Kidney compensates ion losses in copper exposed exercised shubunkin (Carassius auratus auratus)

Copper toxicity causes gills ionoregulatory and respiratory dysfunction in freshwater fish. However, not much is known about the effect on kidney. This research was conducted to investigate sublethal Cu effects on the ionoregulation in both gill and kidney of shubunkin, Carassius auratus auratus. Fish were not fed and exposed to 0 μmol/L (N=16, control), 0.34 μmol/L (N=16) and 0.84 μmol/L (N=16) of copper (CuSO4 5H2O) for 24 or 168 hours. An additional fed control group (N=8) was sampled to reveal the effect of food deprivation alone. All fish were exercised to exhaustion prior to sampling. Food deprivation alone had no effect on ionoregulation; and swimming performance (measured as critical swimming speed) was not affected by either fasting or Cu exposure. Low plasma osmolality level was noticed in fish exposed to the low Cu level for 168 hours. Cu induced a dose dependent Na+ loss in all Cu exposed groups. Both gill Na+/K+ ATPase and H+ ATPase (ATPase) activities were largely undisturbed. Except when fish were exposed to the high Cu level for 168 hours, where these ATPase activities were down-regulated and remarkable Na+ lost. Interestingly, both kidney ATPase activities were up-regulated when challenged with Cu. These ATPase activities were increased more prominent in fish exposed to the high Cu level. At both Cu levels, kidney ATPase activities were up-regulated likely act as a compensatory strategy to enhance Na+ reabsorption. However, this up-regulation was not sufficient to restore Na+ to control levels in the highest exposure group