Responses of the sea anemone, Exaiptasia pallida, to ocean acidification conditions and zinc or nickel exposure.

Ocean acidification, caused by increasing atmospheric carbon dioxide (CO), is a growing concern in marine environments. Land-based sources of pollution, such as metals, have also been a noted problem; however, little research has addressed the combined exposure of both pollutants to coral reef organisms. In this study we examined tissue metal accumulation and physiological effects (activity of anti-oxidant enzymes, catalase and glutathione reductase) in the sea anemone, Exaiptasia pallida after exposure to increased CO, as well as zinc (Zn) or nickel (Ni). After exposure to four concentrations (nominal values=control, 10, 50, 100μg/L) of Zn or Ni over 7days, both metals accumulated in the tissues of E. pallida in a concentration-dependent manner. Anemones exposed to elevated CO (1000ppm) accumulated significant tissue burdens of Zn or Ni faster (by 48h) than those exposed to the same metal concentrations at ambient CO. No differences were observed in catalase activity due to Zn exposure; however, 50μg/L Ni caused a significant increase in catalase activity at ambient CO. No significant effect on catalase activity from CO exposure alone was observed. Glutathione reductase activity was affected by increased Zn or Ni exposure and those effects were influenced by increased CO. Results of this study provide insight into the toxic mechanisms and environmental implications of CO and Zn or Ni exposure to the cnidarian E. pallida.