Abstract
In recent decades, the production of silver nanoparticles (AgNPs) has shown exponential growth. They are widely used as high-potency antimicrobial agents in a range of medical and consumer products and increasingly in the agricultural sector as a component of plant protection nanoproducts. Due to the risk of environmental hazards, the mechanisms of AgNPs toxicity should be thoroughly investigated to deepen our understanding of the potential negative impact on human health. As oxidative stress (OS) is known to be one of the major mechanisms of AgNP-induced toxicity, in the present study, we have evaluated OS-related changes in cytotoxicity parameters in AgNP-treated cerebellar granule cells (CGCs), as well as the effectiveness of antioxidant defence systems, such as glutathione (GSH), superoxide dismutases (SOD1 and SOD2) and catalase. The results indicate that exposure of CGCs to AgNPs decreases cell viability and mitochondrial potential and increases intracellular calcium concentration and free radical production. The level of intracellular GSH significantly decreases in cells after short-term exposure, but overexpression of SOD1 is observed. In contrast, after long-term exposure, catalase activity is substantially reduced. Supplying extracellular GSH prior to AgNPs significantly improved cell survival and reversed most of the changes in the investigated parameters. This suggests that GSH may be considered as a protective agent suitable for counteracting the negative effects of exposure to AgNPs.
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