Metabolic disturbances in fish exposed to sodium pentachlorophenate (NaPCP) and 3,3',4,4',5-pentachlorobiphenyl (PCB126), individually or combined

The Swan River Estuary is the recipient of multiple urban and agricultural contaminants which have the potential to induce liver detoxication enzymes as well as altering the metabolism of aquatic organisms. To test if altered liver metabolism would influence liver detoxication capacities, pink snapper (Pagrus auratus) were i.p. injected with peanut oil (controls), or pentachlorobiphenyl #126 (PCB126), with sodium pentachlorophenate (NaPCP), or PCB126+NaPCP. Relative to controls, ethoxyresorufin-O-deethylase (EROD) activity was induced in the PCB126 and PCB126+NaPCP fish, but not in the NaPCP group. In the liver, cytochrome c oxidase (CCO) activity was enhanced by the treatments while citrate synthase (CS) activity remained unchanged and lactate dehydrogenase (LDH) activity was increased in the NaPCP treatment only. The results suggest that liver CCO activity may be a suitable biomarker of effect following exposure to PCBs or phenolic compounds. In the white muscle, only the PCB126+NaPCP treatment enhanced CCO activity, with all other enzymatic activities remaining unchanged. It appears that the resilience to metabolic perturbations is greater for white muscle than for liver. Low serum sorbitol dehydrogenase (sSDH) activity and histopathology of the liver indicated no significant alteration of cellular structure, albeit the lipid droplet size was increased in the PCB126 and in the PCB126+NaPCP treatments. It is concluded that the hepatic metabolic changes correspond to histopathological observations, but an altered metabolic capacity do not influence the metabolism of xenobiotics by liver enzymes, as measured by EROD activity.