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Maternal toxicity, embryolethality and abnormal fetal development in CD‐1 mice following one oral dose of T‐2 toxin
Author(s) -
Rousseaux C. G.,
Schiefer H. B.
Publication year - 1987
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.2550070410
Subject(s) - gestation , fetus , offspring , toxin , toxicity , trichothecene , pregnancy , in utero , developmental toxicity , teratology , medicine , physiology , endocrinology , biology , biochemistry , genetics
An experiment was undertaken to determine the teratogenic effect of oral administration of T‐2 toxin, a trichothecene mycotoxin. Firstly, a dose response study using 0,0.5, 1.0, 2.0, 3.0, 3.5 and 4.0 mg/kg T‐2 toxin in propylene glycol, on day 9 of pregnancy, was undertaken. Maternal deaths and toxicity was noted in the 4.0 and 3.5 mg/kg groups post‐toxin administration. These groups gained less weight throughout gestation than the rest of the groups, because no fetuses were found in the 4.0 mg/kg group and the 3.5 mg/kg group had significantly fewer fetuses than the remaining groups. The total fetal weight was similar among all groups with fetuses, and normal sex ratio of offspring was seen. More major and minor defects were seen in the 3.0 mg/kg T‐2 toxin treated group than any other group. Secondly, a day response trial using a single dose of 3.0 mg/kg T‐2 toxin given on either days 6, 7, 8, 10, 11 or 12 of gestation was undertaken. Maternal mortality, with placental hemorrhage, was observed. Fetal loss was greater in the T‐2 toxin treated groups than in the starved controls. The greatest number of dead term fetuses was seen in mice treated on day 9 of gestation. Normal sex ratios were present in the offspring. Major skeletal defects were more numerous in mice treated on day 7 of gestation, whereas minor defects, retardations and variants were more common in mice treated on day 8. It was concluded that a single oral dose of T‐2 toxin in propylene glycol is primarily maternotoxic and embryolethal, and that defective development was possibly secondary to maternal toxicity.