氧化应激
神经毒性
褪黑素
细胞毒性
谷胱甘肽
内分泌学
内科学
化学
钴
神经保护
活性氧
生物化学
生物
药理学
毒性
医学
体外
无机化学
酶
作者
Gianfranco Olivieri,Christian Heß,Egemen Savaskan,Chuong V. Ly,Fides Meier,Ginette Baysang,Manfred Brockhaus,F. Müller‐Spahn
标识
DOI:10.1034/j.1600-079x.2001.310406.x
摘要
Heavy metals are increasingly being implicated as causative agents in neurodegenerative diseases such as Alzheimer's disease (AD). Cobalt, a positively charged transition metal, has previously been shown to be in elevated levels in the brain of AD patients compared with age-matched controls. In this study, we investigate the effects of cobalt as an inducer of oxidative stress/cell cytotoxicity and the resultant metabolic implications for neural cells. We show that cobalt is able to induce cell cytotoxicity (reduced MTT metabolism) and oxidative stress (reduced cellular glutathione). The pre-treatment of cells with the pineal indoleamine melatonin, prevented cell cytotoxicity and the induction of oxidative stress. Cobalt treatment of SHSY5Y cells increased the release of beta-amyloid (Abeta) compared with untreated controls (ratio Abeta 40/42). Melatonin pre-treatment reversed the deleterious effects of cobalt. These findings are significant as cobalt is an essential nutritional requirement, usually bound to cobalamin (vitamin B12), for all animals which in the unbound form could lead to neurotoxicity.
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