Single hair analysis by X-ray fluorescence spectrometry detects small changes in dietary zinc intake: A nested randomized controlled trial.

The aim of this study was to determine whether X-ray fluorescence spectrometry (XRF) could be used to detect changes in hair zinc concentration in response to a modest daily increase in zinc from the consumption of zinc biofortified wheat flour. This study was conducted as part of an effectiveness trial (BiZiFED2) exploring the potential for zinc biofortified wheat to alleviate zinc deficiency in adolescent girls aged 10-16 years in Pakistan (trial registration ID ISRCTN17107812). A randomized controlled design was used. Participants received either control flour or zinc biofortified flour for 6 months. Consumption of biofortified flour resulted in an average daily increase in dietary zinc intake of 1.5 mg per day above that of the control flour. At baseline and at the end of the intervention, individual hair samples (control: n = 59, intervention: n = 64) were analyzed for zinc and sulfur content by XRF. Data were analyzed using linear mixed effects models to contrast between trial groups the changes from baseline to end point and also to compare baseline and end point values within each trial group. Increases from baseline to endpoint in both sulfur and zinc were significantly greater in the intervention group compared to control (sulfur counts. CONTROL: baseline = 119.87 ± 20.33 and endpoint = 121.58 ± 23.58/intervention: baseline = 122.67 ± 24.19 and endpoint = 131.60 ± 21.34); (Zinc counts. CONTROL: baseline = 50.88 ± 14.33 and endpoint = 54.82 ± 14.61/intervention: baseline = 49.61 ± 10.77 and endpoint = 58.79 ± 12.20). For these parameters, there were also significant increases from baseline to endpoint in the intervention group but not in control. Furthermore, for Zn:S count ratio there were no differences in terms of the magnitude of the change from baseline to endpoint in the control group, although significant increases from baseline to endpoint were evident in the intervention group (Zn:S count ratio. CONTROL: baseline = 0.42 ± 0.10 and endpoint = 0.45 ± 0.08/intervention: baseline = 0.41 ± 0.08 and endpoint = 0.45 ± 0.08). A modest increase in dietary zinc over 6 months resulted in a detectable increase in both sulfur and zinc counts in individual hairs measured using XRF. This offers a sensitive, non-invasive method to monitor changes within subjects in response to dietary zinc interventions.

Synaptic release of zinc from brain slices: factors governing release, imaging, and accurate calculation of concentration.

Cerebrocortical neurons that store and release zinc synaptically are widely recognized as critical in maintenance of cortical excitability and in certain forms of brain injury and disease. Through the last 20 years, this synaptic release has been observed directly or indirectly and reported in more than a score of publications from over a dozen laboratories in eight countries. However, the concentration of zinc released synaptically has not been established with final certainty. In the present work we have considered six aspects of the methods for studying release that can affect the magnitude of zinc release, the imaging of the release, and the calculated concentration of released zinc. We present original data on four of the issues and review published data on two others. We show that common errors can cause up to a 3000-fold underestimation of the concentration of released zinc. The results should help bring consistency to the study of synaptic release of zinc.

Is zinc the link between compromises of brain perfusion (excitotoxicity) and Alzheimer's disease?

Prior brain injury is a major risk factor in the development of Alzheimer's disease. This is true for traumatic brain injury, stroke or ischemic brain injury, and (more speculatively) for brain injury resulting from the hypo-perfusion-reperfusion in cardiac arrest or cardiac bypass surgery and even hypo- or hypertension. Here we propose that the release of excess, toxic, "floods" of free zinc into the brain that occurs during and after all excitotoxic brain injury is a key factor that sets the stage for the later development of Alzheimer's disease. Rapid and aggressive administration of zinc buffering compounds to patients suffering brain injury may therefore not only ameliorate the acute injury but might also reduce the risk of subsequent development of Alzheimer's disease.