Thermal plasticity of the cardiorespiratory system provides cross-tolerance protection to fish exposed to elevated nitrate

Exposure to nitrate is toxic aquatic animals due the formation of methaemoglobin and a subsequent loss blood-oxygen carrying capacity. Yet, toxicity can be modulated by other stressors in environment, such as elevated temperatures. Acclimation temperatures has been shown offset negative effects on whole animal performance fish, but mechanisms underlying this cross-tolerance interaction remain unclear. In study, juvenile silver perch (Bidyanus bidyanus) were exposed factorial combination temperature (28 °C or 32 °C) concentrations (0, 50 100 mg NO3− L−1) treatments test hypothesis that thermal acclimation offsets via compensatory changes cardiorespiratory system (gills, ventricle blood oxygen capacity). Following 21 weeks acclimation, we found fish acclimated experienced an expansion gill surface area increase ventricular thickness regardless exposure concentration. (both reduced capacity increases concentration right shift oxygen-haemoglobin binding curves from both treatments. These results indicate plasticity gills warm are potential which may provide protection despite induced reductions transport.