中文摘要：

钴是参与维生素B12合成和许多生命活动中必不可少的微量元素,然而一旦机体细胞内的钴离子含量因职业暴露或因饮食摄取钴过量或因钴合金人工假体内源性释放超过安全标准,则可导致严重的金属沉着疾病,这种金属沉着病的症状主要包括感音神经性耳聋、神经性耳鸣、视觉缺陷、认知缺陷、心肌病、心衰、甲状腺疾病、皮肤感觉异常等,在上述病症中,感音神经性耳聋和视神经萎缩是最明显的钴中毒症状。钴中毒引起的细胞损害机制主要涉及细胞的氧化应激和缺氧性损害以及线粒体损害引起的细胞凋亡。因此,钴中毒引起的细胞损害模型尤其适用于听觉系统和视觉系统以及神经系统中因细胞内氧化/抗氧化失衡和细胞缺氧以及线粒体凋亡通路等方面的医学实验研究。

英文摘要：

Cobalt is an important essential element that is required for the synthesis and functional activity of vitamin B 12. Therefore, cobalt is necessary for life. However, if intracellular concentrations of cobalt are excessive due to occupation- al exposure, dietary intake, or endogenous exposure from cobalt-chromium implants, it can also lead to a severe disorder, called metallosis characterized by sensorineural hearing loss, nervous tinnitus, visual impairment, cognitive impairment, pe- ripheral neuropathy, cardiomyopathy, heart failure, thyroid problems, skin rashes, etc. Among these toxicities by cobalt, senso- ry deafness and optic atrophy are the most noticeable symptoms. The toxic mechanisms of cobalt mainly involve oxidative stress, hypoxic injury and mitochondrial-induced apoptosis. Therefore, animal models of cobalt intoxication are applicable to research examining an imbalance in oxidation/antioxidation equilibrium, intracellular hypoxia, and mitochondria initiated apoptotic pathways, especially in the auditory, vision and nervous systems.