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Atomic Absorbance Spectroscopy to Measure Intracellular Zinc Pools in Mammalian Cells
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Zinc Deprivation and the Nervous System
1a Department of Biochemistry, 112 Animal Science Research Center , University of Missouri , Columbia , MO 65211 , USA.
Nutritional Neuroscience
|July 15, 2016
Summary
Dietary zinc deprivation causes neurological issues, including behavioral changes and neuropathy. Early signs suggest a protective role for vulnerable zinc pools against oxidative damage in nerve cells.
Area of Science:
- Neuroscience
- Nutritional Biochemistry
Background:
- Zinc is crucial for nervous system function.
- Zinc deficiency rapidly induces pathological signs in animals.
- The precise biochemical mechanisms of zinc deficiency in the nervous system are not fully understood.
Purpose of the Study:
- To review the role of zinc in nervous system function.
- To emphasize the effects of dietary zinc deprivation on neurological health.
- To identify potential limiting zinc pools and their functions.
Main Methods:
- Review of existing literature on zinc metabolism and neurological function.
- Analysis of pathological signs and behavioral changes associated with zinc deficiency.
- Examination of zinc-dependent proteins and zinc pools in neural tissue.
Main Results:
- Zinc deficiency leads to behavioral changes, abnormal stance, and peripheral neuropathy.
- Essential zinc metalloproteins remain stable during early deficiency.
- Candidate limiting zinc pools include 'chelatable' and plasma membrane pools.
- Zinc deficiency affects calcium uptake in synaptosomes and may impair protective mechanisms against oxidative damage.
Conclusions:
- The initial limiting role of zinc in nerve tissue may be protective against oxidative damage, particularly to plasma membrane proteins and calcium channels.
- This protective role is distinct from catalytic or neurotransmitter functions.
- Further research is needed to identify specific zinc-dependent proteins affected early in deficiency.
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