As a result of living in a hyperosmotic environment, marine fish lose water, and one adaptation to this problem is to drink continuously. The salt water that they ingest is then desalinated in the oesophagus before it enters the intestine where fluid is absorbed into the body. Unfortunately, any pollutants that are present in the water will also enter the intestine as the fish drinks. The toxicity of waterborne copper to freshwater fish has been widely documented and we know that, in particular, excess copper disturbs sodium and chloride homeostasis and alters nitrogenous waste excretion. However, little is known about the effects of copper on marine fish, which live in a completely different osmotic environment and additionally expose their intestines to waterborne contaminants by drinking.
In a recent study published in Aquatic Toxicology, Martin Grosell and colleagues set out to identify the key mechanisms of both acute and chronic copper exposure in a marine fish: the gulf toadfish. The toadfish is an interesting study species, firstly because it is particularly resistant to other environmental stressors such as hypoxia and air exposure and, secondly,unlike most other teleost fish, it can switch from producing ammonia as a waste product to producing urea.
Toadfish were exposed to a variety of waterborne copper concentrations either as an acute challenge for 96 h or for 30 days. Following exposure, the team measured physiological parameters to assess the impacts of copper on osmoregulation and nitrogen excretion processes. Drinking rates during copper exposure were also measured in a separate group of toadfish using a radioisotope marker.
In response to copper exposure, toadfish produced excess mucus that bound copper and formed blue-green-stained mucus-copper precipitates in the tanks. At first, toadfish showed an apparent aversion to the taste of copper and reduced their drinking rate but, after three days of copper exposure, the drinking rate was increased beyond that of controls. The authors concluded that the eventual increase in drinking rate was a compensatory adjustment to osmoregulatory disruptions, which included elevated plasma sodium, chloride and magnesium levels.
Direct contact between water and the gastrointestinal tract resulted in copper accumulation in the intestine, although this occurred later than accumulation in the gills. Amazingly, toadfish accumulated copper in their gills at levels 10-15 times higher than background. This unusually high gill accumulation has also been demonstrated in the freshwater eel. Interestingly,these two species, which exhibit high gill copper accumulation, are among the most copper-tolerant teleosts.
Finally, as well as osmoregulatory disturbances, the authors demonstrated a dramatic, copper-induced elevation of plasma urea. While, in other teleosts, a stress-induced elevation in plasma ammonia has been associated with copper exposure, an increase in urea appears novel to the toadfish. As ammonia is also toxic in excess, Grosell and colleagues pose the intriguing hypothesis that the ability of toadfish to convert ammonia to urea could function here in preventing ammonia toxicity.
