Department of Biochemistry, Faculty of Biotechnology and Biomolecular Sciences, Universiti Putra Malaysia, 43400, UPM, Serdang, Selangor, Malaysia.
Faculty of Science and Natural Resources, Universiti Malaysia Sabah, Jalan UMS, 88400, Kota Kinabalu, Sabah, Malaysia.
Environ Sci Pollut Res Int. 2017 Oct;24(28):22510-22523. doi: 10.1007/s11356-017-9923-3. Epub 2017 Aug 13.
The release of pollutants, especially heavy metals, into the aquatic environment is known to have detrimental effects on such an environment and on living organisms including humans when those pollutants are allowed to enter the food chain. The aim of this study is to analyse the damage to Clarias gariepinus' liver caused by exposure to different concentrations of copper. In the present study, samples of C. gariepinus were exposed to sub-lethal copper sulphate (CuSO) concentrations (from 0.2 to 20.0 mg/L) for 96 h. Physiological and behavioural alterations were observed with respect to their swimming pattern, mucus secretion and skin colour. Mortality was also observed at high concentrations of copper. Histopathological alterations of the liver were analysed under light, transmission and scanning electron microscopies. The liver of the untreated group showed normal tissue structures, while histopathological abnormalities were observed in the treated fish under light and electron microscopes with increased copper concentrations. Histopathological abnormalities include necrosis, melanomacrophage, hepatic fibrosis and congested blood vessels. In addition, the enzyme activity of liver cholinesterase (ChE) was also found to be affected by copper sulphate, as 100% of cholinesterase activity was inhibited at 20.0 mg/L. Thus, liver enzyme activity and histopathological changes are proven to be alternative sources for biomarkers of metal toxicity.
已知污染物（尤其是重金属）排放到水生环境中会对环境和包括人类在内的生物产生有害影响，如果这些污染物进入食物链。本研究旨在分析暴露于不同浓度铜对蓝圆鲹肝脏的损害。在本研究中，将蓝圆鲹样本暴露于亚致死浓度的硫酸铜（CuSO）（0.2 至 20.0mg/L）中 96 小时。观察了游泳模式、黏液分泌和皮肤颜色等生理和行为变化。在高浓度铜的情况下也观察到了死亡率。在光镜、透射电镜和扫描电镜下分析了肝脏的组织病理学变化。未经处理组的肝脏显示正常的组织结构，而在暴露于增加的铜浓度的处理鱼中，在光镜和电子显微镜下观察到组织病理学异常。组织病理学异常包括坏死、黑色素巨噬细胞、肝纤维化和充血的血管。此外，还发现硫酸铜还影响肝脏胆碱酯酶（ChE）的酶活性，因为在 20.0mg/L 时，胆碱酯酶活性被抑制了 100%。因此，肝脏酶活性和组织病理学变化被证明是金属毒性生物标志物的替代来源。
