4-tert-Octylphenol Exposure Disrupts Brain Development and Subsequent Motor, Cognition, Social, and Behavioral Functions

The endocrine-disrupting chemical 4-tert-octylphenol (OP) is a widespread estrogenic chemical used in consumer products such as epoxy resins and polycarbonate plastic. However, the effects of OP on brain development are unknown. The present study examined the effects of OP on neuron and neurobehavioral development in mice. By using primary cortical neuron cultures, we found that OP-treated showed a decreased length of axons and dendrites and an increased number of primary and secondary dendrites. OP reduced bromodeoxyuridine (BrdU), mitotic marker Ki67, and phospho-histone H3 (p-Histone-H3), resulting in a reduction of neuronal progenitor proliferation in offspring mouse brain. Moreover, OP induced apoptosis in neuronal progenitor cells in offspring mouse brain. Furthermore, offspring mice from OP-treated dams showed abnormal cognitive, social, and anxiety-like behaviors. Taken together, these results suggest that perinatal exposure to OP disrupts brain development and behavior in mice.

Bisphenol A Induces Oxidative Stress in Bone Marrow Cells, Lymphocytes, and Reproductive Organs of Holtzman Rats

Bisphenol A (BPA) is an estrogenic chemical used in the production of polycarbonate plastics and epoxy resins. Our earlier studies have demonstrated that BPA is a potent reproductive and genotoxic agent and affects the normal physiological functions. The objective of this study was to evaluate whether exposure to BPA induces oxidative stress. The male Holtzman rats were orally gavaged with BPA (0.01 mg and 5.0 mg/kg/bw) over the period of 6 days. Animals were euthanized by cervical dislocation at the end of the treatments; bone marrow cells and blood lymphocytes were aspirated; testis and epididymis were collected, immediately frozen in liquid nitrogen, and stored at −80°C. These samples were utilized for the determination of lipid peroxidation and various antioxidant enzymes such as superoxide dismutase, catalase, and nonenzymatic reduced glutathione. The results demonstrated that BPA caused an increase in lipid peroxidation and a decrease in activity of various enzymatic and nonenzymatic antioxidants in bone marrow cells, blood lymphocytes, and testicular and epididymal tissues. The findings of the current study suggest that BPA exposure induced oxidative stress, which could be one of the possible mechanisms causing reproductive and genetic toxicity.