The Palaemonid shrimp Palaemon macrodactylus is widely distributed in coastal areas and estuaries which are easily contaminated by various pollutants. However, the responses of this species to environmental toxicants are not well described. In the present study, adult individuals of P. macrodactylus were exposed to gradient concentrations of Cadmium (Cd) to evaluate its acute toxic effects, including bioaccumulation, induced oxidative stress and changed energy metabolism in this species. The medium lethal concentration (LC₅₀) of Cd at 24 h, 48 h, 72 h, and 96 h were 2.60, 0.88, 0.49 and 0.37 mg/L, respectively. Cd bioaccumulations in tissues of shrimp increased in a concentration-dependent manner, and higher concentration (50% 96 h-LC₅₀, 0.185 mg/L) of Cd exposure led to a maximum increase of Cd concentration by 14.8, 145.5 and 15.8 folds in gill, hepatopancreas and abdominal muscle. Cd exposure caused a significant inhibition on the activity of catalase (CAT), and total superoxide dismutase (T-SOD), decrease in the total antioxidant capacity (T-AOC), and an increase of malonadehyde (MDA) content, which indicated a damage to the antioxidant system of shrimp. Meanwhile, Cd exposure also led to a significant up-regulation in the expression level of metallothionein gene (MT), and down-regulations at the mRNA level of heat shock protein 70 (HSP70) and CAT. Moreover, Cd exposure significantly inhibited the oxygen consumption rate (22%), and increased the ammonia excretion rate (43%), hence lead to a significant decrease of the O:N ratio (45%) in shrimp. The results indicated that Cd exposure could induce obvious oxidative stress, energy metabolic dysfunction and bioaccumulation of Cd in P. macrodactylus. The data obtained from the present study would provide useful information for further understanding on the toxicological mechanism of Cd to crustaceans in coastal areas and estuaries.

emon龙虾emon龙广泛分布在沿海地区和河口，容易被各种污染物污染。但是，该物种对环境有毒物质的反应还没有很好地描述。在本研究中，成年P. macrodactylus个体暴露于浓度梯度的镉（Cd）中以评估其急性毒性作用，包括该物种的生物蓄积，诱导的氧化应激和改变的能量代谢。Cd在24小时，48小时，72小时和96小时时的中等致死浓度（LC ₅₀）分别为2.60、0.88、0.49和0.37 mg / L。虾组织中镉的生物积累以浓度依赖的方式增加，并且浓度更高（50％96 h-LC ₅₀（0.185 mg / L）的Cd暴露导致g，肝胰腺和腹肌中的Cd浓度最大增加14.8、145.5和15.8倍。镉暴露对过氧化氢酶（CAT）和总超氧化物歧化酶（T-SOD）的活性有显着抑制作用，总抗氧化能力（T-AOC）降低，丙二醛（MDA）含量增加，表明损害虾的抗氧化系统。同时，镉暴露还导致金属硫蛋白基因（MT）的表达水平显着上调，而热休克蛋白70（HSP70）和CAT的mRNA水平则下调。。此外，Cd暴露显着抑制了耗氧率（22％），并增加了氨的排泄率（43％），因此导致虾中O：N比率显着降低（45％）。结果表明，镉暴露可引起明显的氧化应激，能量代谢功能障碍和镉的富集在P.趾鼠耳蝠。从本研究中获得的数据将为进一步了解镉对沿海地区和河口甲壳类的毒理机制提供有用的信息。