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Background: Bisphenol A (BPA), an endocrine disruptor, may be involved in the etiology of autism spectrum disorders (ASD); however, the mechanism of neuronal and astrocytic damage remains ambiguous. A possible role of altered expression of p21 in autistic‐like behavior in rat offspring was examined with prenatal and postnatal BPA exposure. Methods: Wistar albino dams were exposed to BPA (5 mg/kg) intraperitoneally throughout pregnancy and until the third postnatal day (PND). Pups were examined on 21st PND for behavioral test. Blood samples were collected for serum lactate levels and pups were sacrificed. Right frontal cortices were dissected out and processed for H&E, immunohistochemical analysis, and gene expression. Results: Anxiety like behavior and thigmotaxis along with reduction in serum lactate concentrations were observed in pups exposed to BPA. Decline in neuronal number and decreased astrocytic population with reduced dendritic spines were revealed by H&E and immunohistochemical analysis, respectively, in right frontal cortices. Over expression of p21 was also detected in BPA‐exposed offspring. Conclusions: Over expression of p21 may be associated with autistic behavior. Further studies are recommended to explore the structural alterations in other white matter pathways in frontal cortices. [ABSTRACT FROM AUTHOR]

Background: Bisphenol A (BPA) is a well‐recognized endocrine disruptor and is globally used in the manufacture of many plastic items. Multiple studies suggest links between prenatal BPA exposure and alterations in neurodevelopment and behaviors in children, even at lower levels. This study was conducted to reveal the role of astrocyte morphology and Gamma aminobutyric acid (GABA) signaling in BPA induced cognitive defects in the offspring of Wistar albino rats when exposed during the prenatal and postnatal periods. Methods: Dams of Wistar albino rats were exposed to a dose of 5 mg/kg body weight of BPA throughout the pregnancy and lactation period until the third postnatal day (PND). After delivery of pups, cognitive tests were carried out on the 21st, 24th, and 28th PNDs. Blood samples were collected for measurement of serum GABA levels. On the same day as the blood collections, pups were sacrificed and their right frontal cortices were dissected out. Immunohistochemical analysis for glial fibrillar acidic protein + astrocytes was conducted. Results: Pre and postnatal BPA exposure led to anxiety like behavior in pups. This exposure also resulted in reduced serum GABA concentrations. Immunohistochemical analysis revealed reduced astrocyte numbers as well as decreased numbers of dendritic spines in the BPA exposed pups. Conclusion: BPA exposure during critical periods of development leads to cognitive impairments that correlate with the defects in the GABA signaling pathways and deteriorated morphology of the astrocytes in the offspring of the Wistar rats. [ABSTRACT FROM AUTHOR]

Objective(s): Bisphenol A (BPA) that is a monomer of plastic products may possibly interfere with epigenetics and be involved in onset and progression of several diseases. This study was aimed to detect the epigenetic effects of in utero BPA exposure in mice offspring. Materials and Methods: All experiments were performed according to the national guidelines for laboratory animals and after ethical approval. Thirty adult BALB/c female mice were divided into 3 equal groups, G1 (controls), G2 (ethanol 0.10 ml/100ml of PBS so that final concentration would be 0.01%) vehicle control and G3 (BPA 10 mg/kg). Chemicals were given twice a week throughout the pregnancy. Once delivered at term, female offspring were observed for body weight, behavior and movements. Blood glucose, serum insulin, cholesterol and high-density lipoprotein cholesterol (HDLc) were measured at 5 and 15 months postnatal. Animals were sacrificed at 15 months and pancreas, kidney, adipose tissue and uterine tissue were taken and stained with either Hematoxylin and eosin (H & E) or immunostaining and examined under light microscope. Results: Offspring of group G3 revealed abnormal changes of body weight, behavior and movements. Blood glucose, serum insulin, cholesterol and HDLc were high in group G3 offspring compared to controls. H & E staining showed changes in the parenchyma of pancreas, kidneys and uterus, which were confirmed by staining with anti-islet-1, kidney-specific (Ksp) cadherin, and anti-MLH antibody. Conclusion: In utero exposure of BPA exerts diabetogenic and atherogenic effects with less parenchymal tissue in endocrine pancreas, kidney and uterus. [ABSTRACT FROM AUTHOR]