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Updated: Feb 23, 2026

Toxicity Study of Zinc Oxide Nanoparticles in Cell Culture and in Drosophila melanogaster
Published on: September 19, 2019
Neurotoxicity of Zinc
Deborah R Morris1, Cathy W Levenson2,3
1Department of Biomedical Sciences, The Florida State University College of Medicine, Tallahassee, FL, 32306-4300, USA.
Abstract:
Zinc-induced neurotoxicity has been shown to play a role in neuronal damage and death associated with traumatic brain injury, stroke, seizures, and neurodegenerative diseases. During normal firing of "zinc-ergic" neurons, vesicular free zinc is released into the synaptic cleft where it modulates a number of postsynaptic neuronal receptors. However, excess zinc, released after injury or disease, leads to excitotoxic neuronal death. The mechanisms of zinc-mediated neurotoxicity appear to include not only neuronal signaling but also regulation of mitochondrial function and energy production, as well as other mechanisms such as aggregation of amyloid beta peptides in Alzheimer's disease. However, recent data have raised questions about some of our long-standing assumptions about the mechanisms of zinc in neurotoxicity. Thus, this review explores the most recent published findings and highlights the current mechanistic controversies.
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