科研之友
微信
新浪微博
Facebook
分享链接
摘要
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.
