Abstract
The present study explored the mechanism of cytotoxic and genotoxic effects of AgNPs on a primary culture of mouse Sertoli cells in vitro. To understand the possible molecular mechanisms of testicular lesions following exposure to AgNPs, isolated Sertoli cells were exposed to 5, 10, or 15 μg/ml. DNA damage in the Comet assay and apoptosis in the TUNEL assay were evaluated. The mRNA expression of p53 and bcl-2 genes and their proteins involved in apoptosis was also investigated. The antioxidant status of treated Sertoli cells was determined by measuring superoxide dismutase (SOD-1), catalase (CAT) and glutathione peroxidase (GPX-1) using quantitative polymerase chain reaction (qPCR). The superoxide anions were detected using the nitroblue tetrazolium (NBT) reduction assay. Results indicated that AgNP exposure causes increased oxidative stress levels. The activation of p53, repression of bcl-2 and reduction of endogenous antioxidant enzymes were also involved in these mechanistic pathways, leading to reduced cell numbers and cell detachment.
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