In this work, the widely used plastic additives bisphenol A (BPA), diisononyl phthalate (DINP) and dibutyl phthalate (DBP) were analyzed for developmental and oxidative stress effects on PC12 cells and chicken embryos. Genes studied in fetogenesis were PAX6, including studies of the upstream target GLI and downstream target MMP9. PAX6 is responsible for proper brain, eye and pancreas development. For oxidative stress, GCL, which is the rate-limiting enzyme for glutathione-production was studied. Glutathione is an important molecule in ROS and RNS defense in cells. For PAX6, MMP9 and GCL promoter or GLI response element activity, luciferase assays were used. For semiquantification of PAX6 levels, western blots were used. BPA increased PAX6 levels in embryo cerebella, but no change of PAX6 P1 promoter activity in primary cultures of cerebellar granule neurons was seen. Neither GLI nor MMP9 gave significant changes. GCL transcription was reduced with both BPA and DBP in lowest concentration (1nM). It is therefore estimated that low molecular phthalates and BPA have effects in oxidative stress responses by lowering GCL transcription.