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Background <p>Titanium dioxide (TiO<sub>2</sub>) is widely present in a variety of food and personal care products, leading to frequent human exposure primarily via oral ingestion. Although the oral bioavailability of TiO<sub>2</sub> nanoparticles is generally considered low, the gastrointestinal tract represents the primary site of exposure and may undergo local molecular and metabolic disturbances following repeated contact.</p> Methods <p>In this study, we investigated the impact of TiO<sub>2</sub> exposure on gene expression and cellular metabolism in intestinal epithelial cells using integrated transcriptomic and metabolomic approaches.</p> Results <p>Transcriptomic analysis identified differentially expressed genes associated with disruptions in cellular components, molecular functions, and biological processes, collectively pointing to mechanisms underlying TiO<sub>2</sub>-induced cytotoxicity. Metabolomic profiling further revealed that TiO<sub>2</sub> exposure perturbed key metabolic pathways, as evidenced by significant alterations in critical metabolites—including acetylcholine, glutathione, cytosine, deoxyadenosine, and pantothenic acid—indicative of broad metabolic dysfunction. Notably, integrative correlation analysis demonstrated that TiO<sub>2</sub> disrupts lipid metabolism, amino acid metabolism, nucleotide metabolism, energy metabolism, and redox homeostasis.</p> Conclusions <p>In conclusion, our findings elucidate the metabolic mechanisms driving TiO<sub>2</sub>-induced intestinal toxicity. Moreover, this work underscores the power of integrated transcriptomic-metabolomic analysis as a robust strategy for mechanistic toxicological evaluation and risk assessment of nanomaterial exposure.</p>

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Elucidating metabolic dysfunction induced by titanium dioxide in intestinal epithelial cells using an integrative approach of metabolomics and transcriptomics

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月21日

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  • Xinchen Wang,
  • Shilong Jiang,
  • Zhengyu Gu

摘要

Background

Titanium dioxide (TiO2) is widely present in a variety of food and personal care products, leading to frequent human exposure primarily via oral ingestion. Although the oral bioavailability of TiO2 nanoparticles is generally considered low, the gastrointestinal tract represents the primary site of exposure and may undergo local molecular and metabolic disturbances following repeated contact.

Methods

In this study, we investigated the impact of TiO2 exposure on gene expression and cellular metabolism in intestinal epithelial cells using integrated transcriptomic and metabolomic approaches.

Results

Transcriptomic analysis identified differentially expressed genes associated with disruptions in cellular components, molecular functions, and biological processes, collectively pointing to mechanisms underlying TiO2-induced cytotoxicity. Metabolomic profiling further revealed that TiO2 exposure perturbed key metabolic pathways, as evidenced by significant alterations in critical metabolites—including acetylcholine, glutathione, cytosine, deoxyadenosine, and pantothenic acid—indicative of broad metabolic dysfunction. Notably, integrative correlation analysis demonstrated that TiO2 disrupts lipid metabolism, amino acid metabolism, nucleotide metabolism, energy metabolism, and redox homeostasis.

Conclusions

In conclusion, our findings elucidate the metabolic mechanisms driving TiO2-induced intestinal toxicity. Moreover, this work underscores the power of integrated transcriptomic-metabolomic analysis as a robust strategy for mechanistic toxicological evaluation and risk assessment of nanomaterial exposure.