Department of Experimental and Applied Medicine, Section of Occupational Health and Industrial Hygiene, University of Brescia, Italy.
Hum Exp Toxicol. 2012 May;31(5):421-37. doi: 10.1177/0960327111414280. Epub 2011 Jul 5.
Cobalt exerts well-known and documented toxic effects on the thyroid, heart and the haematopoietic system, in addition to the occupational lung disease, allergic manifestations and a probably carcinogenic action. Cobalt neurotoxicity is reported in isolated cases, and it has never been systematically treated. Bilateral optic atrophy and retinopathy, bilateral nerve deafness and sensory-motor polyneuropathy have been described long ago as a result of chronic occupational exposure to cobal powder or during long-term treatment of anaemia with cobalt chloride. Recently, some patients with high levels of cobalt released from metal prosthesis have been referred as presenting with tinnitus, deafness, vertigo, visual changes, optic atrophy, tremor and peripheral neuropathy. The aim of this work is to group these cases and to identify a possible mechanism of cobalt neurotoxicity, focusing on hypothetic individual susceptibility such as altered metal-binding proteins, altered transport processes in target cells or polymorphic variation of genetic background.
钴除了会引起职业性肺病、过敏表现和可能的致癌作用外，还会对甲状腺、心脏和造血系统产生众所周知和有文件记录的毒性作用。据报道，钴具有神经毒性，但从未得到系统治疗。很久以前就有报道称，长期接触钴粉或长期用氯化钴治疗贫血会导致双侧视神经萎缩和视网膜病变、双侧神经性耳聋和感觉运动性多发性神经病。最近，一些因金属假体释放出高浓度钴的患者被转介为出现耳鸣、耳聋、眩晕、视力改变、视神经萎缩、震颤和周围神经病。这项工作的目的是将这些病例分组，并确定钴神经毒性的可能机制，重点关注个体易感性的假设，如改变的金属结合蛋白、靶细胞中的转运过程改变或遗传背景的多态性变化。
