Affiliation:
1. Laboratory of Functional Neurophysiology and Pathology, Research Unit UR/11ES09, Department of Biological Sciences, Faculty of Science of Tunis, University Tunis El Manar, 2092 Tunis, Tunisia
Abstract
AbstractCadmium (Cd) accumulates in the brain and can damage neurons via complex processes involving oxidative stress induction. In this study we used a homogenous population of neurons which are cerebellar granule neurons (CGNs) to investigate damage induced by Cd and its effects on antioxidant enzyme activity. The exposure of CGNs to increasing concentrations of Cd (2.5 μM-100 μM) during 24 h, 48 h, or 72 h led to the induction of neuronal death in a dose- and exposure time-dependent manner. The necrotic and/or apoptotic pathway involved in the cell death trigged by Cd seems to depend on the concentration of Cd and the exposure time. In addition to its cell damage, Cd was shown to affect the activity of superoxide dismutase (SOD) and catalase (CAT) depending on the concentration of Cd and the exposure time. We also found that the exposure to Cd induces a bigger change in SOD activity than in CAT activity. Taken together, our findings explain, in part, the mechanism of Cd toxicity in a specific type of neuron which can provide information related to neurological pathologies ascribed to Cd toxicity.
Subject
General Agricultural and Biological Sciences,General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Neuroscience
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