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EC number: 203-906-6
CAS number: 111-77-3
It should be noted that the zebra fish model does not have metabolic
capacity, which explains why methoxyethanol produced no effects. It is
well established that the proximate toxicant is the acid metabolite and
not the parent glycol ether. This study established that the acid
metabolite of DEGME does not appear to share the same developmental
toxicity characteristics as MAA.
2-(2-methoxyethoxy)acetic acid, the main metabolite of
2-(2-methoxyethoxy)ethanol was evaluated using the zebrafish
embryotoxicity test (ZET) usingt a modified protocol desinge as fast and
simple method to study chemical toxicity after exposure of the complete
vertebrate embryo during embryogenesis in ovo. The protocol included a
novel quantitative evaluation method to assess the development of the
zebrafish embryo based on specific endpoints in time, the general
morphology score (GMS) system , and a teratogenic evaluation using
separate scoring system based on that used for whole embryo cultures.
Methoxyethoxy acetic acid did not show any evidence of developmental
toxicity up to the maximum tested dose of 10mM. In contrast, the know
methoxyacetic acid and ethoxyacetic acid caused both growth retardation
and malformations. A comparison of the results obtained with this
substance and the others tested with the available mammalian
developmental toxicity data showed the potency ranking of the compounds
within their class in the ZET was comparable to their in vivo ranking.
There were no effects on any reproductive parameters apart from a slight
increase in resorptions in the high dose group. Fetal body weights
appeared to be slightly lower in the mid and high dose groups but this
difference was not statistically significant.
There was no evidence of teratogenicity in any dose group.
Weight gain (GD 6-18) g
*Significantly different from control (p 0.05). For
weight gain only GD 9-11 but overall difference considered biologically
Forelimb flexure (mild)
Dilated renal pelvis
Hyoid delayed ossification
Sternebrae delayed ossification
different from control (p 0.05)
All of these variations seen have been reported as background variants
in NZ rabbits (Palmer 1968, 1972, 1977; Stadler 1983). Mild forelimb
flexure and delayed ossification of the sternebral bones are
characteristic of smaller than average fetuses whilst delayed
ossification of the hyoid and sternebrae is characteristic of delayed
fetal development. These variations correlated with lower fetal body
weights in the mid and high dose groups. No pattern of malformation is
evident. The frequency and distribution of malformations seen do not
indicate teratogenicity, particularly in the context of the relatively
high incidence of spontaneous malformations seen with this species
In a study to examine the developmental toxicity of 2 -(2
-methoxyethoxy)ethanol by the dermal exposure route, pregnant rabbits
were exposured during GD6 -18. Some evidence of maternal toxicity was
seen in the high dose animals, mainly manifest as adverse haematological
changes. The percentage of resorbed implantations increased markedly at
750 mg/kg b.w. At terminal examination a significantly increased
incidence of pups with mild forelimb flexure, dilated renal pelvis,
retrocaval ureter was observed at the highest dose. The incidence of
delayed ossification of the hyoid and sternebrae and cervical spur were
observed at 250 and 750 mg/kg b.w. The NOAEL for maternal toxicity was
250 mg/kg b.w and that for fetotoxicity was 50 mg/kg b.w from this
study. No teratogenic effects were observed. The developmental effects
produced are seen primarily in conjunction with maternal toxicity and
are in the range of what might be expected from compromised mothers. The
variations seen are consistent with those associated with maternal
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