Abstract
Zinc is the trace element considered the one of the etiological agents involved in nerve cell damage in certain human neurodegenerative disorders. Growing evidence indicates the diverse effect of zinc ions, associated with its neuroprotective and neurotoxic abilities. We examined the effect of zinc on the evolution of anoxia‐induced neuronal injury in the organotypic cultures of rat hippocampus. The cultures had been pretreated with ZnCl2 (25–500 μm) 30 min prior anoxia. The ultrastructural findings documented dose‐dependent ability of Zn to reduce anoxia‐induced neuronal changes in hippocampal neurones in vitro. The significant neuroprotection involved the development of late apoptotic changes, whereas the early necrotic anoxia‐induced neuronal injury was not significantly reduced. However, the quite‐well preserved pyramidal neurones displayed the mitochondrial abnormalities, reflecting the combined neuroprotective and neurotoxic Zn properties.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
