The route of NO(2)(-) uptake and subsequent physiological effects were examined in the marine teleost, European flounder (Platichthys flesus), during exposure to 1 mM ambient NO(2)(-) for up to 11 days. Drinking of seawater resulted in a similar nitrite concentration in the anterior part of the intestine as in the ambient water. The NO(2)(-) concentration decreased along the gastro-intestinal tract, suggesting NO(2)(-) uptake across the intestinal epithelium. Comparison of NO(2)(-) uptake in fish that drank NO(2)(-)-contaminated seawater with fish that did not (i.e. had the intestine perfused with a NO(2)(-)-free saline during NO(2)(-) exposure) revealed that the intestinal route contributed some 66% of whole-body NO(2)(-) uptake. Plasma [NO(2)(-)] stayed below the ambient level. It reached a maximum of 0.35-0.4 mM on days 3-6 and then declined to 0.2 mM on day 11. The physiological effects of NO(2)(-) exposure were relatively minor compared with those reported in freshwater fish. Blood methemoglobin levels increased from approximately 4% in non-exposed fish to a maximum of 18% of total hemoglobin in exposed fish. An extracellular hyperkalemia was observed from day 3 of NO(2)(-) exposure, with a maximal increase in plasma K(+) concentrations of 38%. No mortality occurred during the 11 days of NO(2)(-) exposure. The lack of mortality can be related to the relatively low NO(2)(-) accumulation in the plasma and the relatively minor physiological disturbances.