Maternal exposure to the environmental pollutant "BDE-47" impairs the postnatal development of rat cerebellar cortex by modulating neuronal proliferation, synaptogenesis, NGF and BDNF pathways

. 2,2’,4,4’-Tetrabromodiphenyl ether (BDE47) is an environmental contaminant that crosses the blood placental barrier and interferes with the homeostasis of fetal thyroid hormones. Aim of work. This study was designed to investigate the perinatal effect of BDE-47 exposure on the postnatal development of the rat cerebellar cortex. Materials and methods. This study was carried out on 20 pregnant rats and 36 of their offspring. The pregnant rats were divided equally into control and BDE-47 treated mother groups; supplemented orally with BDE-47 (0.2 mg/kg/day from day 8 of gestation until the day of weaning). The offspring of both mother groups were subdivided, according to their developmental age, into three subgroups; PND14, PND21and PND42. SerumT3, T4 and TSH were assessed for dams and their offspring. Testing the motor coordination of the offspring via the rotarod test was conducted. Sections of the cerebellar cortex from offspring subgroups were stained with hematoxylin and eosin alongside immunohistochemical reactions and optical density of nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), proliferating cell nuclear antigen (PCNA) and synaptophysin (SYN) were assessed. Also, the thickness of different layers of the cerebellar cortex was histomorphometrically measured. Results. BDE-47 treated mothers and their offspring subgroups showed a significant decrease in the serum free T3, T4 and increased TSH. The BDE-47 offspring displayed incoordination of the motor activity together with disturbed cytoarchitecture of the cerebellar cortical layers, and impaired migration of its germinative neuronal zones, particularly on PND14 and PND21. Moreover, these offspring displayed a decrease of the immune-expression and optical density of NGF, BDNF in the cerebellar cortical layers with impaired proliferation, and synaptogenesis. Conclusion. Maternal exposure to BDE-47 during pregnancy and lactation effectuated a potential deleterious retarding effect on the postnatal development of the rat cerebellar cortex mostly via modulating neuronal proliferation, synaptogenesis, NGF and BDNF pathways secondary to its hypothyroid effect

Effect of high fat diet on structure of liver and gallbladder of adult male mice – an experimental study

Introduction. High fat diet (HFD) intake induces obesity and adversely affects different body organs including liver and gallbladder. Aim. It was to clarify the effects of HFD on the liver and gallbladder structure using light microscopic (LM) examination. Material and methods. 16 healthy adult male mice were equally divided into 2 groups. Control group mice were fed normal diet. HFD group was fed using HFD. At the end of the 8-week experiment, mice were anesthetized. Liver and gallbladder were removed and prepared to histological processing. Sections were stained with hematoxylin and eosin (H&E) and immunostaining for cyclooxygenase-2 (COX-2) cellular localization. Oil Red O (ORO)-stained frozen liver sections were prepared. Results. H&E-stained sections of HFD group revealed rounded swollen hepatic cells with pale cytoplasm suggesting cellular ballooning. Dilated congested sinusoids and portal vein, cellular degeneration and collection of inflammatory cells were observed between hepatic cells and in portal region. Gallbladder sections showed epithelial stratification and cellular vacuolation. Strong immunoexpression of COX-2 was observed in Kupffer and hepatic cells of the liver and gallbladder mucosal epithelial cells. Conclusion. HFD is suggested to alter the normal histological features of liver and gallbladder represented by fatty liver and gallbladder epithelial hyperplasia and inflammatory reaction