The lethal concentration of
nitrite to the Chinese mitten crab Eriocheir sinensis was tested by exposing the animals to 17.78, 23.71, 31.62, 42.17, and 56.23 mg NaNO2 L(-1) at 20 degrees C for 24, 48, 72, and 96 h. The corresponding LC50 value for each time exposure was 43.87 (38.70-51.70), 40.24 (34.88-46.01), 38.87 (33.72-46.01) and 38.87 (33.72-46.01) mg NaNO2 L(-1) or 29.25 (25.80-34.47), 26.83 (23.25-30.67), 25.91(22.48-30.67), 25.91(22.48-30.67) mg NO2-N L(-1), respectively. The physiological response of the crab to
nitrite toxicity was further investigated by exposing the crab to 0, 10, 20, 30 and 40 mg NaNO2 L(-1) for 2 d. The changes of nitrogenous compounds in haemolymph,
oxyhemocyanin and metabolism were measured at 3, 6, 24 and 48 h upon exposure. Haemolymph
nitrite was significantly enhanced by the increase of
nitrite from 10 to 40 mg NaNO2 L(-1) during the 2-day exposure. The concentrations of
nitrate,
urea and
glutamate in haemolymph increased concomitantly with the exposing time and ambient
nitrite levels, suggesting that the formation of
nitrate,
urea and
glutamine may be the possible end products of
nitrite detoxification in crabs. The diffusion of
nitrite caused a reduction of
oxyhemocyanin, resulting to
hypoxia in tissues. Under a
hypoxia condition, crabs increased energy demand for metabolism as indicated by the elevated levels of
glucose and
lactate in haemolymph. Our data showed that ambient
nitrite could affect
oxygen carrying capacity through
oxyhemocyanin reduction and the increase of energy catabolism in crabs. This study suggests that
nitrite could be detoxified through the pathway of
nitrate,
urea and
glutamine formation in crabs.