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Cadmium-induced hepatotoxicity: Interconnecting molecular and cellular pathways
Devaraj Ezhilarasan1, Muthusethupathi Sharmila1
1Department of Pharmacology, Hepatology and Molecular Medicine Lab, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences (SIMATS), Chennai, Tamil Nadu 600 077, India.
Toxicology
|April 24, 2026
Summary
Cadmium exposure causes liver damage through oxidative stress and mitochondrial dysfunction. This persistent toxicant overwhelms detoxification, leading to inflammation and DNA damage in liver cells.
Area of Science:
- Environmental toxicology
- Hepatology
- Cellular toxicology
Background:
- Cadmium (Cd) is a persistent environmental toxicant accumulating in the liver.
- Cd exposure leads to hepatotoxicity via oxidative stress, mitochondrial dysfunction, inflammation, and DNA damage.
Purpose of the Study:
- To elucidate the interconnected mechanisms of cadmium-induced hepatotoxicity.
- To highlight the central role of oxidative stress and its downstream effects.
Main Methods:
- Review of experimental studies in murine and rat models.
- Analysis of molecular and cellular pathways involved in Cd toxicity.
Main Results:
- Cd overwhelms metallothionein detoxification, leading to free Cd accumulation in mitochondria and ER.
- Oxidative stress, Nrf2/ARE pathway inhibition, mitochondrial dysfunction, and ER stress are key mechanisms.
- Cd stimulates inflammatory pathways (TLR4/NF-κB, NLRP3 inflammasome) and cell death (apoptosis, ferroptosis).
Conclusions:
- Oxidative stress is a central mechanism driving Cd-induced hepatotoxicity.
- Disrupted redox homeostasis, inflammation, and DNA damage contribute significantly to liver injury.
- Understanding these pathways is crucial for mitigating Cd-induced liver disease.
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