Here's one of the articles showing that magnesium can increase 5'-nucleotidase activity. I don't know which 5'-nucleotidase enzyme they're talking about here, actually, yet:
http://www.jbc.org/cgi/content/abstract/246/9/3057
(pubmed: http://www.ncbi.nlm.nih.gov/pubmed/4324346?dopt=Abstract)
That's the type of article that doesn't allow you to tell if the effect would be significant under normal circumstances. Magnesium normally helps buffer and maintain adenine nucleotide pools, and one mechanism explaining that buffering effect is the calcium-channel-blocking effect of magnesium (the other main one is to form MgATP2- and other complexes with adenine nucleotides). But it would probably be a double-edged sword, the effect of Mg2+ on 5'-nucleotidase activity. It would help provide extracellular adenosine, and that can be cardioprotective/antiatherogenic. But excessive amounts of Mg2+ could conceivably cause that kind of purine and pyrimidine "wasting" effect. It would probably only occur at some of the really high doses of magnesium some people talk about.
In the case of zinc, though, the activation of CD73 (ecto-5'-nucleotidase) activity and cytosolic 5'-nucleotidase activity by zinc would, in concert with other derangements of nucleotide metabolism that can be produced by excessive amounts of zinc, have more clear potential to be detrimental. CD73 activity is sensitive to changes in zinc intake and increases in response to zinc supplementation, but I just don't think this would necessarily be a good thing, really. That effect can help decrease platelet aggregation in the short term, but it doesn't mean that zinc "should" be increasing CD73 activity or that the CD73 enzyme is somehow subsaturated or deficient in activity in the absence of a large excess of zinc. This article talks a bit about the way zinc is a component of both 5'-nucleotidases and cyclic nucleotide phosphodiesterase enzymes:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1132794
To the extent that an excess of free zinc could increase the activities of phosphodiesterase enzymes or adenosine deaminase (a zinc metalloenzyme), those wouldn't necessarily be good things (especially in the case of phosphodiesterases). This article shows that zinc can directly inhibit adenylate cyclase, and the authors implicate this and other mechanisms in the neurotoxicity of zinc in diseases such as Alzheimer's:
http://www.jbc.org/cgi/content/full/277/14/11859
(pubmed: http://www.ncbi.nlm.nih.gov/pubmed/11805091?dopt=Abstract)
That inhibition of adenylate cyclase was not due to the binding of Zn2+ or ZnATP or some other zinc-containing species to one of the two metal binding sites, given that Mg2+ did not antagonize the effects of Zn2+. Magnesium increases adenylate cyclase activity to some extent, and the authors of that article, above, note that adenylate cyclase has two (apparently catalytic or allosteric) metal binding sites that normally bind Mg2+. The presence of a catalytic binding site for a metal is different from the presence of a "metal binding function" of a protein. That study on zinc shows that adenylate cyclase can bind zinc and be inhibited by it, but that doesn't mean that adenylate cyclase is "supposed" to be bound by zinc. It's pretty clear that it's a toxic effect that can result from an excess of free zinc.
A lot of the research on the supposed nutritional effects of zinc seems strange to me. One thing I'm seeing, as I do some hasty searches on zinc and CD73, is that part of the enhancement of CD73 activity is apparently due to a zinc-induced increase in CD73 expression. That's not really a "nutritional" effect in the traditional sense, because the effect of zinc on CD73 activity doesn't really seem to emerge in a predictable or even saturable way. The CD73 enzyme has more than one zinc binding site, and I'm sure that some level of dietary zinc is required for some normal level of CD73 activity. I'm not saying zinc is not essential, because it obviously is. But an increase in CD73 activity in response to zinc does not mean that the CD73 activity, in the absence of that level of zinc availability to CD73 itself or to the zinc finger transcription factors that mediate an increase in the expression of the CD73 gene, was "deficient" before the extra zinc was provided. This article looks like a good one that might talk about some of these issues related to zinc safety:
http://www.ncbi.nlm.nih.gov/pubmed/16632171
Zinc supplementation seems questionable to me, and single servings of many "meats" contain 4 and 5 mg of zinc, etc. The case reports on neurodegeneration induced by high-dose zinc supplementation or intractable hyperzincemia are appalling, and the neurotoxic effects of an excess of free zinc are unlikely to be attributable to merely a zinc-induced decrease of copper availability to the brain (here's the posting in which I link to some of those case reports: (http://hardcorephysiologyfun.blogspot.com/2008/12/zinc-toxicity-and-parp.html). I've never seen anything like that in the context of hypermagnesemia.
Hypermagnesemia is difficult to even achieve, given that the kidneys rapidly clear an excess of Mg2+ in the blood. Hypermagnesemia can cause a strange sort of almost paralytic effect, by inhibiting acetylcholine release at the neuromuscular junction, and there are reports in the literature of postoperative, intravenous infusions of magnesium inducing "recurarization" (http://www.ncbi.nlm.nih.gov/pubmed/8652332). The effect may have to do with calcium channel blockade by magnesium, I think, but it's mainly from i.v. magnesium. I've never seen a report of magnesium-induced, direct neurotoxicity, of the kind that very high-dose zinc supplementation has been shown to produce.
This animal study shows "neurotoxicity" following the direct injection of large amounts of magnesium into the spinal cord (http://www.ncbi.nlm.nih.gov/pubmed/9124662), but the abstract also shows that lower-level, inhibitory effects on neuromuscular functions, effects that occurred in response to half that dose of intrathecal magnesium, were accompanied by "warning signs" of magnesium-induced sedation and anesthetic effects (effects that could be explained by Mg2+-mediated NMDA receptor antagonism and calcium channel blockade, at least partially). The point is that similar warning signs have usually been evident in humans with hypermagnesemia, and I haven't heard of similar warning signs with Zn2+. But the main idea is that Zn2+ is known to have the potential to be neurotoxic, and even intravenous Mg2+ hasn't really been associated with those kinds of effects.
This is off the original topic, but this article shows the dynamic and somewhat nonspecific quality with which some metals/minerals can interact in the body (and calcium and magnesium are actually essential). Many metals are not essential but can still have effects on the body. That's part of my rationale for exploring all of the mechanisms involved in these topics. This article shows that magnesium activates type 5 adenylate cyclase, and calcium can antagonize this effect. The authors discuss the way magnesium can allosterically activate adenylate cyclase or participate in the binding of a substrate, ATP (as MgATP2-), to adenylate cyclase:
http://www.jbc.org/cgi/content/full/277/36/33139
(pubmed: http://www.ncbi.nlm.nih.gov/pubmed/12065575?dopt=Abstract)
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