Nutrition and Traumatic Brain Injury Improving Acute and Subacute Health Outcomes in Military Personnel (2011) / Chapter Skim
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16 Zinc
16 Zinc
Pages 233-246
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From page 233... ...
Neurons in brain regions with high concentrations of free zinc, such as the hippocampus, are thus particularly vulnerable to zinc-mediated damage and death. Additionally, after CNS injury, large quantities of free zinc can be released, not only from presynaptic vesicles but also from metalloproteins and from mitochondrial zinc pools, result 233
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From page 234... ...
Because the metal-binding metallothioneins have been shown to play an antioxidant role, these data suggest that zinc deficiency may impair antioxidant mechanisms that are needed to protect neurons and other cell types in the brain after TBI. A relevant selection of human and animal studies (from the year 1990)
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From page 235... ...
group placebo- mg or supplementation on serum zinc level, the supplemented controlled at 12 mg for 15 days, group had significantly higher levels of trial then tablets of 22 mg zinc in urine at days 2 (p=0.0001) and 10 elemental zinc or placebo (p=0.01)
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From page 236... ...
Hellmich TBI, fluid Adult, male Lamotrigine or At 4 hours post-TBI, injured rats had et al., percussion Sprague- nicardipine significant increase in number of neurons 2007 injury (FPI) Dawley rats with Flouro-Jade (FJ, showing injured cells)
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From page 237... ...
Yeiser TBI, Adult, male Postinjury, Compared to rats fed with standard et al., unilateral Sprague- zinc diets (standard: amount of zinc (controls) , serum 2002 cortical stab Dawley rats 30 mg/kg; moderately zinc level was significantly lower in zinc-deficient rats (p ≤ 0.05)
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From page 238... ...
isoforms I and II in injured, zinc-deficient rats was greater compared to uninjured controls (p < 0.001) , but lower compared to injured, normally fed rats (p < 0.05)
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From page 239... ...
. However, zinc supplementation appears to be associated with improvements in markers of immune function in a variety of other noncritically ill patients.
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From page 240... ...
While controlled cortical impact resulted in significant performance deficits on the Morris water maze test in animals fed a diet adequate in zinc, rats that were fed the zinc-supplemented diet (180 ppm) prior to TBI showed no differences from sham-operated control rats at any point during the 10-day cognitive trial, suggesting that zinc supplementation may improve cognitive resilience in the event of brain injury (Cope et al., unpublished)
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From page 241... ...
Zinc supplementation resulted in increased levels of serum pre-albumin and retinol-binding protein, suggesting improved protein synthesis and a role for supplemental zinc in maintaining visceral protein in TBI patients. Two weeks after injury, patients in the zinc-supplemented group had better Glasgow Coma Scale scores than control patients given adequate zinc.
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From page 242... ...
-positive cells at the site of injury compared to animals with adequate zinc. TUNEL staining, a marker of DNA fragmentation and cell death, in combination with nuclear morphology and cell-specific markers, revealed that moderate zinc deficiency caused both apoptosis and necrosis of macrophages and ameboid microglia involved in the clearance of debris following TBI (Yeiser et al., 2002)
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From page 243... ...
In the acute care situation, the available clinical evidence suggests that after TBI, zinc deficiency should be prevented to maintain visceral protein and optimize the potential for neurological recovery. The only acute dose of supplemental zinc that has been tested in a clinical setting is 12 mg/day administered intravenously for the first 15 days after injury.
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From page 244... ...
2008. Chelation of neurotoxic zinc levels does not improve neurobehavioral outcome after traumatic brain injury.
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From page 245... ...
2002. Moderate zinc deficiency increases cell death after brain injury in the rat.
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