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EC number: 907-672-2
CAS number: -
Neurotoxicity was evaluated in two studies. The results suggest that DBPP does not induce delayed neurotoxicity in chickens.
Neurotoxicity was evaluated in two studies (Abou-Dania 1987 (supporting
study); Abou-Dania 1988 (supporting study)).
In the study of Abou-Donia (1988) the effects of DBPP in chickens on
brain neurotoxic esterase (NTE), acetylcholinesterase (AChE) and plasma
butyrylcholinesterase (BuChE) were investigated. The oral LD50 of
di-n-butylphenyl phosphate (DBPP) was determined to be 1863 mg/kg body
weight in leghorn hens unprotected against its cholinergic effects. The
acute effect of this dose was studied on hen brain NTE, AChE and BuChE
24 h after dosing. While this treatment had no effect on brain AChE, it
produced statistically significant inhibition of brain NTE (38%
inhibition) and plasma BuChE (70% inhibition). Because it is generally
assumed that approximately 75% inhibition of hen brain NTE 24h after
dosing is required for an organophosphorous compound to have the
potential to produce delayed neurotoxicity, the present results suggest
that DBPP does not produce delayed neurotoxicity in chickens. These
results, however, are equivocal since the oral LD50 dose of DBPP caused
statistically significant inhibition of hen brain NTE and plasma BuChE,
enzymes that are sensitive to inhibition by delayed neurotoxic
organophosphorous compounds. The positive control, tri-o-cresyl
phosphate (TOCP) also caused a statistically significant inhibition of
hen brain NTE (87% inhibition) and plasma BuChE (62% inhibition). TOCP
did not produce a significant effect on brain AChE activity (11%
In another study (Abou-Donia 1987) the potential delayed neurotoxicity
of DBPP was investigated in hens. A group of hens treated with TOCP
served as a positive control. Although 12 out of the 20 hens treated
with one or two oral doses (at a 21-day interval) of the LD50 of DBPP
died, none of the hens that survived developed delayed neurotoxicity.
The lack of delayed neurotoxicity potential of DBPP was demonstrated by
a) the absence of any neurologic dysfunction such as leg weakness,
ataxia, or paralysis characteristic of organophosphorous
compound-induced delayed neurotoxicity (OPIDN) and b) the absence of
neuropathology lesions pathognomonic of OPIDN such as Wallerian-type
degeneration reported in the literature (Cavanagh 1973; Abou-Donia and
Graham 1978, 1979a,b; Abou-Donia et al. 1983,1986) and seen in positive
control hens treated with TOCP.
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