# Cadmium Toxicity Effects on Histone Modifiers, Enzyme Activity and Adipokines in Human Adipose Tissue Cells

**Authors:** Victor Tadeu Gonçalves Plata, Júlia Fernandes Barcella, Raphael Justa Saran, Artur Francisco da Silva Neto, Yasmin Alaby Martins Ferreira, Andressa Bolsoni-Lopes, Lila Missae Oyama, Lucia Maria Armelin-Correa, Maria Isabel Cardoso Alonso-Vale

PMC · DOI: 10.3390/molecules31061056 · Molecules · 2026-03-23

## TL;DR

Cadmium exposure disrupts fat cell function through epigenetic changes, oxidative stress, and inflammation, potentially leading to long-term metabolic issues.

## Contribution

This study reveals novel mechanisms by which cadmium affects adipose tissue through epigenetic and metabolic pathways.

## Key findings

- Cadmium altered histone modifiers linked to H3K27 in adipose cells.
- Cd exposure disrupted redox balance and impaired fat cell differentiation.
- Cadmium modulated inflammatory and adipokine responses in a concentration-dependent manner.

## Abstract

Environmental exposure to heavy metals, particularly cadmium (Cd), has been increasingly associated with obesity, metabolic dysfunction, chronic inflammation, and related disorders such as type 2 diabetes and cardiovascular diseases. Adipose tissue (AT), a paracrine and endocrine organ central to systemic energy and inflammatory homeostasis, is a major site of heavy metal accumulation and a key target of Cd toxicity. However, the mechanisms by which Cd disrupts adipocyte function, especially through epigenetic pathways, remain poorly understood. In this study, we investigated the effects of Cd on epigenetic regulators, antioxidant enzyme activity, inflammatory mediators, and adipogenic programming in human adipose-derived stromal/stem cells (hASCs) and differentiated adipocytes. Cd exposure altered histone modifiers associated with lysine 27 of histone 3 (H3K27), disrupted redox balance in a concentration-dependent manner, impaired adipogenic differentiation and lipid accumulation, and modulated inflammatory and adipokine responses according to differentiation stage and Cd concentration. Our findings suggest that Cd compromises adipose cell homeostasis through mechanisms involving epigenetic dysregulation, oxidative stress imbalance, and altered adipogenic and inflammatory signalling. These observations point to possible long-term metabolic consequences of environmental Cd exposure due to its accumulation in adipose tissue.

## Linked entities

- **Chemicals:** cadmium (PubChem CID 23973), Cd (PubChem CID 23973)
- **Diseases:** type 2 diabetes (MONDO:0005148)

## Full-text entities

- **Diseases:** cardiovascular diseases (MESH:D002318), Toxicity (MESH:D064420), chronic inflammation (MESH:D007249), metabolic dysfunction (MESH:D008659), type 2 diabetes (MESH:D003924), obesity (MESH:D009765)
- **Chemicals:** lipid (MESH:D008055), Cadmium (MESH:D002104), heavy metal (MESH:D019216)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13029247/full.md

## References

42 references — full list in the complete paper: https://tomesphere.com/paper/PMC13029247/full.md

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Source: https://tomesphere.com/paper/PMC13029247