AChE-inhibitors: inhibiting the replication & development of both neurons & glial
Subject: AChE-inhibitors: inhibiting the replication & development of both neurons & glial
Date: Sat, 20 Oct 2001 17:51:23 -0400
From: Stephen Tvedten <steve@getipm.com>
Organization: Get Set Inc. (www.getipm.com)
To: Paul Helliker <phelliker@cdpr.ca.gov>
Director, State of
California, Department of Pesticide Regulation
cc: Christine Whitman whitman.christine@epa.gov
Dear Mr. Helliker, I thought you might like to read this scientific article.
'Developmental Neurotox. of Chlorpyrifos...and Other Chlinesterase Inhibitors on DNA Synthesis...' _Env Health Perspectives_:109:909-913 (9/'01), http://ehpnet1.niehs.nih.gov/docs/2001/109p909-913/qiao/abstract.html ...
...by Duke U Med. Center authors, summarizes (and new experiments reported on) a massive *non-AChE* effect of organo-phosphates and other AChE-inhibitors: inhibiting the replication & development of both neurons & glial cells.
Using transformed (synchronous mitosis) neuronal & glial cell lines in vitro, a rapid inhibition of DNA synthesis and thus cell replication is shown by the *non-AChE-active* molecules chlorpyrifos and its catabolic product trichlorpyridinol. The AChE-active metabolite chlorpyrifos oxon also inhibited these cells. TCP is more persistant in the body and had a greater inhibition than the oxon. These transformed cell lines are less responsive in some way/s to chlorpyrofos than are normal neural cells.
The o-p diazinon and physostigmine (a carbamate) also inhibited neural replication [not all agents tested here or previously had equivalent effects, see the paper or the abstract].
Although apparantly AChE plays some additional non-enzymatic role in the proliferation of glial cells, there may still be some link of cell replication w/ the AChE-inhibiting neurotransmiter role of chemicals. But neural cell division is here clearly shown to be inhibited by molecules apparantly well-established as not inhibiting AChE. [Also, as far as I know, the ACh/AChE neurotransmission system is only present in the parasympathetic autosomal (involuntary) nerves, not in the sympathtetic autosomal nerves, or the voluntary nerves. I don't know its ditribution in the brain...].
Glial cell creation was inhibited more in most cases than were neurons, and it's glions that continue to develop well into childhood. Also, children's known faster recovery from AChE-inhibition becomes more irrelevant, even as their glial development make them more vulnerable!
The enzymes in serum or plasma that bind &/or hydrolize AChE-inhibitors (as AChE hydrolizes ACh) protect against o-p's & carbamate neurotransmiter effects. Neonates however are deficient in these binding proteins or hydrolytic enzymes. Thus, not only are they more vulnerable to AChE-inhibition, but they are likely more vulnerable to the effect of the same chemicals on the creation of neurons & glions.
In vivo, sea urchin embryos have had their neural cell development inhibited by o-p's.
Well Mr. Helliker, the ever unfolding dangers of your "registered" POISONS never cease to amaze me, especially when I realize that Rachel Carson's Silent Spring published in 1962 was concerned with the use of only about 700,000 pounds of pesticide POISONS used in the USA each year. We now use about 4.5 BILLION pounds of your "registered" POISONS and we lose more crops to insect pests than we did when we did not have any of your "crop protection products"! Using my non-toxic, food-grade and/or GRAS alternatives, I have removed all pest problems inside and outside in over 350 schools. Yet you will not allow their unregistered use. Why? Protect the people and not the POISON "industry" profits!
Respectfully, Stephen L. Tvedten
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