Cardiac and branchial physiology associated with copper accumulation and detoxication in the mytilid mussel Perna viridis (L.)

Acute, sublethal, copper exposures induced bimodal physiological responses in the mytilid mussel Perna viridis. Whole animal studies revealed that copper increased heart rate (mild tachycardia) whilst clearance rates and hence gill cilia were simultaneously inhibited. The inhibitory bioamine dopamine reversed tachycardia, indicating that elevated heart rates were due to nervous (serotonergic) stimulation of the myocytes. The excitatory bioamine 5-hydroxytryptamine failed to reverse copper-induced inhibition of clearance rates, suggesting that mechanical damage or blockage of the cilia rather than overt neurotoxicity was impairing the function of the gill. The digestive diverticula was the major copper-accumulating organ although rapid metal exocytosis was evident when individuals were allowed to depurate in uncontaminated seawater. Waste products are expelled from the digestive diverticula into the intestine and as the rectum passes through the heart, elevated rates of ventricular contraction may facilitate egestion of metal-rich faeces. Elevated cardiac activity during exposure to copper may serve to increase ventricular pulsatile pressure on the rectum for the expulsion of metal-rich faecal inclusions (coproliths) derived from the digestive diverticula lysosomes. This study describes a relationship between the heart, alimentary canal and digestive diverticula lysosomes as a pathway for metal detoxication in mytilid mussels.