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EC number: 200-300-3
CAS number: 56-93-9
Table 1 Concentration of BTMAC-derived radioactivity in tissues
following i.v. administration of 0.63 mg/kg to the rat
a Mean + SD for three animals.
b All extracted 14C consisted of BTMAC
Values are ng equivalents/g tissue.
Results obtained from the toxicity experiments demonstrated that acute
toxicity of BTMAC was characterized by severe cholinergic symptoms
including salivation, chromodacryorrhea, and sedation. Diarrhea,
tremours, clonic convulsions, and respiratory distress were also usually
present. The incidence of spontaneous convulsions could be readily
increased by handling or otherwise disturbing the animals. Rats that did
not survive exhibited a series of regular convulsions, loss of
consciousness, rapid heart rate, and shallow respiration with gasping,
just before death. Death or survival of each animal was generally
determined within 3 h of dose administration.
The effects of atropine and neostigmine on BTMAC-induced salivation and
chromodacryorrhea were also examined. The atopine groups were clearly
protected against BTMAC-induced salivation and chromodacryorrhea. In
contrast, neostigmine appeared to potentiate the salivation response at
125 and 175 mg/kg. At the higher doses, salivation was already near
maximum and potentiation of this response by neostigmine was difficult
to determine. Neostigmine appeared to potentiate chromodacryorrhea only
at the lowest dose, probably because this response was at or near the
biological maximum at the next highest dose. In the non-BTMAC treated
rat (n = 3) administration of neostigmine resulted in slight but readily
detectable salivation and chromodacryorrhea.
The high dose that was used in the toxicity modulation experiments was
the reported oral LD50 in rat (DeWitt et al. 1953), therefore some
mortality among animals was expected. However, BTMAC appeared to be more
toxic than previously reported, since mortality in the present study was
near 100% at the high dose. Although these experiments were not designed
to be an LD50 study, death was dose related, and, in an effort to
ascertain as much information from this work as possible, estimates of
toxicity were calculated. Treatments did not appear to alter BTMAC
lethality significantly, since there were no left or right shifts in the
curves, only minimal differences in slopes were observed, and the LD50’s
for each group were essentially identical. Mortality was identical at 11
of 20 animals for each of the three treatment groups (saline-, atropine-
, and neostigmine-treated rat).
DEWITT, J. B., BELLACK, E., KLINGENSMITCH. W., WARD, J. C., and
TREICHLER, R., 1953, Relationship Between Chemical Structure and Toxic
Action on Rats. Chemical Biological Research Center, Review No. 5
(National Research Council, Washington), p. 39.
Benzyltrimethylammonium chloride (BTMAC)-derived radioactivity was
rapidly eliminated from the F344 rat following p.o. administration of 0.63-63
mg/kg of [ring-U-14C]BTMAC. Greater than 90% of the
radioactivity was excreted in urine and faeces within 24-h post-dosing.
2. BTMAC was poorly to moderately absorbed from the GI tract following
p.o. administration. The percent of total dose absorbed did not exceed
either 40% in the rat.
3. Absorption was linear, but limited, over time following dermal
administration of 63 mg/kg to the rat. Less than 10% of the total dose
was absorbed from the skin within 24 h of BTMAC application.
4. Metabolism of BTMAC was minimal in the rat. Toxicity (excessive
cholinergic stimulation and mortality) appears to be attributable to the
5. The limited absorption and rapid elimination of BTMAC should result
in little or no bioaccumulation in tissues following repeated exposure
to low levels of this compound. The results suggest that greater human
health risks may be associated with acute high level
exposure rather than chronic low level exposure.
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