Background and Objectives: Sertraline is a selective serotonin reuptake inhibitor (SSRI) that is frequently prescribed during pregnancy to treat mood disorders. Studies indicate that chronic use of sertraline is associated with elevated liver enzymes, oxidative stress, and histological alterations in the liver. Folic acid, a recommended supplement currently used during the first trimester of pregnancy, has antioxidant and anti-inflammatory effects. Hence, folic acid might be a potential protective agent against sertraline-induced liver injury. The current study aimed to investigate the possible hepatotoxic effects of sertraline administration during pregnancy and early postpartum. In addition, we sought to evaluate the potential protective effects of folic acid supplementation in alleviating any sertraline-induced liver damage. Materials and Methods: Eighty pregnant albino rats were randomly divided into four groups: control, folic acid-treated, sertraline-treated, and folic acid–sertraline-treated. Each group was divided into rats euthanized immediately after giving birth (0 h) or 14 days postpartum. Biochemical, histological, and immunohistochemical evaluations of liver function and structure were conducted. Results: Administration of sertraline was associated with a significant increase in hepatic enzymes (ALT and AST) and disrupted lipid profile (elevated cholesterol, triglycerides, and LDL-c) compared to the control group. Increased apoptosis was evidenced by increased caspase 3 expression and histological alterations, including vacuolation and inflammatory infiltrates, in sertraline-treated rats. Folic acid supplementation effectively mitigated these effects by preserving liver architecture, normalizing biochemical markers (ALT, AST, and lipid profile changes), and reducing apoptotic activity (lower caspase 3 expression). Conclusions: Folic acid mitigated sertraline-induced hepatic damage in pregnant rats. This suggests the potential benefits of using folic acid during the whole duration of pregnancy in patients treated with sertraline.

Background: Cadmium is a common toxic heavy metal of great concern for environmental pollution and human health. It is extensively used in many industries as radiation screens, rechargeable batteries and pigments. Montelukast is a powerful highly effective anti-inflammatory drug. Recently it shows significant antioxidant properties.Aim of the Study: evaluate the effect of Cadmium on thyroid glands and to assess the possible protective role of MontelukastMaterials and Methods: Forty adult male albino rats were divided into four equal groups received treatment for 6 weeks: (I) (Control group) received distilled water. (II) (Cadmium group)"3mg/kg". (III) (Recovery group) kept untreated for another 6 weeks after Cadmium administration with the same dose and period as pervious group. (IV) (Montelukast and Cadmium group) received Montelukast "10mg/kg" and Cadmium"3mg/kg". At the end, all animals were sacrificed. Thyroid gland samples were obtained for histological and immunohistochemical studies. Blood samples were obtained for hormonal assay. Data was statistically analyzed.Results: Histological examination of thyroid glands of Cadmium treated rat’s showed disorganization and irregularity in the follicles. The follicular cells appeared distorted with pyknotic nuclei and some cell desquamated in follicular lumen. Colloid retraction within the follicles, cellular infiltration around congested blood vessels and marked collagen fibers deposition in connective tissue septae were detected. Significant increase in Caspase-3 immune expression in the follicular cell’s cytoplasm was noticed. High significant decrease of thyroid hormone (T3, T4) level was noticed. These changes were still seen in the recovery group. Co-administration of Montelukast showed obvious protection against the hazardous effects of Cadmium. Conclusion: Cadmium induces marked thyroid tissue damage via, fibrosis and apoptosis. These structural changes can be alleviated by combined treatment with Montelukast.

Background: Aluminum chloride is the most abundant metal present on the earth's crust. It is found in our daily life as in drinking water, soil and in commonly used cosmetics. The lung epithelium is the site for aluminum chloride accumulation. Propolis is wax-like bee product. It has a powerful anti-inflammatory antioxidant property.Objectives: evaluation of aluminum chloride toxicity on lung tissue and the possibility of Propolis to play a protective roleMaterials and Methods: fifty adult male albino rats were divided into five equal groups received treatment for 6 weeks: (I) Control group received distilled water (II) Propolis group "50mg/kg ". (III) Aluminum chloride group "475mg/kg". (IV) Recovery group" kept untreated". (V) Propolis and aluminum chloride group. Finally, all animals were sacrificed. Lung samples were obtained for histological and immunohistochemical studies. Data was statistically analyzed.Results: groups (I& II) showed normal structure of lung tissues. Aluminum chloride group (III) revealed distorted lung tissues. Some alveoli were collapsed and the others showed compensatory dilatation. Lung tissue had numerous hemosiderin granules. Pneumocyte II showed condensed nucleus, cytoplasmic vacuolations, distended irregular mitochondria, dilated rough endoplasmic reticulum and degeneration of their lamellar bodies. There was thickening in the inter-alveolar septa, numerous inflammatory infiltrate and eosinophilic materials. Blood vessels were congested and surrounded by inflammatory cells. The bronchioles showed distortion. Marked collagen fibers and numerous accumulations of mast cells in connective tissue septae were detected. A significant decrease in BCL2 immune expression was noticed. These changes were moderately alleviated in the recovery group. Co-administration of Propolis with aluminum chloride restored lung tissue integrity Conclusion: Aluminum chloride induces marked lung tissue damage via, fibrosis and apoptosis. These changes can be alleviated moderately by stopping treatment for 2 weeks and markedly by combined treatment with Propolis. So we recommend Propolis supplementation for people exposed to aluminum chloride

Background: Olanzapine (OLZ) is an atypical antipsychotic drug, has been used as approved therapy for schizophrenia and bipolar disorder. Hypericum perforatum (HP) is a herbaceous plant, has been described as a neuroprotective agent with potent antioxidant and anti-inflammatory effects. Objectives: to evaluate the effects of chronic use of olanzapine on the anterior pituitary gland and the possible protective role of hypericum perforatum Material and method: Fifty six adult male albino rats were divided into 4 groups, received treatment orally for 8 weeks; (I) control group, (II) HP supplemented group (80 mg/kg/day), (III) OLZ treated group (10 mg/kg/day), (IV) OLZ and HP group (10 mg of OLZ and80 mg of HP/kg/day) . Finally, rats were weighted, anesthetized and sacrificed. Blood samples were collected for biochemical study. Pituitary gland were dissected out and processed for histological study. Results: Olanzapine treated rats exhibited a high significant increase in rat`s body weight. Plasma levels of luteinizing hormone (LH) and follicle stimulating hormone (FSH) were significantly decreased but thyroid stimulating hormone (TSH) and prolactin hormone were increased. OLZ induced degeneration of pars distalis cells. Where, cells had small dark nuclei and cytoplasmic vacuolization. Eosinophilic material deposition and congestion of blood sinusoid were noticed. Most chromophiles contained degenerated mitochondria and dilated rough endoplasmic reticulum. Furthermore, there was a high significant increase in the number of positive caspase-3 immune-stained cells. Hypericum perforatum co-administration induced improvement of these changes occurred by OLZ. Conclusion: Olanzapine induced morphological and biochemical changes in the anterior pituitary gland. Hypericum perforatum could ameliorate these changes.