Abstract
For several reasons the central nervous system is particularly sensitive to metal-induced oxidative stress (Verstraeten et al. 2008, this issue): the brain contains a high fraction of oxidizable polyunsaturated fatty acids, only relatively low activities of the antioxidant enzymes catalase, superoxide dismutase and glutathione peroxidase, has a high oxygen consumption and a high iron content. Parkinson’s disease is one of the neurodegenerative diseases where metal toxicity is suspected to play an important role (Verstraeten et al. 2008, this issue). This is based on the observation of high aluminium concentrations in post-mortem brains of patients with Parkinson’s disease and on animal studies where administration of aluminium caused a strong decrease in the dopamine content of the striatum. Metals are not degraded and may accumulate to toxic levels. This and the diversity of not yet fully understood mechanisms is the reason why metal toxicity is one of the hot topics of our journal (Hengstler et al. 2003; Barbosa et al. 2006a, b; Brulport et al. 2007; Devi et al. 2007; Hengstler and Bolt 2007; Kobayashi et al. 2007; M’Bemba-Meka et al. 2007; Montes et al. 2007; Nampoothiri et al. 2007; Periyakaruppan et al. 2007; Posser et al. 2007; Santos et al. 2007; Beyersmann and Hartwig 2008; Glahn et al. 2008). The editors are happy that Sandra Verstraeten from Buenos Aires and Lucila Aimo as well as Patricia Oteiza from the University of California present an extensive review about molecular mechanisms of brain toxicity in this issue of the Archives of Toxicology. The authors revisit the mechanisms of aluminium and lead toxicity and focus on the recent literature about deregulation of cell signalling, the impairment of neurotransmission, membrane biophysics and reactive oxygen species as key factors. This review is a must for everybody interested in metal-induced neurotoxicity.
Published Version
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