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Collecting Variable-concentration Isothermal Titration Calorimetry Datasets in Order to Determine Binding Mechanisms
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TiO

Lan-Min Wang1, Ke Jia1, Zhen-Fang Li1

  • 1The Sperm Laboratory, College of Life Sciences, Zhejiang University, Hangzhou, 310058, China.

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|June 3, 2023
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Summary
This summary is machine-generated.

Titanium dioxide nanoparticles (TiO2-NPs) harm male reproductive health in the crustacean Eriocheir sinensis. Exposure disrupts the haemolymph-testis-barrier and spermatogenesis, linked to oxidative stress and mTOR signaling pathways.

Keywords:
Adhesion junctionEriocheir sinensisSpermatogenesisTiO(2) nanoparticlesmTOR

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Area of Science:

  • Environmental Toxicology
  • Reproductive Toxicology
  • Nanomaterial Safety

Background:

  • Titanium dioxide nanoparticles (TiO2-NPs) are known to cause male reproductive toxicity.
  • Limited research exists on TiO2-NP toxicity in aquatic crustaceans.
  • The freshwater crustacean Eriocheir sinensis is a relevant model for studying environmental contaminant effects.

Purpose of the Study:

  • To investigate the male reproductive toxicity of TiO2-NPs in Eriocheir sinensis.
  • To elucidate the underlying mechanisms of TiO2-NP-induced reproductive damage.
  • To explore the role of oxidative stress and mTOR signaling in TiO2-NP toxicity.

Main Methods:

  • Exposure of E. sinensis to 3 nm and 25 nm TiO2-NPs.
  • Assessment of apoptosis, haemolymph-testis-barrier (HTB) integrity, and seminiferous tubule structure.
  • Evaluation of adherens junction (AJ) protein expression and tubulin organization.
  • Measurement of reactive oxygen species (ROS) generation and mTORC1/mTORC2 signaling pathway activity.
  • Intervention with ROS scavenger N-acetylcysteine (NAC) and mTORC1 inhibitor rapamycin.

Main Results:

  • TiO2-NP exposure induced apoptosis and damaged the HTB and seminiferous tubules.
  • Smaller 3-nm TiO2-NPs caused more severe spermatogenesis dysfunction than 25-nm TiO2-NPs.
  • TiO2-NPs affected AJ expression, induced tubulin disorganization, and caused ROS generation.
  • An imbalance in mTORC1-mTORC2 signaling was observed (increased mTORC1/Akt, unchanged mTORC2).
  • NAC treatment rescued mTORC1-mTORC2 imbalance and AJ alterations; rapamycin partially restored AJ and tubulin.

Conclusions:

  • TiO2-NP exposure poses a significant risk to male reproductive health in E. sinensis.
  • Oxidative stress and subsequent mTORC1-mTORC2 pathway dysregulation are key mechanisms in TiO2-NP-induced reproductive toxicity.
  • Disruption of adherens junctions and the haemolymph-testis-barrier contributes to spermatogenesis dysfunction.