Recent findings found that TiO₂ nanoparticles (TiO₂-NPs) have male reproductive toxicity. However, few reports have studied the toxicity of TiO₂-NPs in crustaceans. In this study, we first chose the freshwater crustacean Eriocheir sinensis (E. sinensis) to explore the male toxicity of TiO₂-NP exposure and the underlying mechanisms. Three nm and 25 nm TiO₂-NPs at a dose of 30 mg/kg bw induced apoptosis and damaged the integrity of the haemolymph-testis-barrier (HTB, a structure similar to the blood-testis-barrier) and the structure of the seminiferous tubule. The 3-nm TiO₂-NPs caused more severe spermatogenesis dysfunction than the 25-nm TiO₂-NPs. We initially confirmed that TiO₂-NP exposure affected the expression patterns of adherens junctions (α-catenin and β-catenin) and induced tubulin disorganization in the testis of E. sinensis. TiO₂-NP exposure caused reactive oxygen species (ROS) generation and an imbalance of mTORC1-mTORC2 (mTORC1/rps6/Akt levels were increased, while mTORC2 activity was not changed). After using the ROS scavenger NAC to inhibit ROS generation, both the mTORC1-mTORC2 imbalance and alterations in AJs were rescued. More importantly, the mTORC1 inhibitor rapamycin abolished mTORC1/rps6/Akt hyperactivation and partially restored the alterations in AJs and tubulin. Collectively, the mTORC1-mTORC2 imbalance induced by TiO₂-NPs was involved in the mechanism of AJ and HTB disruption, resulting in spermatogenesis in E. sinensis.

最近的研究发现，TiO ₂纳米粒子（TiO ₂ -NPs）具有男性生殖毒性。_{然而，很少有报道研究过TiO 2} -NPs对甲壳类动物的毒性。在这项研究中，我们首先选择了淡水甲壳动物中华绒螯蟹（E. sinensis ）来探索 TiO ₂ -NP 暴露的雄性毒性及其潜在机制。剂量为 30 mg/kg bw 的 3 nm 和 25 nm TiO 2 -NPs 诱导细胞凋亡并破坏血淋巴-睾丸屏障（HTB，一种类似于血-睾丸屏障的结构）的完整性_和曲细精管。3 纳米 TiO ₂-NPs 比 25-nm TiO ₂ -NPs 引起更严重的精子发生功能障碍。我们初步证实，TiO ₂ -NP 暴露会影响黏附连接（α-连环蛋白和β-连环蛋白）的表达模式，并诱导中华桉睾丸中的微管蛋白解体。_二氧化钛-NP 暴露导致活性氧 (ROS) 生成和 mTORC1-mTORC2 失衡（mTORC1/rps6/Akt 水平增加，而 mTORC2 活性未改变）。在使用 ROS 清除剂 NAC 抑制 ROS 生成后，mTORC1-mTORC2 失衡和 AJ 的改变都得到了挽救。更重要的是，mTORC1 抑制剂雷帕霉素消除了 mTORC1/rps6/Akt 过度激活并部分恢复了 AJ 和微管蛋白的改变。_{总的来说，由 TiO 2} -NPs诱导的 mTORC1-mTORC2 失衡参与了 AJ 和 HTB 破坏的机制，导致了E. sinensis 的精子发生。