| Autor: |
Mello DF; Center for the Environmental Implications of Nanotechnology, Nicholas School of the Environment, Duke University, Durham, North Carolina 27708, United States., Maurer LL; Center for the Environmental Implications of Nanotechnology, Nicholas School of the Environment, Duke University, Durham, North Carolina 27708, United States., Ryde IT; Center for the Environmental Implications of Nanotechnology, Nicholas School of the Environment, Duke University, Durham, North Carolina 27708, United States., Songr DH; Simulation Group, Samsung SDI, Suwon-si 17084, Gyeonggi-do, Republic of Korea., Marinakos SM; Center for the Environmental Implications of Nanotechnology, Department of Civil & Environmental Engineering, Duke University, Durham, North Carolina 27708, United States., Jiang C; College of Environmental Science and Engineering, Ministry of Education Key Laboratory of Pollution Processes and Environmental Criteria, Tianjin Key Laboratory of Environmental Remediation and Pollution Control, Nankai University, Tianjin 300350, P. R. China., Wiesner MR; Center for the Environmental Implications of Nanotechnology, Department of Civil & Environmental Engineering, Duke University, Durham, North Carolina 27708, United States., Hsu-Kim H; College of Environmental Science and Engineering, Ministry of Education Key Laboratory of Pollution Processes and Environmental Criteria, Tianjin Key Laboratory of Environmental Remediation and Pollution Control, Nankai University, Tianjin 300350, P. R. China., Meyer JN; Center for the Environmental Implications of Nanotechnology, Nicholas School of the Environment, Duke University, Durham, North Carolina 27708, United States. |
| Abstrakt: |
Silver nanoparticles (AgNPs) are extensively used in consumer products and biomedical applications, thus guaranteeing both environmental and human exposures. Despite extensive research addressing AgNP safety, there are still major knowledge gaps regarding AgNP toxicity mechanisms, particularly in whole organisms. Mitochondrial dysfunction is frequently described as an important cytotoxicity mechanism for AgNPs; however, it is still unclear if mitochondria are the direct targets of AgNPs. To test this, we exposed the nematode Caenorhabditis elegans to sublethal concentrations of AgNPs and assessed specific mitochondrial parameters as well as organismal-level endpoints that are highly reliant on mitochondrial function, such as development and chemotaxis behavior. All AgNPs tested significantly delayed nematode development, disrupted mitochondrial bioenergetics, and blocked chemotaxis. However, silver was not preferentially accumulated in mitochondria, indicating that these effects are likely not due to direct mitochondria-AgNP interactions. Mutant nematodes with deficiencies in mitochondrial dynamics displayed both greater and decreased susceptibility to AgNPs compared to wild-type nematodes, which was dependent on the assay and AgNP type. Our study suggests that AgNPs indirectly promote mitochondrial dysfunction, leading to adverse outcomes at the organismal level, and reveals a role of gene-environment interactions in the susceptibility to AgNPs. Finally, we propose a novel hypothetical adverse outcome pathway for AgNP effects to guide future research. |
