Department of Biochemistry, Maharshi Dayanand University, Rohtak, India.
Department of Biochemistry, Maharshi Dayanand University, Rohtak, India; Department of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Neurotoxicology. 2014 Mar;41:154-66. doi: 10.1016/j.neuro.2014.02.004. Epub 2014 Feb 20.
Aluminium is light weight and toxic metal present ubiquitously on earth which has gained considerable attention due to its neurotoxic effects. The widespread use of products made from or containing aluminium is ensuring its presence in our body. There is prolonged retention of a fraction of aluminium that enters the brain, suggesting its potential for accumulation with repeated exposures. There is no known biological role for aluminium within the body but adverse physiological effects of this metal have been observed in mammals. The generation of oxidative stress may be attributed to its toxic consequences in animals and humans. The oxidative stress has been implicated in pathogenesis of various neurodegenerative conditions including Alzheimer's disease and Parkinson's disease. Though it remains unclear whether oxidative stress is a major cause or merely a consequence of cellular dysfunction associated with neurodegenerative diseases, an accumulating body of evidence implicates that impaired mitochondrial energy production and increased mitochondrial oxidative damage is associated with the pathogenesis of neurodegenerative disorders. Being involved in the production of reactive oxygen species, aluminium may impair mitochondrial bioenergetics and may lead to the generation of oxidative stress. In this review, we have discussed the oxidative stress and mitochondrial dysfunctions occurring in Al neurotoxicity. In addition, the ameliorative measures undertaken in aluminium induced oxidative stress and mitochondrial dysfunctions have also been highlighted.
铝是一种轻量级且有毒的金属，广泛存在于地球上，由于其神经毒性作用而受到广泛关注。由铝制成或含有铝的产品的广泛使用确保了其在我们体内的存在。进入大脑的铝的一部分会被长时间保留，这表明它在反复暴露时可能会积累。体内没有已知的生物作用，但已在哺乳动物中观察到这种金属的不良生理影响。氧化应激的产生可能归因于其在动物和人类中的毒性后果。氧化应激与包括阿尔茨海默病和帕金森病在内的各种神经退行性疾病的发病机制有关。尽管目前尚不清楚氧化应激是与神经退行性疾病相关的细胞功能障碍的主要原因还是仅仅是后果，但越来越多的证据表明，受损的线粒体能量产生和增加的线粒体氧化损伤与神经退行性疾病的发病机制有关。铝参与活性氧的产生，可能会损害线粒体生物能，并可能导致氧化应激的产生。在这篇综述中，我们讨论了铝神经毒性中发生的氧化应激和线粒体功能障碍。此外，还强调了在铝诱导的氧化应激和线粒体功能障碍中采取的改善措施。
