Fig. 1

Mouse model exhibiting cranial neural tube defect after trimethoprim exposure. a Control mouse embryo (untreated) at E10.5 (24 somites stage) age matched against b mouse embryo with exencephaly at E10.5 (23 somites stage) harvested from TELSE tablet (0.5% w/v containing 0.1% w/v trimethoprim) administered female CD1 mouse. The arrows indicate the open cranial neural tube. c Mouse embryo with cranial neural tube defect at E10.5 (22 somites stage) harvested from pure trimethoprim (containing 0.05% w/v trimethoprim) administered female CD1 mouse. d Transverse section through the cranial region of embryo C showing open hindbrain (Scale bar for A-C represent 0.5 mm and D represent 0.1 mm). e TELSE tablet administered female CD1 mouse showed significantly increased number of exencephalic embryos (n = 8) compared to control embryos (n = 24) (*P < 0.0001) (ANOVA). f, g No significant differences were seen between crown-rump length and number of somites in the E10.5 embryos between affected (n = 8) and not affected embryos of both treated mice (n = 14) and untreated mice (n = 24) (P < 0.0001) (ANOVA) (Value of bars are medians ± standard deviation). h, i Chromatogram of trimethoprim showed a single peak at 1.54 min and mass spectrometry analysis of the TELSE tablet confirmed the presence of trimethoprim as the active compound, with an exact mass of 291 and 230 for parent and daughter ions respectively