Nickel-induced oxidative stress and apoptosis in Carassius auratus liver by JNK pathway

• Nickel (Ni) induced Carassius auratus liver injury.
• Ni induced immunotoxicity and behavioral changes.
• Ni induced oxidative stress and apoptosis in fish liver by JNK and mitochondrial pathway.
• Ni regulated Bax, Bcl-2 and caspase-3 activities.

Nickel (Ni) is ubiquitous in the biosphere and is a common component of natural fresh waters. When present in high concentrations, it becomes toxic to aquatic organisms. It is known that Ni toxicity may induce oxidative stress and apoptosis. However, the precise mechanism and the pathways that are activated in fish are still unclear. Thus, this study aimed to assess which apoptotic pathways are triggered by Ni in Carassius auratus liver, the main target of waterborne pollutants. Fish were exposed to 10, 25, 50 and 100 mg/L of nickel sulfate for 96 h. Our data showed that Ni exposure caused fish weight loss (by 10–12%) and decreased locomotory activity (by 1–25%). Ni exposure significantly decreased the relative lymphocyte count (by 1–24%) and increased the relative count of monocytes (by 25–111%) and neutrophils (by 10–322%) as compared to controls. Ni induced oxidative stress, as evidenced by increasing of lipid peroxidation level (29–91%) and depleting of the glutathione levels (7–79%) in fish liver. Ni also suppressed the activities of superoxide dismutase (by 39–55%) and glutathione peroxidase (16–24%) and decreased ATP levels (13–51%) in livers. Moreover, liver caspase-3, one of the key executioners of apoptosis, was markedly activated by the Ni exposure. Ni exposure also increased expression levels of phosphorylated Jun N-terminal kinases (JNK) in liver, which in turn activated pro-apoptotic signaling events by breaking the balance between pro-apoptotic and anti-apoptotic Bcl-2 proteins. In conclusion, these results suggested that Ni induced oxidative stress and apoptosis, at least, via the JNK signaling pathway.