The effects of chloridazon (Ch) and its metabolite chloridazon-desphenyl (Ch-D) at the environmentally relevant concentrations of 0.45 µg/L and 2.7 µg/L on signal crayfish Pacifastacus leniusculus were assessed in a 30-day exposure followed by a 15-day depuration period. Locomotion, biochemical haemolymph profile, oxidative and antioxidant parameters, and histopathology were evaluated. Crayfish exposed to Ch at 0.45 µg/L and 2.7 µg/L showed significantly (p < 0.01) higher CAT activity and GSH level in hepatopancreas and gill compared to controls. The concentration of Ch at 2.7 µg/L was associated with significantly (p < 0.01) higher levels of GLU, LACT, ALT, AST in haemolymph compared to controls. Chloridazon-desphenyl exposure at both tested concentrations caused significantly higher (p < 0.01) GLU, LACT, ALT, AST, NH₃, and Ca in haemolymph; lipid peroxidation (TBARS) levels in hepatopancreas; and CAT activity and GSH level in hepatopancreas and gill. Alterations of structure including focal dilatation of tubules, increased number of fibrillar cells, and haemocyte infiltration in the interstitium were observed with 2.7 µg/L Ch and with both Ch-D exposures. Locomotion patterns did not vary significantly among groups. A 15-day recovery period was insufficient to restore normal physiological parameters in exposed groups. Chloridazon and its metabolite Ch-D exerts harmful effects on crayfish.

与环境有关的浓度分别为0.45 µg / L和2.7 µg / L的氯达松（Ch）及其代谢产物氯达松-去苯基（Ch-D）对小龙虾Pacifastacus leniusculus的影响在30天的暴露之后评估15天的净化期。评估了运动，生化血淋巴分布，氧化和抗氧化参数以及组织病理学。与对照组相比，暴露于Ch浓度分别为0.45 µg / L和2.7 µg / L的小龙虾的CAT活性和GSH水平显着提高（p <0.01）。与对照组相比，血淋巴中Ch的浓度为2.7 µg / L与GLU，LACT，ALT，AST的显着（p <0.01）水平相关。两种测试浓度下的氯达唑烷-去苯酚暴露均导致较高的（p <0.01）GLU，LACT，ALT，AST，NH ₃以及血淋巴中的Ca；肝胰腺脂质过氧化（TBARS）水平；肝胰腺和g中的CAT活性和GSH水平。在2.7 µg / L Ch和两次Ch-D暴露下均观察到结构改变，包括肾小管的局部扩张，原纤维细胞数量增加和间质中的血细胞浸润。各组之间的运动模式没有显着差异。15天的恢复期不足以恢复暴露组的正常生理参数。氯达唑酮及其代谢物Ch-D对小龙虾具有有害作用。