Keywords: 
• nano-nickel oxide /
• Crassostrea gigas /
• oxidative stress /
• antioxidase /
• defense protein

Abstract: Nano-nickel oxide (nNiO) is a widely used nanoparticle, and the research on aquatic toxicological effects of nNiO was limited, especially for marine organisms. To explore the mechanism of toxicity of nNiO to marine bivalve molluscs, the Pacific oysters (Crassostrea gigas) were exposed to nNiO at different concentrations (0, 1, 10, 100 mg·L^-1) for 96 h in the present study. The activities of superoxide dismutase (SOD), peroxidase (POD), catalase (CAT) and malondialdehyde (MDA) content in gill and digestive glands were measured. The expression changes of the shock protein HSP70 and AOX gene in gill and digestive gland were also determined by real-time fluorescence quantitative PCR. The results showed that the content of the MDA in both tissues increased significantly (P<0.01) in the 100 mg·L^-1 treatment group, suggesting that the nanoparticles caused lipid peroxidation of oysters and may cause oxidative damage. Meanwhile, nNiO exposure also induced changes in the antioxidant enzymes (SOD, CAT, and POD) activities of oysters. The SOD and CAT activities reached the maximum in the 10 mg·L^-1 treatment group, while the POD activity reached the highest in the 1 mg·L^-1 concentration group. At high concentrations of nNiO (100 mg·L^-1) group, the activities of the three antioxidant enzymes were lower than those in lower concentrations (1 and 10 mg·L^-1), indicating that the activities of antioxidant enzymes were repressed by higher concentrations of nNiO exposure. However, heat shock protein (hsp70) and alternative oxidase (aox) genes were up-regulated in digestive glands and gills, respectively (P<0.01). It is indicated that the stress protein (HSP70 and AOX) played a key role with higher nNiO exposure concentration. The results provided basic data for the study on the toxicity mechanism of nano-nickel oxides to marine bivalve molluscs.