When oceans acidify: Metal toxicity, uptake-depuration, and ion homeostasis in the copepod Nitokra sp

Mechanisms governing metal kinetics help maintain trace element levels required for physiological functions and ion regulation in aquatic organisms. However, both essential and non-essential metals can become toxic at excessive concentrations. Water physicochemical properties, including pH and dissolved anions, influence metal speciation, bioavailability, and toxicity. Under acidic conditions, bioavailability may increase as H⁺ competes with metal cations for binding sites, increasing free metal ions. Greater bioavailability may also disrupt uptake of essential macronutrients such as calcium (Ca) and sodium (Na) through competition at biotic binding sites. In the present study, we assessed the toxicity (half maximal lethal concentration [LC₅₀]), toxicokinetics (bioaccumulation at the 10% lethal concentration [LC₁₀] followed by depuration), and the impacts on Ca and Na levels of cadmium (Cd), copper (Cu), and zinc (Zn) in the estuarine copepod Nitokra sp. at pH 8.1 (natural) and pH 7.6 (acidified, as projected by the Intergovernmental Panel on Climate Change). All tested metals followed typical dose-response toxicity curves, with Cu being the most toxic, followed by Cd and Zn, with no significant differences between pH 8.1 and 7.6. Contrary to our hypothesis, bioconcentration factors were higher at pH 8.1 than at pH 7.6. Metal exposure did not significantly affect Ca and Na, but trends suggest early physiological disturbance, with Ca decreasing with exposure to Cd or Zn and increasing with exposure to Cu. During elimination, Ca levels were higher in Cu-exposed copepods than in Cd-exposed ones and similar to controls, suggesting that Cd competes with Ca at the cellular level.