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Reactive oxygen species trigger NF-κB-mediated NLRP3 inflammasome activation involvement in low-dose CdTe QDs
Yanting Pang1, Daming Wu1, Ying Ma1
1Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing, 210009, China.
Abstract:
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.
Insights
Low-dose Cadmium telluride (CdTe) quantum dots (QDs) activate hepatic macrophages (Kupffer cells), causing liver injury and inflammation via oxidative stress and the NF-κB/NLRP3 pathway.
Area of Science:
- Toxicology
- Nanomedicine
- Immunology
Background:
- Cadmium telluride (CdTe) quantum dots (QDs) show promise in imaging and drug delivery.
- The toxicological effects and underlying mechanisms of low-dose CdTe QD exposure remain largely unknown.
- Hepatic macrophages (Kupffer cells, KCs) are critical in liver injury and inflammation.
Purpose of the Study:
- To investigate the toxic effects of low-dose CdTe QDs on hepatic macrophages (KCs).
- To elucidate the mechanisms of CdTe QD-induced liver injury and inflammation.
- To explore the role of the NF-κB and NLRP3 inflammasome pathways in CdTe QD toxicity.
Main Methods:
- In vivo studies using rodent models exposed to varying doses of CdTe QDs.
- In vitro experiments utilizing a KC cell model exposed to low concentrations of CdTe QDs.
- Assessment of oxidative stress markers, inflammatory cytokine levels, and key pathway protein expression (NF-κB, caspase-1, NLRP3).
- Intervention with N-acetylcysteine (NAC) and Dehydroxymethylepoxyquinomicin (DHMEQ) to investigate mechanistic pathways.
Main Results:
- Low-dose CdTe QDs (2.5 and 10 μM/kg·bw) induced liver injury and inflammation in vivo by disturbing antioxidant levels.
- CdTe QDs were absorbed by KCs in vitro, leading to significant reactive oxygen species (ROS) production, oxidative stress, and inflammation.
- ROS-mediated activation of the NF-κB pathway was identified as a key driver, promoting inflammatory factors and indirectly mediating NLRP3 inflammasome assembly.
- Inhibition of ROS and NF-κB signaling pathways attenuated CdTe QD-induced inflammation.
Conclusions:
- Low-dose CdTe QDs pose a risk, causing liver injury and inflammation primarily through Kupffer cell activation.
- Oxidative stress and subsequent NF-κB pathway activation are central mechanisms in CdTe QD-induced hepatic inflammation.
- The NF-κB and NLRP3 inflammasome pathways are crucial in mediating the inflammatory response to CdTe QDs in KCs.
