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Titanium Dioxide Nanoparticles Induce Cell Cycle Arrest and Apoptosis through Inhibiting PI3K/AKT/mTOR Pathway in

Ruoyun Dong1, Xiaojia Meng2, Hongmei Chang1

  • 1Department of Preventive Medicine / the Key Laboratory for Prevention and Control of Emerging Infectious Diseases and Public Health Security, the Xinjiang Production and Construction Corps, School of Medicine, Shihezi University, Shihezi, 832000, Xinjiang, China.

Biological Trace Element Research
|December 11, 2023
PubMed

Insights

Titanium dioxide nanoparticles (TiO2 NPs) harm sperm production by causing cell cycle arrest and apoptosis in spermatogonia. This occurs via the PI3K/AKT/mTOR pathway, explaining reduced sperm counts.

Area of Science:

  • Toxicology
  • Cell Biology
  • Nanotechnology

Background:

  • Titanium dioxide nanoparticles (TiO2 NPs) are linked to reduced sperm counts.
  • The underlying mechanisms, particularly concerning spermatogonia, require elucidation.

Purpose of the Study:

  • To investigate TiO2 NPs' effects on spermatogonial cell cycle and apoptosis.
  • To explore the role of the PI3K/AKT/mTOR signaling pathway in these effects.

Main Methods:

  • Mouse spermatogonia (GC-1) were exposed to varying TiO2 NP concentrations.
  • Cell viability, cell cycle, apoptosis, and key signaling proteins were analyzed.
  • PI3K pathway modulation using IGF-1 (agonist) and LY294002 (inhibitor) was performed.

Main Results:

  • TiO2 NPs inhibited proliferation, induced G0/G1 cell cycle arrest, and promoted apoptosis.
  • Downregulation of CDK4, CDK2, Cyclin D1, Cyclin E1, and upregulation of p21, p53 were observed.
  • TiO2 NPs inhibited the PI3K/AKT/mTOR pathway; IGF-1 reversed effects, while LY294002 exacerbated them.

Conclusions:

  • TiO2 NPs induce spermatogonial G0/G1 cell cycle arrest and apoptosis by inhibiting the PI3K/AKT/mTOR pathway.
  • This pathway inhibition is a likely cause of TiO2 NP-induced reduction in sperm numbers.
Keywords:
ApoptosisCell cycleGC-1 cellsPI3K/AKT/mTOR pathwayTitanium dioxide nanoparticles

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