Fishery College, Huazhong Agricultural University, Hongshan District, Wuhan 430070, PR China.
Ecotoxicol Environ Saf. 2011 Jul;74(5):1156-63. doi: 10.1016/j.ecoenv.2011.02.015. Epub 2011 Mar 9.
The present study was conducted to determine antioxidant responses, hepatic intermediary metabolism, histology and ultrastructure in Synechogobius hasta after a 15-days of waterborne cadmium (Cd) exposure at the concentrations of 0 (control), 0.10, 0.17 and 0.29 mg Cd/l (corresponding to 0, 12.6%, 21.5% and 36.7% of 96 h LC₅₀), respectively. Growth performance and survival declined, but hepatosomatic index (HSI) increased with increasing waterborne Cd levels (P < 0.05). Waterborne Cd exposure also significantly increased lipid contents in whole body and liver (P < 0.05), and Cd accumulation in whole body, muscle and vertebrae. Waterborne Cd exposure changed hepatic enzymatic activities involved in intermediary metabolism, induced antioxidant responses and increased lipid peroxidation level in the gill, liver and spleen. Waterborne Cd exposure also caused considerable histological alterations of gill, liver and spleen, led ultrastructures damage of liver and spleen of fish, and induced fatty liver for this fish species.
本研究旨在探讨连续 15 天暴露于不同浓度(0、0.10、0.17 和 0.29 mg Cd/L,分别对应 96 h LC₅₀ 的 0、12.6%、21.5%和 36.7%)水镉环境下,褐牙鲆(Synechogobius hasta)的抗氧化反应、肝中间代谢、组织学和超微结构的变化。随着水镉浓度的增加,褐牙鲆的生长性能和存活率下降,但肝体比(HSI)增加(P < 0.05)。水镉暴露还显著增加了鱼体和肝脏的脂质含量(P < 0.05),以及鱼体、肌肉和脊椎的镉积累。水镉暴露还改变了参与中间代谢的肝酶活性,诱导了抗氧化反应,并增加了鳃、肝和脾的脂质过氧化水平。水镉暴露还导致了鳃、肝和脾的组织学改变,引起了鱼的肝损伤和脂肪肝。