Recent studies have revealed that excess Cu exerts pro-inflammatory effects by stimulating receptor-mediated signalling molecules such as nuclear factor-kappa B (NF-κB) (10), resulting in infiltration and activation of immune cells in inflamed organs (11). The recruited innate immune cells to the site of injury are again exposed to Cu to become activated and subsequently transmit activation signals to T lymphocytes, the key players of adaptive immunity (12). Following activation, the infiltrating immune cells produce a large amount of mediators and inflammatory cytokines causing clinical damage to living tissues (11, 12). Liver injury is characterized by accelerated serum levels of alanine transaminase (ALT) and aspartate transaminase (AST) (12), and impaired kidney function is reflected by a significant elevation of serum urea and creatinine concentrations (2, 13). After activation, the immune cells undergo programmed cell death characterized by extracellular exposure of phosphatidylserine (PS), various caspase activities and DNA fragmentation (14). Several recent studies reported that the pro-apoptotic property of Cu is mediated through oxidative stress and DNA damage in different cell types (15, 16). Because the accumulation of Cu in blood circulation and various organs of mammals can cause growth disorders (2, 17, 18), the biological safety issues of Cu content provided for animal feed is needed to be investigated.