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Related Experiment Video

Updated: Jul 3, 2026

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse

Published on: October 6, 2023

Thyroid hormone effect in human hepatocytes.

Eliana A Miler¹, María Del Carmen Ríos de Molina, Gabriela Domínguez

¹Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina.

Redox Report : Communications in Free Radical Research

|July 24, 2008

Summary

This summary is machine-generated.

Thyroid hormone (T3) increases oxidative stress markers like malondialdehyde (MDA) and oxidized glutathione (GSSG) in liver cells. Ascorbic acid partially counteracted these effects, but high T3 doses induced cell death, indicating significant cellular damage.

Related Experiment Videos

Last Updated: Jul 3, 2026

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse

Published on: October 6, 2023

Area of Science:

Endocrinology
Molecular Biology
Hepatology

Background:

Hyperthyroidism is linked to increased oxidative stress and free radical production.
Thyroid hormones, particularly triiodothyronine (T3), may directly contribute to cellular oxidative damage.

Purpose of the Study:

To investigate the in vitro effects of T3 on oxidative stress markers in human hepatocytes.
To assess the protective role of ascorbic acid against T3-induced oxidative stress.

Main Methods:

Human hepatocyte cell line (Hep G2) exposed to varying doses of T3 (0.1-20.0 nM) for 1-24 hours.
Measurement of oxidative stress markers: malondialdehyde (MDA), oxidized glutathione (GSSG), superoxide dismutase (SOD), catalase, and glutathione peroxidase.
Inclusion of ascorbic acid and assessment of its effects on T3-treated cells.

Main Results:

T3 significantly increased MDA and GSSG levels, indicating lipid peroxidation and oxidative damage.
Superoxide dismutase (SOD) activity increased with T3, but catalase and glutathione peroxidase activities remained unchanged.
Ascorbic acid reduced MDA levels and enhanced SOD activity.
High T3 concentrations (200 nM) induced significant apoptosis (69%) in Hep G2 cells.
Even with increased SOD activity, MDA and GSSG remained elevated, suggesting insufficient antioxidant defense against T3 toxicity.

Conclusions:

Thyroid hormone T3 directly induces oxidative stress and cell death in hepatocytes.
Ascorbic acid demonstrates a protective effect against T3-induced oxidative stress, though it may not fully mitigate the damage at high hormone levels.
The findings highlight the potential role of oxidative stress in hyperthyroidism pathogenesis and suggest antioxidant strategies may be beneficial.