Aging & Oxidative Stress & Zinc & Neurodegeneration Baste on 23 Feb 2007 11:16 am
Zinc in ‚Inflam-aging’ of the Brain
Source: Biogerontology (200), 7: 307-314
Article Type: Review
Authors: V Frazzini, E Rockabrand, E Mocchegiani, SL Sensi
Image Taken From:
http://upload.wikimedia.org/wikipedia/commons/thumb/7/79/
Zinc_finger_DNA_complex.png/300px-Zinc_finger_DNA_complex.png
Zinc (Zn) is the second most abundant trace element in the body (total amount approx. 2 g) and essential for human survival. Zics’s role in human physiology include a) catalytic (about 300 enzymes are Zn-dependent), b) structural (‘Zn-finger motifs in proteins) and c) regulatory (metallothioneins, immunes response, insulin metabolism) function.
Currently, a daily Zn intake of 10 mg is considered adequate. Dietary surveys showed widespread, worldwide prevalence of inadequate Zn intakes with, however, considerably lower risk in North America and Europe than other parts of the world.
Well-known clinical Zn-deficiency symptoms include a) skin lesions & delayed wound healing, b) immune deficiency, c) impaired taste and appetite and d) eye lesions. Consequently, Zn is nowadays commonly found in dietary/food supplements.
As with any nutrient, too much is too much. This brings us to the recent article by Frazzini et al. who asked the question whether Zn could actually be a link between oxidative stress and brain aging.
What caught my interest are the in nerve cells observed regional differences of Zn dysregulation, which have been suggested to trigger ‘normal’ brain aging and especially neurodegeneration.
The figure below summarizes the key aspects of the mechanisms possibly explaining Zn’s potential to induce brain cell death.
Does this now mean we should be aware of our daily Zn intake to protect our brain?
Most probably not. Although Zn toxicity (here especially peripheral symptoms) has been described in individuals repeatedly consuming more than 50 mg per day, the blood brain barrier, which regulates Zn homeostasis of the brain, is comparatively impermeable to changes in the concentration of blood metal ions. This does, of course, not mean that one cannot deplete the brain of Zn when significantly cutting down oral Zn intake.
In terms of neurodegeneration, for example Alzheimer’s disease, current believe is that the toxic effects of Zn are due to disruption of the brain endogenous Zn homeostasis, a hypothesis which is supported by studies in neuronal-specific Zn-transporter knockout mice.
As a general comment, I think Zn deficiency is a far bigger problem that chronic Zn overload for the majority of people. So, despite the increasing number of studies linking brain Zn with neurodegeneration, the above mentioned facts hopefully made clear that there’s only little - better to say no - hope of preventing neurodegeneration by reducing Zn intake. Vice versa, increase Zn intake above the current RDA to boost the body’s antioxidant and subsequently disease resistance, as suggested in various publications, must also be discouraged due to lack of evidence.
FIGURE: Mechanism of Zn-mediated Neurodegeneration