Department of Biology, Faculty of Science, University of Sarajevo, 71 000, Sarajevo, Bosnia and Herzegovina.
Department of Biology, Faculty of Science, University of Sarajevo, 71 000, Sarajevo, Bosnia and Herzegovina.
Environ Pollut. 2023 Apr 1;322:121174. doi: 10.1016/j.envpol.2023.121174. Epub 2023 Feb 4.
Nickel (Ni) is a widespread environmental pollutant commonly released into effluent due to industrial activities, the use of fuels, or wastewater disposal. Many studies confirm the toxic effects of this heavy metal. However, there is a lack of knowledge and data on bioaccumulation patterns in tissues as well as cellular and molecular responses following the exposure of living organisms to Ni. In this study, Japanese quails were exposed to low (10 μg/L) and high (2000 μg/L) Ni concentrations in the form of nickel(II) chloride via drinking water. Sub-chronic exposure lasted 30 days while nominal concentrations represented average Ni content in drinking water (low dose) and average Ni levels in highly polluted aquatic environments (high dose). It was revealed that a high dose of Ni was correlated with increased water intake and decreased body weight. Overall, Ni exposure induced the development of microcytic anemia and alterations in measured blood indices. Moreover, Ni exposure impaired immunological activation as seen through the increased number of the white blood cells, increased heterophile/lymphocyte (H/L) ratio, and pronounced thrombocytosis. Ni elicited changes in the albumin, glucose, cholesterol, and triglyceride serum levels in a concentration-dependent manner. Alterations of plasma protein fractions suggested liver functional impairment while high levels of urea and creatinine indicated potential kidney injury. Granulation of heterophiles and an increase in erythroblasts in the bone marrow showed that the hematopoietic tissue was also impacted by Ni toxicity. On average each quail bioaccumulated 5.87 μg of Ni per gram of tissue. Moreover, the distribution and bioaccumulation of Ni in terms of relative concentration were as follows: feathers > kidneys > heart > liver > pectoral muscles. Assessed bioaccumulation levels and associated cellular and metabolic alterations have revealed new multilayer toxicological data that will help in the extrapolation of Ni toxicity in other vertebrates, including humans.
镍（Ni）是一种广泛存在的环境污染物，通常由于工业活动、燃料使用或废水处理而释放到废水中。许多研究证实了这种重金属的毒性作用。然而，对于生物体暴露于镍后组织中的生物累积模式以及细胞和分子反应，我们的了解和数据还很缺乏。在这项研究中，通过饮用水的形式，日本鹌鹑被暴露于低（10μg/L）和高（2000μg/L）浓度的镍（Ni），即氯化镍。亚慢性暴露持续 30 天，而名义浓度代表饮用水中的平均镍含量（低剂量）和高度污染的水生环境中的平均镍水平（高剂量）。结果表明，高剂量的镍与饮水量增加和体重减轻有关。总的来说，镍暴露会导致小细胞性贫血和测量血液指标的改变。此外，镍暴露会损害免疫激活，表现为白细胞数量增加、异嗜性/淋巴细胞（H/L）比值增加和明显的血小板增多。镍以浓度依赖的方式引起白蛋白、葡萄糖、胆固醇和甘油三酯血清水平的变化。血浆蛋白谱的改变表明肝脏功能受损，而尿素和肌酐水平升高则表明潜在的肾脏损伤。异嗜性粒细胞的颗粒化和骨髓中红细胞生成增加表明造血组织也受到镍毒性的影响。平均而言，每只鹌鹑组织中生物累积了 5.87μg 的镍。此外，镍在组织中的分布和生物累积按相对浓度表示如下：羽毛>肾脏>心脏>肝脏>胸肌。评估的生物累积水平以及相关的细胞和代谢变化揭示了新的多层毒理学数据，有助于将镍毒性外推到其他脊椎动物，包括人类。
