Taurine attenuates nano-copper-induced oxidative hepatic damage via mitochondria-dependent and NF-κB/TNF-α-mediated pathway

Abstract

Manufactured nano-copper particles are now being widely used in various fields. However, there is a serious lack of information regarding the human health and environmental implications of copper nanomaterials. In earlier studies, we have shown that nano-copper induces hepatotoxicity. The purpose of the present study was to evaluate whether taurine plays any protective role against nano-copper-induced hepatic damage, and if so, what pathways it undergoes for the mechanism of its protective action. Nano copper (15–20 nm) administration increased intracellular reactive oxygen species (ROS) and NO production, decreased glutathione level and induced apoptotic cell death via mitochondria-dependent pathways. Signal transduction studies showed that nano-copper exposure significantly elevated iNOS, Bax, cytochrome c, cleaved caspase 9 and cleaved caspase 3. In addition, the same exposure altered the protein expression of NF-κB/IκBα in association with an enhanced level of TNF-α. Taurine treatment could, however, significantly reverse all these adverse effects in nano-copper-intoxicated mice.