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Aspects of Cadmium Neurotoxicity

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Metal Ion in Stroke

Abstract

Occupational and environmental exposure to Cd leads to a progressive and almost irreversible accumulation of the metal in the body determined by various host factors such as Cd body burden, age, gender, body status of vitamins, and essential elements. Cadmium absorption rate is increasing by low Fe, Zn, and Ca levels. Metallothioneins play a critical role in the protection of human health from Cd toxic effects. Today besides many organs toxicity and carcinogenicity, Cd is considered also as a neurotoxin. Although Cd does not easily penetrate BBB barriers in adults, this heavy metal can disturb CNS function either via alterations in the trace elements brain contents or/and via disturbances of crucial brain enzymes interfering in neurotransmitters release and neurotransmission. Chronic low level to Cd exposure in developing organisms may cause serious behavioral problems in later life. Experimental in vitro and in vivo data refer to effects of Cd on the hypothalamus–pituitary axis at different levels which may lead to disorders of the endocrine and/or immune system. In conclusion, Cd-induced brain dysfunction may be related to disruption of metal ion homeostasis, reduction of the total brain antioxidant status, inhibition of oxidative DNA repair systems, alteration in signal transduction, stimulation in the production of ROS, which may act as signaling molecules in the induction of gene expression and apoptosis. Antioxidants to some extent may protect the brain from Cd oxidative stress.

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Carageorgiou, H., Katramadou, M. (2012). Aspects of Cadmium Neurotoxicity. In: Li, Y., Zhang, J. (eds) Metal Ion in Stroke. Springer Series in Translational Stroke Research. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-9663-3_33

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