> Jim seems to be suggesting that it is building up to a toxic dose.
> Randy is denying it. Are different things meant here?
If by "toxic", you mean "fatal", I do not think anyone means "fatal".
The "toxicity" here would only be some low level of "intoxication".
"No Observed Effect" vs a "Measureable Effect" is the terminology people
use.
(Yes, a navigational or behavioral issue from a claimed low "chronic"
exposure could mean that the bee does not return from a flight, so the bee
is just as dead either way, but no one expects the bee to keel over from
acute pesticide poisoning from a low chronic dose.)
And I don't think that Randy is "denying" anything, as I don't think that
there is a conversation.
Christina said:
> ALL of the molecules persist for days, especially the top
> two metabolites, and ALL of them can bind to synapses.
> So one IMI molecule binds to one synapse. But its two
> metabolites can bind to TWO synapses, that was Jim's point.
Yes that was my point, but hold on there... maybe you can tell us if I
neglected to consider what Richard brings up - he's claiming that there is
only one unique binding point for an imidacloprid molecule, and that the
breakdown thereof yields two or more molecules, but only one that can bind
to a receptor, and one (or more) that cannot. Apparently, there's no way to
tell which one ends up with the bit that does the binding, which runs
counter to what I thought I knew about how enzymes do their jobs.
>> You can never make two metabolites
>> from one IMI that both retain the binding
>> site and block two nerves.
If the above is true, then I don't understand how anyone could ever get away
with saying things like "the metabolites are more toxic than the
imidacloprid", which has been said multiple ways by multiple people. The
toxicity should, in this scenario, be no different before or after the
initial breaking up of the imidacloprid, and no metabolite could ever be
"more toxic" to the bee.
What gave me the impression that each of the two major metabolites could
bind to a receptor was the lack of any qualification to the statements I've
read about their abilities to bind. If only one of the two can bind, I'd
have expected someone to mention it. I also remembered this older paper:
http://onlinelibrary.wiley.com/doi/10.1046/j.1471-4159.2000.751294.x/pdf
"First-generation (CP) and second-generation (CT) neonicotinoids bind at the
same site in the same way
Structure-activity relationships developed for the action of neonicotinoids
at the nAChRs of two Dipterans and two Homopterans provide a unique data set
to evaluate the first- and second-generation insecticides. Adding the CP or
CT substituent to nithiazine-type Molecules greatly increases the
insecticidal activity.
Thus, the CT substituent generally confers higher potency in the
clothianidin and desmethylthiamethoxam series, and the CP moiety is
preferred in the IMI, thiacloprid, acetamiprid, and nitenpyram series."
In the above, the specific use of the term "moiety" may have a different
meaning than I interpreted.
Re-reading it now, I have to concede that these paragraphs are no basis for
any conclusion on this.
It gaves me the impression that there are two "working parts" to the
"CP"-type pestcides, each of them able to "work" (block receptors).
But I cannot point to anything authoritative. As I have said before,
structural work seems appropriate, as knowing the actual structures of each
metabolite would help to resolve many unresolved issues of contention. I
don't think anyone has looked at the actual structures, although there seem
to be many who are acting as if what they have been told had some firm basis
in fact, when it seems to be pure assumptions, based upon what was intended
by the chemists who developed the pesticide.
> As Jim pointed out in an earlier post...
If I am pointing anything out, I hope it is that many of the flat statements
made here on Bee-L about the nuts and bolts of pesticide metabolization and
toxicity seem to have nothing to support them that can be considered
"authoritative evidence". If someone has done some LC-MS work, and has a
list of weights of each metabolite, I've yet to see it. If someone has some
actual structural data from looking at real molecules as metabolized by real
bees, subjected to "field-realistic" doses, I've yet to hear of it. Without
either one, I don't understand how anyone has any idea of what's going on
in the early stages of metabolization, which is a very big missing
prerequisite, given the stentorian tones with which these points have been
proclaimed.
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