Cadmium telluride (CdTe) quantum dots (QDs) can be employed as imaging and drug delivery tools; however, the toxic effects and mechanisms of low-dose exposure are unclear. Therefore, this pioneering study focused on hepatic macrophages (Kupffer cells, KCs) and explored the potential damage process induced by exposure to low-dose CdTe QDs. In vivo results showed that both 2.5 μM/kg·bw and 10 μM/kg·bw could both activate KCs to cause liver injury, and produce inflammation by disturbing antioxidant levels. Abnormal liver function further verified the risks of low-dose exposure to CdTe QDs. The KC model demonstrated that low-dose CdTe QDs (0 nM, 5 nM and 50 nM) can be absorbed by cells and cause severe reactive oxygen species (ROS) production, oxidative stress, and inflammation. Additionally, the expression of NF-κB, caspase-1, and NLRP3 were decreased after pretreatment with ROS scavenging agent N-acetylcysteine (NAC, 5 mM pretreated for 2 h) and the NF-κB nuclear translocation inhibitor Dehydroxymethylepoxyquinomicin (DHMEQ, 10 μg/mL pretreatment for 4 h) respectively. The results indicate that the activation of the NF-κB pathway by ROS not only directly promotes the expression of inflammatory factors such as pro-IL-1β, TNF-α, and IL-6, but also mediates the assembly of NLRP3 by ROS activation of NF-κB pathway, which indirectly promotes the expression of NLRP3. Finally, a high-degree of overlap between the expression of the NF-κB and NLRP3 and the activated regions of KCs, further support the importance of KCs in inflammation induced by low-dose CdTe QDs.

碲化镉 (CdTe) 量子点 (QD) 可用作成像和药物输送工具；然而，低剂量暴露的毒性作用和机制尚不清楚。因此，这项开创性研究侧重于肝巨噬细胞（Kupffer 细胞，KCs），并探讨了暴露于低剂量 CdTe 量子点引起的潜在损伤过程。体内结果表明，2.5 μM/kg·bw和10 μM/kg·bw均可激活KCs引起肝损伤，并通过扰乱抗氧化水平产生炎症。肝功能异常进一步验证了低剂量接触 CdTe 量子点的风险。KC 模型表明，低剂量 CdTe QD（0 nM、5 nM 和 50 nM）可被细胞吸收并导致严重的活性氧 (ROS) 产生、氧化应激和炎症。此外，用 ROS 清除剂N预处理后，NF-κB、caspase-1 和 NLRP3 的表达降低。-乙酰半胱氨酸（NAC，5 mM 预处理 2 小时）和 NF-κB 核转位抑制剂去羟甲基环氧喹啉（DHMEQ，10 μg/mL 预处理 4 小时）。结果表明，ROS对NF-κB通路的激活不仅直接促进pro-IL-1β、TNF-α、IL-6等炎症因子的表达，而且通过ROS激活介导NLRP3的组装。 NF-κB 通路，间接促进 NLRP3 的表达。最后，NF-κB 和 NLRP3 的表达与 KCs 的激活区域之间的高度重叠，进一步支持了 KCs 在低剂量 CdTe QDs 诱导的炎症中的重要性。