Effects of prolonged copper exposure in the marine gulf toadfish (Opsanus beta). I. Hydromineral balance and plasma nitrogenous waste products.

Acute (96 h) and prolonged (30 days) copper exposure induced osmoregulatory disturbance and impaired nitrogenous waste excretion in the marine teleost, the gulf toadfish (Opsanus beta), which was found to be extremely tolerant to acute copper exposure with a 96 h LC50 exceeding 340 microM but exhibited disturbed mineral balance in response to both acute and prolonged exposure to approximately 12 microM copper. The main cause of copper toxicity was found to be Na+ and Cl- regulatory failure leading to elevated plasma [Na+] and [Cl-] and osmolality which in turn led to fluid loss from muscle tissue. Analysis of intestinal fluid composition revealed a complicated pattern of effects of copper exposure. Intestinal transport physiology was directly influenced by copper exposure with Cl- absorption being the most sensitive parameter. Evidence for increased Na+ and fluid absorption when the fish exhibited elevated plasma osmolality indicates that the intestine may also exhibit a compensatory response to impairment of branchial transport processes, suggesting at least two target organs (gill and intestine) for copper toxicity in marine fish. Plasma Mg2+ was elevated from approximately 1.5 mM to as much as 4.0 mM, likely as a result of increased branchial permeability. While plasma [ammonia] clearly responded to copper exposure, plasma [urea] exhibited a much more sensitive and pronounced response to both acute and prolonged copper exposure, resulting in as much as a three-fold increase in circulating urea levels. This response is most likely the result of the unique ability of this teleost to convert ammonia to urea.