Laboratory of Ecology, Biology and Physiology of Aquatic Organisms, Department of Biology, Faculty of Science of Tunis, University of Tunis El Manar, 2092, Tunis, Tunisia.
High Institute of Aquaculture and Fishing of Bizerte, BP15, 7080, Menzel Jemil, Tunisia.
Environ Sci Pollut Res Int. 2024 Aug;31(39):51658-51672. doi: 10.1007/s11356-024-34578-y. Epub 2024 Aug 9.
The present investigation was undertaken to evaluate the toxic effects of CoCl-induced hepatotoxicity and fatty acid changes in juvenile Cyprinus carpio. Fish were divided into six experimental groups in duplicate. The first group served as controls. The second group received the lowest exposure dose at 2.5 µg/L. In the third group, fish were exposed to 25 µg/L of CoCl. The fourth group was exposed to 50 µg/L of CoCl. The last two groups were exposed to the highest doses, 100 and 500 µg/L of CoCl. Total antioxidant activities were estimated using a colorimetric method. Liver fatty acid compositions were analyzed by high-performance gas chromatography (GC). Hepatopathy was identified through microscopic analysis. Exposure of C. carpio to CoCl resulted in hepatotoxicity, indicated by increased levels of malondialdehyde (MDA), hydrogen peroxide (HO), protein carbonyls (PCO), and alterations in the ferric reducing antioxidant power system (FRAP). Superoxide dismutase (SOD), glutathione-S-transferase (GST), glutathione peroxidase (GPx), reduced glutathione (GSH), metallothioneins (MTs), and low thiol levels (L-SH) significantly increased, particularly under exposure to the highest CoCl doses (100 and 500 µg/L). Acetylcholinesterase activity decreased significantly in C. carpio exposed to graded CoCl doses. Additionally, there was a decrease in polyunsaturated fatty acids (PUFA), primarily n-3 PUFA, docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA), while an increase in monounsaturated (MUFA) and saturated fatty acids (SFA), including palmitic (C16:0), stearic (C18:0), palmitoleic (C16:1), and oleic (C18:1) acids, was observed. Histopathological examination of the liver confirmed hepatopathy revealing characteristic tissue changes such as leucocyte infiltration, hepatic cell membrane degradation, vacuolization, and lipid inclusions. The study provided ethnophysiology insights into the responses of C. carpio to CoCl-induced oxidative stress and lipidomic alteration, underscoring its potential as a bioindicator for assessing environmental impacts and metal contamination.
本研究旨在评估 CoCl 诱导的幼鲤肝毒性和脂肪酸变化的毒性作用。将鱼分为六组，每组重复两次。第一组作为对照组。第二组接受最低暴露剂量 2.5μg/L。第三组暴露于 25μg/L 的 CoCl。第四组暴露于 50μg/L 的 CoCl。最后两组暴露于最高剂量，100 和 500μg/L 的 CoCl。使用比色法测定总抗氧化活性。采用高效气相色谱法（GC）分析肝脂肪酸组成。通过显微镜分析鉴定肝病变。CoCl 暴露导致鲤肝毒性，表现为丙二醛（MDA）、过氧化氢（HO）、蛋白羰基（PCO）水平升高，铁还原抗氧化能力系统（FRAP）改变。超氧化物歧化酶（SOD）、谷胱甘肽-S-转移酶（GST）、谷胱甘肽过氧化物酶（GPx）、还原型谷胱甘肽（GSH）、金属硫蛋白（MTs）和低硫醇水平（L-SH）显著升高，尤其是在暴露于最高 CoCl 剂量（100 和 500μg/L）时。CoCl 剂量递增暴露的鲤乙酰胆碱酯酶活性显著降低。此外，多不饱和脂肪酸（PUFA），主要是 n-3 PUFA、二十二碳六烯酸（DHA）和二十碳五烯酸（EPA）减少，而单不饱和（MUFA）和饱和脂肪酸（SFA）增加，包括棕榈酸（C16:0）、硬脂酸（C18:0）、棕榈油酸（C16:1）和油酸（C18:1）。肝组织学检查证实肝病变，显示特征性组织变化，如白细胞浸润、肝细胞膜降解、空泡化和脂质包涵体。该研究为鲤对 CoCl 诱导的氧化应激和脂质组改变的反应提供了民族生理学见解，强调其作为评估环境影响和金属污染的生物标志物的潜力。
