zinc & EDTA - interesting i never would have hypothesized this one (take note best betters):
Dietary Metal-complexing Agents and Zinc Availability in the Rat
Donald Oberleas, Merle E. Muhrer and Boyd L. O’Dell
The growth rate of weanling rats was used to determine the effects of phytate, calcium and ethylenediaminetetraacetate (EDTA) upon the physiological availability of zinc. Phytate decreased availability and the effect was augmented by excess dietary calcium. Calcium had no effect in the absence of phytate so that its effect must be mediated through an interaction with phytate. EDTA increased zinc availability when the diet contained phytate but had no significant effect upon the growth rate in the absence of phytate
. In vitro experiments showed that zinc phytate is highly insoluble at the pH range encountered in the small intestine. Addition of calcium to the medium produced an even more insoluble complex containing zinc, calcium and phytate. The results suggest that the formation of such complexes with phytate is the mechanism whereby zinc is made less available and the more complete precipitation of zinc in the presence of calcium explains the effect of excess calcium. In vitro studies with intestinal strips and 65Zn showed that zinc uptake was progressively decreased as the ratio of calcium to phytate was increased. This effect was counteracted in part by the addition of EDTA. It appears that EDTA increases zinc availability by competing with phytate and forming a soluble complex which allows absorption across membranes
zinc & cell death:
2005 The American Society for Nutritional Sciences J. Nutr. 135:359-362, March 2005
Recent Advances in Nutritional Sciences
Roles for Cell Death in Zinc Deficiency1,2
Pamela J. Fraker
Studies of zinc deficiency (ZD) have become important for demonstrating that nutritional imbalances can readily induce programmed cell death (PCD) or apoptosis in a variety of kinds of cells
. In mice, ZD caused a 300% increase in the amount of apoptosis among pre T-cells, which was a major cause of thymic atrophy that alters host defense. Embryogenesis was significantly altered in ZD mice due to increased apoptosis in the neural crest, optic, and head regions. Insufficient zinc initiated PCD in hepatocytes, glioma, kidney, monocytes, fibroblasts, and testicular cells, demonstrating the scope of this phenomenon. New forms of cell death continue to emerge. For example, autophagy is initiated by starvation and various nutritional and metabolic imbalances. Autophagy is a form of PCD whereby the cell digests some of its own organelles to provide needed nutrients. Understanding the interplay between these different forms of cell death and nutritional imbalances is very important because of their profound impact on development, growth, immune function, and health.
zinc & microhemorrhage:
Matrix metalloproteinase-9 and spontaneous hemorrhage in an animal model of cerebral amyloid angiopathy
Jin-Moo Lee, MD, PhD et al
We examined the potential role of the extra-cellular matrix-degrading enzyme, matrix metalloproteinase-9 (MMP-9), in the pathogenesis of cerebral amyloid angiopathy (CAA)-induced spontaneous hemorrhage. The amyloid-beta peptide (A) induced the synthesis, release and activation of MMP-9 in murine cerebral endothelial cells, resulting in increased extracellular matrix degradation. Furthermore, extensive MMP-9 immunoreactivity was observed in CAA-vessels with evidence of microhemorrhage in aged APPsw transgenic mice, but not detected in aged wild type or young APPsw mice. These results suggest that increased vascular MMP-9 expression, stimulated by A, may play a role in the pathogenesis of spontaneous intracerebral hemorrhage
in patients with CAA.
for more on zinc and tissue integrity, check this one out:
this one's on zinc deficiency and elevated MMP-9, plus another interesting one on zinc and response to interferon drugs:
that's all for now, time to get ready for work..