Taurine attenuates nano-copper-induced oxidative hepatic damage via mitochondria-dependent and NF-kappa B/TNF-alpha-mediated pathway

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 nano-materials. 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-kappa B/I kappa B alpha in association with an enhanced level of TNF-alpha. Taurine treatment could, however, significantly reverse all these adverse effects in nano-copper-intoxicated mice.