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内质网应激是指细胞内质网钙稳态失衡或蛋白质加工运输障碍,生理功能发生紊乱时的一种亚细胞器应答反应,主要表现为未折叠蛋白反应。内质网应激反应是细胞适应的一种自身保护机制,但持续的或剧烈的应激反应却能激发程序性细胞死亡。内质网应激可以由多种干扰内质网功能的病理生理改变以及其他环境因素变化引起,金属化学物也是重要的诱发内质网应激的外界环境因素。内质网应激作为一种适应和保护机制,研究内质网应激在金属毒性中的作用有助于探讨毒作用机制和化学防护剂的开发。本研究在描述内质网应激与铅、镉、汞、铁、锰、铬等金属毒性关系的基础上,发现不同金属诱导内质网应激具有明显的时间效应和剂量效应特点,基本表现为早期诱导,晚期恢复或抑制;低剂量激活,而高剂量抑制。这为探讨金属毒性机制提供给了新的靶点。
Endoplasmic reticulum stress is a subcellular organelle response response when the cellular endoplasmic reticulum calcium homeostasis or protein processing and transport disorders, physiological function disorder occurs, mainly as unfolded protein response. Endoplasmic reticulum stress response is a self-protection mechanism of cell adaptation, but sustained or severe stress response can stimulate programmed cell death. Endoplasmic reticulum stress can be caused by a variety of pathophysiological changes that interfere with the function of the endoplasmic reticulum and other changes in the environment, and the metal chemistry is also an important environmental factor that induces endoplasmic reticulum stress. Endoplasmic reticulum stress as a mechanism for adaptation and protection, the role of endoplasmic reticulum stress in metal toxicity is helpful to explore the mechanism of toxic effects and the development of chemopreventive agents. In this study, based on the description of the relationship between endoplasmic reticulum stress and the metal toxicity of lead, cadmium, mercury, iron, manganese, chromium and other metals, it was found that different metals have obvious time-effect and dose-response characteristics in endoplasmic reticulum stress. For early induction, late recovery or inhibition; low dose activation, while high-dose inhibition. This provides a new target for exploring the mechanism of metal toxicity.