中华耳科学杂志
中華耳科學雜誌
중화이과학잡지
CHINESE JOURNAL OF OTOLOGY
2015年
1期
57-63
,共7页
李鹏%丁大连%曾祥丽%Richard Salvi%Jerome A. Roth
李鵬%丁大連%曾祥麗%Richard Salvi%Jerome A. Roth
리붕%정대련%증상려%Richard Salvi%Jerome A. Roth
钴%耳毒性%神经毒性
鈷%耳毒性%神經毒性
고%이독성%신경독성
Cobalt%Ototoxicity%Neurotoxicity
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。
鈷是參與維生素B12閤成和許多生命活動中必不可少的微量元素,然而一旦機體細胞內的鈷離子含量因職業暴露或因飲食攝取鈷過量或因鈷閤金人工假體內源性釋放超過安全標準,則可導緻嚴重的金屬沉著疾病,這種金屬沉著病的癥狀主要包括感音神經性耳聾、神經性耳鳴、視覺缺陷、認知缺陷、心肌病、心衰、甲狀腺疾病、皮膚感覺異常等,在上述病癥中,感音神經性耳聾和視神經萎縮是最明顯的鈷中毒癥狀。鈷中毒引起的細胞損害機製主要涉及細胞的氧化應激和缺氧性損害以及線粒體損害引起的細胞凋亡。因此,鈷中毒引起的細胞損害模型尤其適用于聽覺繫統和視覺繫統以及神經繫統中因細胞內氧化/抗氧化失衡和細胞缺氧以及線粒體凋亡通路等方麵的醫學實驗研究。
고시삼여유생소B12합성화허다생명활동중필불가소적미량원소,연이일단궤체세포내적고리자함량인직업폭로혹인음식섭취고과량혹인고합금인공가체내원성석방초과안전표준,칙가도치엄중적금속침착질병,저충금속침착병적증상주요포괄감음신경성이롱、신경성이명、시각결함、인지결함、심기병、심쇠、갑상선질병、피부감각이상등,재상술병증중,감음신경성이롱화시신경위축시최명현적고중독증상。고중독인기적세포손해궤제주요섭급세포적양화응격화결양성손해이급선립체손해인기적세포조망。인차,고중독인기적세포손해모형우기괄용우은각계통화시각계통이급신경계통중인세포내양화/항양화실형화세포결양이급선립체조망통로등방면적의학실험연구。
Cobalt is an important essential element that is required for the synthesis and functional activity of vitamin B12. 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.