Moderate Zinc Deficiency Increases Cell Death After Brain Injury in the Rat

Zinc supplementation has been used clinically to reduce Zn losses and protein turnover in patients suffering from traumatic brain injury. Despite the known role of zinc in cell survival and integrity, the influence of zinc status on central nervous system wound healing in the weeks and months after...

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Bibliographic Details
Published in:Nutritional neuroscience 2002-10, Vol.5 (5), p.345-352
Main Authors: Yeiser, E. Carden, VanLandingham, Jacob W., Levenson, Cathy W.
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Apoptosis - drug effects
Apoptosis - physiology
Brain Injuries - pathology
Cell Death - drug effects
Cell Death - physiology
CNS
Energy Intake
Immunohistochemistry
In Situ Nick-End Labeling
Macrophages
Microglia
Neurons - drug effects
Neurons - pathology
Rats
Rats, Sprague-Dawley
Trauma
TUNEL
Zinc - deficiency
Zinc - pharmacology
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Summary:Zinc supplementation has been used clinically to reduce Zn losses and protein turnover in patients suffering from traumatic brain injury. Despite the known role of zinc in cell survival and integrity, the influence of zinc status on central nervous system wound healing in the weeks and months after brain injury has not been addressed. In this investigation, we examined cell death after unilateral cortical stab wounds in adult rats (n=5 per group) that were provided diets containing adequate zinc (30 mg Zn/kg diet), supplemental zinc (180 mg/kg), or moderately deficient zinc (5 mg/kg). Four weeks following the brain injury there was a 1.82-2.65-fold increase in terminal deoxynucleotidyl transferase-mediated biotinylated dUTP nick-end labeling (TUNEL)-positive cells with DNA fragmentation at the site of injury in animals receiving a moderately zinc deficient diet compared to animals receiving a zinc-adequate or supplemented diet (p#0.05). Examination of the nuclear morphology of these cells suggested the presence of both apoptosis and necrosis. Immunohistochemistry showed that the TUNEL-positive cells expressed both ED-1 and OX-42, identifying them as microglia/macrophages. Thus it appears that adequate zinc status may be necessary to minimize the amount of neuroimmune cell death after brain injury.
ISSN:1028-415X
1476-8305
DOI:10.1080/1028415021000033811