Quotes from organophosphate paper at
http://dx.doi.org/10...6/S0300-483X(02)00447-X
Knew it - organophosphate neurotoxicity is UNRELATED to its cholinergic effects
Exposure to organophosphorus (OP) esters can
cause several syndromes including acute choliner-
gic clinical episodes, the so-called Intermediate
syndrome, organophosphate induced delayed neu-
ropathy (OPIDN) and chronic neurological ef-
fects. Acute toxicity is produced by irreversible
inactivation of the enzyme cholinesterases, the
exact mechanism of the intermediate syndrome is
not understood while the OPIDN is claimed to be
‘marked’ by the inhibition and subsequent ageing
(dealkylation) of a protein enzyme in nerve cells
called neuropathy target esterase (NTE). The
ability to produce OPIDN is not even related to
the degree of inhibition of AchE and there is no
indication that the intermediate syndrome is
related to the cholinergic effect of OP compounds.
It took the medical and scientific body more than
50 years to recognise OPIDN despite its dramatic
nature of clinical presentation.
This is not an argument as such against the
existence of chronic neurotoxicity. We do agree on
the necessity of such studies. We have done some
work in this regard and our early results indicate
that some patients show clear improvement after
cessation of exposure and peripheral neurophysio-
logical parameters may even normalise, while
other patients do not. This is typically seen in
other chronic toxic neuropathies such as those
caused by lead and thallium.
So, I'll try to make a list of further literature to explore (after throwing out all the acute toxicity studies, and all studies before 1980)
NEGATIVE statistical significance (does not indicate absence of effect yet though - must see the odds ratios before firmly concluding)
Maizlish, N., Schenker, M., Weisskopf, C., Seiber, J., Samuels,
S., 1987. A behavioural evaluation of pest control workers
with short-term, low-level exposure to the organophosphate
diazinon. Am. J. Indust. Med. 12, 153 / 172.
Fiedler, N., Kipen, H., Kelly-McNeil, K., Fenske, R., 1997.
Long term use of organophosphates and neuropsychologi-
cal performance. Am. J. Indust. Med 32, 487 / 496.
Ames, R., Steenland, K., Jenkins, B., Chrislop, D., Russo, J.,
1995. Chronic neurologic sequelae to cholinesterase inhibi-
tion among agricultural pesticide applicators. Arch. En-
viron. Health 50, 440 / 443.
==
POSITIVE statistical significance
Misra, U.K., Prasad, M., Pandey, C.M., 1994. A study of
cognitive functions and event related potentials following
organophosphate exposure. Electromyogr. Clin. Neurophy-
siol. 34, 197 / 203.
Stokes, L., Stark, A., Marshall, E., Narang, A., 1995. Neuro-
toxicity among pesticide applicators exposed to organopho-
sphates. Occup. Environ. Med. 52, 648 / 653.
Or actually, just read Table 6.
BAD PESTICIDES:
sarin
pyridostig-mine bromide, DEET, and chlorpyrifos.
NEED MORE INFORMATION pesticides:
diazinon
===
THIS quote possibly related to those who down huperzine A or other nootropics:
What was
also unique among OP exposed patients was that
certain cholinergic functions were selectively pre-
served; for example, the sudomotor function in the
skin and respiratory modulation of cardiac vagal
tone in the bulbar reticular formation in the
brainstem were often not affected and yet other
functions that do not require cholinergic nerves in
the same anatomical sites were abnormal. It is well
known that chronic low level of anticholinesterase
activity protects cholinergic synapses from episo-
dic large anticholinesterase poisoning, but could it
at the same time damage non-cholinergic synapses
in the same area? This is a strong possibility given
the evidence from our patients chronically exposed
to LTLL of OP
Edited by InquilineKea, 20 August 2011 - 01:54 PM.