Nano-copper induces oxidative stress and apoptosis in kidney via both extrinsic and intrinsic pathways

In the modern medicine nano particle has been used as a power tool but recently it has been established that nano particle pathophysiologically affects different organs. Recently, we have investigated the role of copper nano particle in liver dysfunction. In the literature, practically little is known about the nano-copper induced renal dysfunction. We, therefore, conducted the present study as a continuation of our earlier one to investigate the molecular mechanism in nano-copper induced kidney dysfunction. Nano-copper exposure increased the production of reactive oxygen species (ROS), reactive nitrogen species (RNS) and altered the levels of oxidative stress related biomarkers in kidney tissue. Signal transduction mechanism studies showed that nano copper exposure reciprocally regulated Bcl-2 family protein expression, disturbed mitochondrial membrane potential and subsequently helped releasing cytochrome c from mitochondria to cytosol. Apoptotic nature of cell death is confirmed by activation of caspases 3 which is also supported by histological study. In addition, we also observed the activation of Fas, caspase 8 and tBid in kidney tissue in this pathophysiology, suggesting the involvement of extrinsic pathways. Combining all, results suggest that nano copper can trigger both intrinsic and extrinsic apoptotic pathways in oxidative stress mediated kidney dysfunction.

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► Nano-copper induced renal-dysfunction is poorly defined.
► Nano-copper exposure increased the production of ROS and RNS.
► Cell death is apoptotic in nature.
► Involvement of intrinsic and extrinsic cell death pathways.