxygenase-1HumansSignal TransductionAHR protein, humanBasic Helix-Loop-Helix ProteinsHeme Oxygenase-1HMOX1 protein, humanNFE2L2 protein, humanNF-E2-Related Factor 2Polychlorinated BiphenylsReceptors, Aryl HydrocarbonAryl hydrocarbon receptor (AhR)Nuclear factor-2 erythroid related factor-2 (Nrf-2)Oxidative stressPollutantsPolychlorinated biphenyls (PCB)Thyroid autoimmunity

Identifiers

PMID39174753

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.