Background:The most common disorders of the thyroid gland are hyperthyroidism and hypothyroidism. Both have been linked to cell damage. Aim of Work: This study was designed to evaluate the effect of melatonin administration on the testis of both hyperthyroidic and hypothyroidic adult male albino rats models. Materials and Methods: Fifty adult male albino rats were used in this study and divided into five groups; ten rats each. Control group (G1) was given distilled water. Hyperthyroidic group (G2) was given thyroxin (0.2 mg/kg b.w). Hyperthyroidic+melatonin group (G3) was given thyroxin (0.2 mg/kg b.w) and melatonin (2.5 mg / kg b.w). Hypothyroidic group (G4) was given carbimazole (1.35 mg/kg b.w). Hypothyroidic+melatonin group (G5) was given carbimazole (1.35 mg/kg b.w) and melatonin (2.5 mg / kg b.w). All the treatments were given orally for 15 days. At the end of the study, the animals of all groups were sacrificed and their testes were rapidly dissected out. The testicular mass was calculated. Testicular specimens of each group were processed for light and electron microscopic studies. Results: The testicular mass was significantly decreased in both hyperthyroidic group (G2) and hypothyroidic group (G4) when compared with the control. Light and electron microscopy of the hyperthyroidic group (G2) and hypothyroidic group (G4) showed seminiferous tubular germ cells disorganization with increased intercellular spaces, necrosis and cellular damage. Melatonin supplementation to rats given Thyroxin (G3) improved the testicular mass and the cell damage. On the contrary, melatonin supplementation to rats given carbimazole (G5) did not show any improvement on both morphometrical and histological levels. Conclusion: It was concluded that simultaneous melatonin administration effectively depresses the negative effects of hyperthyroidism but not hypothyroidism on the adult male rat testis.

Background: Doxorubicin (Dox) is a powerful and greatly effective drug in cancer. However, its clinical usefulness is still restricted due to its specific toxicity to the cardiac tissue. Vitamin E is a well-known antioxidant used as a dietary supplement. Aim of the work: To evaluate the possible protective effects of vitamin E against Dox-induced cardiotoxicity. Material and Methods: Forty 3-months adult male albino rats weighing 200-250 gm were divided into four equal groups: Group (I): served as a negative control and received no treatment. Group (II): served as a positive control and treated with an intraperitoneal injection of 0.9% sodium chloride saline once daily for one week. Group (III): treated with 4mg Dox/kg b.w./ day intraperitoneally for one week. Group (IV): was pretreated with 100mg vitamin E/kg body weight/day orally for 2 weeks followed by a combination of an intraperitoneal injection of Dox and oral vitamin E for one week in the same previous doses. Then, the animals were anaesthetized and blood samples were utilized for measurement of lactate dehydrogenase (LDH), creatine kinase (CK), triglyceride, total cholesterol and high-density lipoprotein (HDL-C). Animals were sacrificed, and a portion of each heart was taken from all groups for determination of the levels of total cardiac antioxidant capacity (TAC). The remaining portions of the heart muscle were prepared for light and electron microscopic studies. Results: Administration of Dox resulted in histological alterations in the form of vacuolated disorganized cardiac muscle fibers, degenerated mitochondria and congested dilated blood vessels. Also, significant decreases of cardiac TAC and serum HDL-C and increases of serum levels of LDH, CK, triglyceride and total cholesterol of Dox-treated group were noticed in comparison with the control ones. Pre and concomitant administration of vitamin E with Dox improved these alterations. Conclusion: Vitamin E ameliorates the cardiac damage induced by Dox.

INTRODUCTIONThe testis is the male primary reproductive organ. It profits two main functions: secretion of testosterone which is the male sex hormone, and the production of sperms. These functions are key for both maintenances of the male characteristics and preservation of species (Lara et al., 2018).Cisplatin (CIS) is a widely used chemotherapeutic agent. It is used to treat cancer like mesothelioma and osteosarcoma. It has been recommended by the United States Food and Drug Administration since 1978 (Abdel-Moneim, 2014).CIS is an alkylating agent that exerts its effect by persuading DNA cross-links and making breaks in the DNA double strand causing what is called the programmed cell death (PCD) and apoptosis (Reddy et al., 2016). PCD leads to oxidative stress by generating Reactive Oxygen Species and lipid peroxidation, causing cellular necrosis (Fallahzadeh et al., 2017).

Background: Excess fluorides intake produces histopathological changes of many organs. Methionine is a potential natural antioxidant against oxidative radicals. Aim of the Work: To evaluate the possible protective role of methionine against sodium fluoride (NaF)-induced pancreatic toxicity. Material and Methods: Thirty 3-months (200-250gm) adult male albino rats were divided into three equal groups: group I (control), group II (Fluoride group) and group III (Fluoride+methionine group). Control group; was given 1ml distilled water. Fluoride group; was given 10 mg NaF/kg b.w. Fluoride+methionine group; was given 10 mg NaF/kg b.w. and 2 mg methionine/rat. All the treatment was given orally by gastric tube once daily for 35 days. After anesthesia, all groups were sacrificed. The pancreatic specimens were prepared for light and electron microscopic studies and anti-insulin antibody immunohistochemical staining. The mean numbers of zymogen granules and insulin positive β-cells of all groups were counted. Results: The mean numbers of zymogen granules and insulin positive β-cells of the fluoride group were significantly decreased when compared to control. The pancreatic specimens of the fluoride group revealed congested blood vessels, extravasated blood cells, vacuolated pancreatic acini, loss of the acinar cell architecture, dilated rough endoplasmic reticulum and degenerated mitochondria. By anti-insulin antibodies immunohistochemistry, there was a weak positive reactivity in the fluoride treated group when compared to control. The concomitant administration of NaF and methionine improved these changes. Conclusion: The concurrent administration of NaF and methionine ameliorates the structural alterations developed in the pancreas following excess NaF intake.

No abstract