Center for Biotechnology, University of Bielefeld, 33615 Bielefeld, Germany; Plant Biotechnology, Faculty of Biology, Bielefeld University, 33615 Bielefeld, Germany.
Physiology and Pathophysiology of Cells and Membranes, Medical School OWL, Bielefeld University, 33615 Bielefeld, Germany.
Environ Int. 2024 Sep;191:109000. doi: 10.1016/j.envint.2024.109000. Epub 2024 Sep 7.
Faced with unpredictable changes in global weather patterns, release and redistribution of metals through land erosion and water movements add to the increasing use of metals in industrial activities causing high levels of environmental pollution and concern to the health of all living organisms. Cadmium is released into the environment by smelting and mining, entering the food chain via contaminated soils, water, and phosphate fertilizers. Bioaccumulation of cadmium in plants represents the first major step into the human food chain and contributes to toxicity of several organs, especially the kidneys, where biomagnification of cadmium occurs over decades of exposure. Even in small amounts, cadmium brings about alterations at the molecular and cellular levels in eukaryotes through mutagenicity, molecular mimicry at metal binding sites and oxidative stress. The epigenome dictates expression of a gene's output through a number of regulatory steps involving chromatin remodeling, nucleosome unwinding, DNA accessibility, or nucleic acid modifications that ultimately impact the transcriptional and translational machinery. Several epigenetic enzymes exhibit zinc-dependence as zinc metalloenzymes and zinc finger proteins thus making them susceptible to deregulation through displacement by cadmium. In this review, we summarize the literature on cadmium-induced epigenetic mechanisms in mammalian kidneys and plants, compare similarities in the epigenetic defense between these bioaccumulators, and explore how future studies could advance our understanding of the cadmium-induced stress response and disruption to biological health.
面对全球气候模式的不可预测变化，通过土地侵蚀和水运动释放和重新分配金属，加上工业活动中金属使用量的增加，导致了高水平的环境污染，并引起了所有生物的健康问题。镉是通过冶炼和采矿释放到环境中的，通过受污染的土壤、水和磷酸盐肥料进入食物链。镉在植物中的生物积累代表了进入人类食物链的第一个主要步骤，并导致几个器官的毒性，特别是肾脏，镉在暴露几十年后发生生物放大。即使在少量的情况下，镉也会通过致突变性、金属结合位点的分子模拟和氧化应激，在真核生物的分子和细胞水平上引起改变。表观基因组通过涉及染色质重塑、核小体解旋、DNA 可及性或核酸修饰的多个调节步骤来决定基因输出的表达，最终影响转录和翻译机制。几种表观遗传酶作为锌金属酶和锌指蛋白表现出锌依赖性，因此它们容易通过镉的置换而失调。在这篇综述中，我们总结了哺乳动物肾脏和植物中镉诱导的表观遗传机制的文献，比较了这些生物积累物之间在表观遗传防御方面的相似性，并探讨了未来的研究如何能增进我们对镉诱导的应激反应和对生物健康的破坏的理解。
