Environmental estrogens are long known to interfere with neurological, reproductive, cardiovascular and musculoskeletal system of human-beings and animals. Chemicals like bisphenol-A and phthalates are just two of many environmental endocrine disruptors that have deleterious effects on the health. Earlier studies on neuronal cultures in rats have shown that both bisphenol-A and phthalates induce reactive oxygen species and apoptosis. Mitogen-activated protein kinase pathway is reported to be involved in the apoptotic signaling. One part of this study is to explore the effects of these chemicals and the mechanisms involved in their toxicity.The research has been done on two alternative cell culture models: PC-12 cells and chicken cerebellar granule neurons. Chicken neurons have given opportunity to investigate toxicity at different stages of neuronal development in vitro. Vitamins C and E, which are ROS scavengers showed protection after bisphenol-A exposure at the early stages of neuron development. Chicken neurons were more sensitive to bisphenol-A and phthalate exposure than PC-12 cells.Since serum-deprivation has been widely used to initiate apoptosis in the PC-12 cells, this model was used as comparison. ROS is known to be generated as a result of such exposure which in turn consumes endogenous glutathione under oxidative stress. Since glutathione is a vital endogenous antioxidant, measuring glutathione has given a better understanding to mechanisms behind the cell death and ROS production. The current study showed that glutathione levels fell after deprivation or when α-estradiol, but not vitamins C and E, was added to the serum-deprived PC-12 cells in accordance with earlier promoter study. However, bisphenol-A and MEHP did not change glutathione level.In conclusion, whereas deprivation induces cell death with reduction in GSH level, bisphenol-A and phthalate induce cell death with no effect on glutathione level.