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Related Concept Videos

Masking and Demasking Agents01:19

Masking and Demasking Agents

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EDTA titrations may necessitate masking and demasking agents to temporarily protect a particular metal ion in a mixture from the EDTA reaction. These agents facilitate the sequential analysis of the metal ions by forming stable complexes with some—but not all—metal ions during certain steps.
There are many masking agents, such as cyanide, fluoride, triethanolamine, thiourea, and 2,3-bis(sulfanyl)propan-1-ol (formerly 2,3-dimercapto-1-propanol), with the masking agent chosen based on...
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Atomic Absorbance Spectroscopy to Measure Intracellular Zinc Pools in Mammalian Cells
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Zinc and Traumatic Brain Injury: From Chelation to Supplementation.

Cathy W Levenson1

  • 1Department of Biomedical Sciences and Program in Neuroscience, College of Medicine, Florida State University, Tallahassee, FL 32306, USA.

Medical Sciences (Basel, Switzerland)
|August 23, 2020
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Summary

Traumatic brain injury (TBI) affects millions globally. Research shows zinc

Keywords:
brain injurychelationexcitotoxicityneuroprotectionsupplementationtraumazinc

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Area of Science:

  • Neuroscience
  • Neurobiology
  • Toxicology

Background:

  • Traumatic brain injury (TBI) is a significant global health issue, causing millions of disabilities and deaths annually.
  • Over 30 years of research have elucidated the complex neurochemical, cellular, and molecular mechanisms underlying TBI.
  • Initial research focused on the neurotoxic effects of excessive zinc accumulation following brain injury.

Purpose of the Study:

  • To review the evolution of research on zinc's role in traumatic brain injury.
  • To highlight the expanded understanding of zinc's involvement in TBI pathophysiology and potential therapeutic applications.

Main Methods:

  • Literature review of research spanning over three decades.
  • Analysis of studies investigating zinc's neurochemical, cellular, and molecular mechanisms in TBI.
  • Examination of research on zinc's impact on gene expression, neurogenesis, and cognitive/behavioral deficits post-TBI.

Main Results:

  • The field has progressed from understanding zinc toxicity to exploring cellular zinc pools after TBI.
  • Zinc plays a critical role in TBI-regulated gene expression and neurogenesis.
  • Interventions involving zinc show promise in mitigating cognitive and behavioral impairments following brain injury.

Conclusions:

  • Research on zinc and TBI has evolved significantly, revealing multifaceted roles beyond initial toxicity.
  • Understanding zinc's complex involvement offers new avenues for therapeutic strategies to improve outcomes after TBI.
  • Further investigation into zinc modulation may lead to effective treatments for TBI-related cognitive and behavioral deficits.