Richard said:
> This simply is not true as I have already pointed
> out, but obviously not very well.
We certainly acknowledge your better general grasp of the mechanics and
terminology at work here, and it would certainly be reassuring to hear that
this was in fact the case, but merely echoing what we have all been told is
not very productive, unless you bring more supporting evidence to the table
than those who are being echoed.
> When you make a metabolite the original IMI is
> converted to the metabolite so the original
> molecule cannot possibly bind as it is no longer there.
> It is true you can make multiple metabolites from one parent molecule.
Since you are making statements about imidacloprid and its metabolites,
perhaps you can sort out the following list from table 3 of this paper:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3827204/
http://tinyurl.com/nckk4z8
IMI 1-(6-chloro-3-pyridylmethyl)-N-nitroimidazolidin-2-ylideneamine
IM-1
1-(6-chloro-3-pyridylmethyl)-N-nitro-5-hydroxyimidazolidin-2-ylideneamine
IM-2 1-(6-chloro-3-pyridylmethyl)-2-nitroguanidine
IM-3
1-(6-chloro-3-pyridylmethyl)-N-nitro-4,5-dihydroxyimidazolidin-2-ylideneamin
e
IM-4 1-(6- chloro-3-pyridylmethyl)imidazolidin-2-ylideneamine
IM-5 1-(6-chloro-3-pyridylmethyl)-Naminoimidazolidin-2-ylideneamine
IM-6 1-(6-chloro-3-pyridylmethyl)-N-nitrosoimidazolidin-2-ylideneamine
IM-7 1-(6- chloro-3-pyridylmethyl)-N-nitroimidazolin-2-ylideneamine
IM-8
N5-[1-[(6-chloropyridin-3-yl)methyl]-2-methyl-1,2,6,7-tetrahydro-imidazo[1,2
-b][1,2,4]triazin-1-one
IM-9 1-(6-chloropyridin-3-ylmethyl)imidazolin-2-one
IM-10 N-nitroimidazolidin-2-ylideneamine
IM-11 N-nitroimidazolin-2-ylideneamine
ICM-1 2-nitroguanidine (1-nitroguanidine)
a) Which metabolites above are created from which of the others?
b) What is the order of the breakdown?
c) What happens differently that results in different metabolites being able
to bind with the same receptors?
d) What is the statistical mix of these differences, which are the most
commonly-found metabolites that can bind?
e) What would happen to change the binding site itself, to make it "bind
more tightly" (or is it really "readily"?) in some metabolites as compared
to others?
f) Why would the metabolites have modified binding sites, yet never be able
to end up with an extra one created as a result of metabolization? What's
the difference between "change" and "create", given that we are talking
about chemistry?
g) What are the odds that the "binding more tightly" is actually "binding
to different receptors"?
h) What are the odds that bee nutrition or some other externality is making
a big difference in metabolization, and hence, the results found in the
various studies?
I've been asking these questions, and no one seems to have a glimmer of an
answer.
And if we don't know the answers to the above, I fail to see how the flat
statements are anything more than a guess, a statement of what SHOULD happen
under ideal conditions.
And as I said, we seem to have "Unexpected Consequences" here.
So if you can actually explain the specifics of what is going on great.
But if you can't back up a flat statement with either specifics or with at
least a statistically-based general statement, then we simply DON'T know,
and we need to take a look, if for no other reason than to put the issue to
rest.
So, when one says "This simply is not true", one cannot support that
statement with a list of even more general statements that may or may not
apply to the specifics of the case at hand.
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