Prenatal Bisfenol A ve/veya Di-2-Etil Hekzil Ftalat Maruziyetinin Nöroendokrin Bozucu Etkilerinin Değerlendirilmesi
Özet
Bisphenol A (BPA) and di(2-ethylhexyl) phthalate (DEHP) are chemical substances that are widely present in the environment and known to have endocine disrupting properties. In the recent years, studies have been conducted showing the exposure to this chemical is related to cognitive deficits, slow neurodevelopment, increases in the incidences of aggression and depression, hyperactivity and attention problems. It can be emphasized that the effects of maternal and childhood exposure may be of particular interest and lead to serious consequences. In addition symptoms are often the consequences of multiple mechanisms being affected together, and it can be anticipated that symptoms may be more significant, particularly as a result of exposure to endorcrine disrupting chemicals (EDCs) as mixtures. In this thesis, toxic effects of prenatal and lactational exposure to BPA and DEHP mixture (vs. single exposures and vs. control group) on central nervous system and neuroendocrine system have been evaluated. Pregnant Sprague-Dawley rats were divided into four groups as control, BPA (50 mg/kg/day), DEHP (30 mg/kg/day) and BPA plus DEHP (BPA;50 mg/kg/day, DEHP; 30 mg/kg/day) and dosed by oral gavage during pregnancy and lactation periods. The male offspring of born from those rats were chosen randomly and assessed for the effects on the neurotransmitter systems in the cerebrum region, the histopathologic changes and apoptosis formation in the hippocampus region when they reach to adulthood (twelfth week). In addition, the occurrence of oxidative stress was evaluated as one of the mechanisms that could be an underlying factor for these harmful effects. The findings showed that prenatal and neonatal exposure to EDCs led to imbalance of neurotransmitter systems. It was also detected that exposure to BPA and/or DEHP caused apoptosis and histopathologic changes in the hippocampus. In particular, the effects of combined exposures were found to be more significant. Oxidative stress was also induced in the study groups. Therefore, it can be suggested that oxidative stress can be considered as one of the underlying mechanisms for neurodevelopmental effects of EDCs. All results indicate adverse effects of prenatal and lactational exposure to BPA and/or DEHP on the central nervous system and neuroendocrine system in male rat offspring.
