ABSTRACT

Heavy metal pollution is a problem that cannot be ignored. Due to the prevalence of cadmium in the environment and its harmful effects on humans, cadmium pollution has become a research hotspot recently. The mechanism of cadmium-induced toxicity has also drawn much attention and most studies have been conducted using whole cells, but the toxicological mechanism of cadmium remains unclear. In this study, we aimed to obtain NRK-52E cells at different growth stages by various methods and analyze the differences in cadmium toxicity. The results show that the cadmium sensitivity of cells in each phase was different and the late apoptotic rate was increased significantly after 5 µM Cd treatment. In addition, cadmium easily induces apoptosis of G0- and S-phase cells, as well as necrosis of S- and M-phase cells, but has no significant effect on G1-phase cells. Overall, we first explored the differences in the effects of cadmium on NRK-52E cells at various growth phases. Besides, the findings of this study might provide a theoretical basis for further exploration of the toxicological mechanism of cadmium.Abbreviations Cd: cadmium; CDK: cyclin-dependent kinases; DAPI 2-(4-amidinophenyl)-1H-indole-6-carboxamidine; TBST: Tris-buffered saline with Tween-20; PI: propidium iodide; DMEM: Dulbecco’s Modified Eagle Medium; BCA: bicinchoninic acid

摘要

重金属污染是一个不容忽视的问题。由于镉在环境中的普遍存在及其对人体的危害，镉污染成为近年来的研究热点。镉致毒性的机制也引起了广泛关注，大多数研究是利用全细胞进行的，但镉的毒理学机制尚不清楚。在本研究中，我们旨在通过各种方法获得不同生长阶段的 NRK-52E 细胞，并分析镉毒性的差异。结果表明，5 μM C​​d处理后，各期细胞对镉的敏感性不同，晚期凋亡率显着增加。此外，镉易诱导G0期和S期细胞凋亡，以及S期和M期细胞坏死，但对 G1 期细胞无显着影响。总体而言，我们首先探讨了镉对不同生长阶段的 NRK-52E 细胞影响的差异。此外，本研究结果可能为进一步探索镉的毒理学机制提供理论依据。缩写Cd：镉；CDK：细胞周期蛋白依赖性激酶；DAPI 2-(4-脒基苯基)-1H-吲哚-6-甲脒；TBST：含有 Tween-20 的 Tris 缓冲盐水；PI：碘化丙啶；DMEM：Dulbecco 改良 Eagle 培养基；BCA：二辛可宁酸