Bisphenol A (BPA) is one of the most common worldwide chemicals involved in the industry of polycarbonate plastics, medical devices, and pharmaceuticals. Forty three-month-old albino rats were randomly classified into four groups. Group Ӏ received a daily corn oil dose (5 mL/kg/ body weight, BW) through a gastric tube for one month, Group ӀӀ received a daily dose of Curcumin (200 mg/kg body weight (B.W.) through a gastric tube for one month, Group ӀӀӀ received a daily dose of BPA (0.5 μg/kg B.W.) through a gastric tube for one month and Group ӀV received concomitant daily doses of Bisphenol A and Curcumin as the regimen described in groups ӀӀ and ӀӀӀ. The rats were sacrificed, and glandular portion of stomach was dissected and processed for light, immunohistochemical and ultrastructural study. BPA induced destructed gastric glands, dilated congested blood vessels, submucosal oedema, decreased PAS-positive reactivity, increased collagen fibres deposition, decrease in the positive BCL2 immunoexpression, increased positive PCNA immunoexpression, reduction in the gastric mucosal height and destructive changes in the enteroendocrine, chief and parietal cells. Curcumin coadministration provoked an obvious improvement in the gastric structure. BPA exposure has toxic effects on the glandular portion of the stomach in rats. Otherwise, Curcumin coadministration has exhibited protective impact on the architecture of the stomach.

Background Alzheimer's disease (AD) is a worldwide severe medical and social burden. Liraglutide (LIR) has neuroprotective effects in preclinical animal models. Aim: To explore the probable neuroprotective impact of Glucagon‐like peptide‐1 (GLP‐1) on rats' behavior and to elucidate its underlying mechanisms. Methods: A total of 24 male albino rats were assigned to control, LIR (300 µg/kg subcutaneously (s.c.)), AD only (100 mg/kg aluminum chloride (AlCl3) orally) and LIR + AD treated groups. Eight radial arm maze was performed. Serum blood glucose, proinflammatory cytokines, oxidative stress markers were measured and hippocampal tissue homogenate neurotransmitters were evaluated. Histopathological and immunofluorescent examinations were performed. Results: LIR prevents the impairment of learning and improves both working memory and reference memory through significant reduction of serum tumor necrosis factor (TNF‐α), interleukin 6 (IL‐6) and interferon‐γ (INF‐γ) and malondialdehyde (MDA) and through the increase of superoxide dismutase (SOD), dopamine, adrenaline, and noradrenaline. LIR also improves hippocampal histological features of ALCL3 administrated rats and decreases the percentage of neuronal loss. Conclusion: LIR normalizes ALCL3‐induced dementia. It improves cognitive dysfunction and ameliorates cerebral damage.

Background Pregabalin (PGB) was approved as new anti-epileptic drugs with little information about its teratogenic effect. Aim of the work to evaluate the developmental toxicity of PGB. Materials and methods 60 pregnant albino rats were divided into three groups. PGB (500 mg/kg body weight/day) was given to group II, PGB (1250 mg/kg body weight/day) was given to Group III and no medications were given to group I. The pups were normally delivered. Liver, kidney and heart specimens were prepared for histological, immunohistochemical, and morphometric studies. Results A dose of 500 mg of PGB had minimal toxic effects in the form of mild collagen deposition and moderate positive caspase-3 immunoexpression. PGB dose of 1250 mg/kg induced gross toxic effects in form of degenerated cardiac myofibres, ruptured blood vessels, vacuolations in the renal cortex, fibrosis and strong positive caspase-3 immunoexpression. Conclusion PGB at dose of 500 mg/kg revealed minimal toxic changes. PGB cause embryotoxicity in a dose-dependent manner, as the higher dose induced more degenerative changes.

Background: One of the popular painkillers, paracetamol is thought to be safe for use in pregnant women, and nursing mothers. Objectives: To observe the effect of paracetamol on the development of the medial prefrontal cortex (mPFC) in albino rats and to evaluate the protective effect of silymarin. Material and Methods: Forty pregnant rats were divided randomly into four equal groups: Group A: received nothing. Group B: was given silymarin at a dose of 200 mg/kg body weight orally once daily. Group C: was given paracetamol at a dose of 350 mg/kg body weight orally once dailly. Group D: was given paracetamol and silymarin. Treatment started at the sixth day of the gestation until the end of lactation. After weaning, the pups received the same regimen until the age of three months. The offspring were selected from each group at the following ages: 1 day, 21 days and 3 months The mPFC was processed for light, ultrastructural and immunohistochemical analyses. Results: Paracetamol exposure led to hypocellularity in different layers of mPFC, shrunken pyramidal neurons, vacuolated neuropil, weak SYN immunoreaction and a decrease in the number of pyramidal cells and thickness of the mPFC. Silymarin coadministration induced a partial restoration of normal arrangement of the mPFC, the cytoarchitecture of pyramidal neurons, SYN immunoreaction as well as an increase in the number of the pyramidal cells and thickness of the mPFC. Conclusion: Paracetamol treatment caused neuronal damage in the mPFC. Silymarin appeared to be beneficial in protecting mPFCʼ structure.

Background: Iron is the most abundant element on earth and an essential metal for life. It is used extensively by proteins involved in the electron transport chain, the active centers of many enzymes and oxygen transport. It is essential for the adequate development and functioning of the brain. The regulation of the iron metabolism is crucial since both the iron deficiency and the iron overload can cause a disease. Aim of the Work: To detect the effects of iron exposure during the postnatal period on the putamen, the subthalamic nucleus and the substantia nigra in adult albino rats. Material and Methods: A total number of twenty albino rats were used in the study. They were equally divided into a control group and an experimental group. The control group received tap water orally. The experimental group received 15 mg/ kg of ferrous gluconate orally. The regimen started at postnatal day 12 and continued until three months old. The rats were anaesthetized and the brains were extracted. The specimens from the fixed brains were dissected and processed for the light and the electron microscopic examination. Morphometric measurements were also done. Results: The light microscopic study of the treated group revealed neurons of putamen had dense darkly stained nuclei and vacuolations appeared within the neuropil. Wide spaces between darkly stained neurons of the subthalamic nucleus were detected. The neuropil of the substantia nigra pars compacta (SNc) had many vacuoles and most of the neurons had darkly stained nuclei. Immunohistochemistry of the putamen using anti-TH demonstrated a reduction of TH expression in a patchy manner. Immunohistochemistry of SNc showed a weak TH immunoreactivity in the neuropil of the treated group and a reduction in the number of TH immunopositive neurons in comparison with the control group. The electron microscopic study of the SNc and putamen of the treated group showed degeneration of the mitochondria, vacuolization of the cytoplasm, heterochromatic nuclei with irregular outline and marked loss of cell organelles in the cytoplasm. Morphometric studies revealed significant reduction in the cell count and surface area of the neurons in SNc and putamen of the treated group in comparison with the control group. Conclusion: Iron overdose during postnatal period produces degeneration of the putamen, subthalamic nucleus and substantia nigra in the adult albino rat.