Nano-silver triggers apoptosis through the mitochondria-dependent pathway in the gills of common carp

Abstract

Although the ecotoxicity of nano-silver has been extensively reported, its toxicological mechanisms in fish gills remain not fully elucidated—particularly, the apoptotic effects and underlying mechanisms induced by nano-silver in fish gills are still unclear. The main goal of the present study is to clarify the potential mechanisms mediating nano-silver-induced gill cell apoptosis in common carp (Cyprinus carpio) by combining terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay and real-time quantitative polymerase chain reaction (RT-qPCR) to detect apoptotic features and related gene expression patterns. The results showed that exposure to nano-silver resulted in a total silver accumulation of up to 0.15 µg g⁻¹ in fish gills, accompanied by an increase in reactive oxygen species (ROS) levels. Nano-silver induced a 21.4% apoptotic rate in fish gill cells and caused the differential expression of related apoptotic genes. In the mitochondrial-dependent pathway, including the mitogen-activated protein kinase (MAPK) and mitochondrial pathways, nano-silver exposure resulted in a significant up-regulation of ap-1 and cytc genes. In the death receptor pathway, nano-silver exposure resulted in a significant down-regulation of fadd and caspase-8 genes. These findings demonstrate that nano-silver likely induces ROS overproduction to activate the MAPK pathway, thereby triggering mitochondria-dependent apoptosis in carp gills. This study enriches the mechanistic understanding of nano-silver toxicity in fish and provides molecular evidence for the risk assessment of nano-silver in aquatic ecosystems.