ArticleBrain research2010
The relationship between transient zinc ion fluctuations and redox signaling in the pathways of secondary cellular injury: relevance to traumatic brain injury.
Article in Brain research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 36 citations in OpenAlex.
- Extremely Low-Frequency and Low-Intensity Electromagnetic Field Technology (ELF-EMF) Sculpts Microtubules.The European journal of neuroscience · 2025Article
- Neuro-Inflammation Modulation and Post-Traumatic Brain Injury Lesions: From Bench to Bed-Side.International journal of molecular sciences · 2022Review
- ZnProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Zinc in the Brain: Friend or Foe?International journal of molecular sciences · 2020Review
- Zinc and Traumatic Brain Injury: From Chelation to Supplementation.Medical sciences (Basel, Switzerland) · 2020Review
- Development of a stretch-induced neurotrauma model for medium-throughput screening in vitro: identification of rifampicin as a neuroprotectant.British journal of pharmacology · 2018Article
- Vitamins and nutrients as primary treatments in experimental brain injury: Clinical implications for nutraceutical therapies.Brain research · 2016Review
- Mechanochemical regulations of RPA's binding to ssDNA.Scientific reports · 2015Article
- Rapid accumulation of endogenous tau oligomers in a rat model of traumatic brain injury: possible link between traumatic brain injury and sporadic tauopathies.The Journal of biological chemistry · 2013Article
- Zinc-mediated allosteric inhibition of caspase-6.The Journal of biological chemistry · 2012Article
- Improving treatments and outcomes: an emerging role for zinc in traumatic brain injury.Nutrition reviews · 2012Review
- Fluorophilia: fluorophore-containing compounds adhere non-specifically to injured neurons.Brain research · 2012Article
- Zinc in the central nervous system: From molecules to behavior.BioFactors (Oxford, England)Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
A major obstacle that hampers the design of drug therapy for traumatic brain injury is the incomplete understanding of the biochemical pathways that lead to secondary cellular injury and contribute to cell death. One such pathway involves reactive species that generate potentially cytotoxic zinc ion fluctuations as a major executor of neuronal, and possibly glial, cell death. Whether zinc ions released during traumatic brain injury are toxic or protective is controversial but can be approached by investigating the exact concentrations of free zinc ions, the thresholds of compromised zinc buffering capacity, and the mechanism of cellular homeostatic control of zinc. Rapidly stretch-injured rat pheochromocytoma (PC12) cells express cellular zinc ion fluctuations that depend on the production of nitric oxide. Chelation of cellular zinc ions after rapid stretch injury, however, increases cellular reactive oxygen species. In a rat model of traumatic brain injury, parasagittal fluid percussion, analysis of the metal load of metallothionein was used as an indicator of changes in cellular zinc ion concentrations. The combined results from the cellular and in vivo investigations caution against interpreting zinc ion fluctuations in the early phase (24h) after injury as a primarily cytotoxic event.
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Registered trials
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