Marwa A. Ahmed

Intake of melatonin is associated with amelioration of physiological changes, both metabolic and morphological pathologies associated with obesity: an animal model

Obesity and its associated metabolic pathologies are the most common and detrimental diseases, affecting over 50% of the adult population. Our knowledge about the protective effects of melatonin against high‐fat diet (HFD)‐induced obesity is still marginal. In this investigation, we hypothesized that melatonin can minimize the metabolic pathologies and morphological changes associated with obesity in animals receiving an HFD. To examine these effects, and to test our hypothesis, an animal model formed of male Boscat white rabbits was established. The animals were divided into three groups: (i) a control group fed regular diet; (ii) an obesity group fed an HFD for 12 weeks; and (iii) a treated group fed HFD for 12 weeks and then treated with melatonin for 4 weeks. The animals were killed and their serum and tissues were evaluated for: (i) lipid profile (cholesterol, triglycerides and low‐density lipoprotein) and glucose; (ii) antioxidant enzyme (serum glutathione peroxidase, GSH‐PX); and (iii) fatty changes (liver, kidney and blood vessels). Compared with the control group, intake of HFD (obesity group) was associated with: (i) a statistically significant increase in blood pressure, heart rate, sympathetic nerve activity, body weight, food consumption, serum lipids, blood glucose levels and atherogenic index; (ii) decreased level of GSH‐PX and high‐density lipoprotein (HDL); and (iii) fatty changes in the liver and kidney as well as atheromatous changes in the blood vessels. Compared with the obesity group, intake of melatonin (treated group) was associated with: (i) a statistically significant decrease in blood pressure, heart rate, sympathetic nerve activity, body weight, food consumption, serum lipids, blood glucose levels and atherogenic index; (ii) increased level of GSH‐PX and HDL; and (iii) disappearance of fatty changes in the liver and kidney as well as atheromatous changes in the blood vessels. The administration of melatonin reduced the metabolic pathologies associated with the intake of HFD, suggesting a protective role. Although the underlying mechanisms are unclear, they may include its antioxidant and receptor‐mediated effects. The clinical ramifications of these effects await further investigations.

Metformin versus laparoscopic ovarian drilling in clomiphene- and insulin-resistant women with polycystic ovary syndrome

To compare the hormonal‐metabolic profiles and reproductive outcomes in clomiphene‐resistant patients with polycystic ovary syndrome and insulin resistance between women receiving metformin and those undergoing laparoscopic ovarian drilling.

Effects of opioid (tramadol) treatment on testicular functions in adult male rats: The role of nitric oxide and oxidative stress.

Nowadays, tramadol hydrochloride is frequently used as a pain reliever, and for the treatment of premature ejaculation. Decreased semen quality was noted in chronic tramadol users. The present study aimed to elucidate the effects of tramadol on the testicular functions of adult male rats. A total of 40 albino adult male rats were divided into control and tramadol groups, with 20 rats for each group. Rats of the tramadol group were subcutaneously injected with 40 mg/kg three times per week for 8 weeks. The control group received normal saline 0.9%. Blood samples from each animal were obtained. Plasma levels of different biochemical substances were determined. Nitric oxide was measured in testicular tissue samples. Those samples together with epididymal tissue samples were processed for histopathological examination. Tramadol significantly reduced plasma levels of luteinizing hormone, follicle‐stimulating hormone, testosterone and total cholesterol, but elevated prolactin and estradiol levels compared with the control group. In addition, tramadol increased the testicular levels of nitric oxide and lipid peroxidation, and decreased the anti‐oxidant enzymes activities significantly compared with the control group. The tramadol group showed decreased sperm count and motility, and numbers of primary spermatocytes, rounded spermatid and Leydig cells. Immunohistochemical examinations showed that tramadol increased the expression of endothelial nitric oxide synthase in testicular tissues. The present study showed that tramadol treatment affects the testicular function of adult male rats, and these effects might be through the overproduction of nitric oxide and oxidative stress induced by this drug.

Role of vitamin C and selenium in attenuation of nicotine induced oxidative stress, P53 and Bcl2 expression in adult rat spleen

UNLABELLED Forty adult female rats were randomly divided into four groups: control, nicotine, nicotine+vitamin C and nicotine+selenium group. Splenic tissues concentrations of thiobarbituric acid reactive substances (TBARS), nitric oxide, superoxide dismutase (SOD) and catalase (CAT) activities were measured. The P53 and Bcl2 proteins were detected by Western blot and their expression in splenic tissues were measured by quantitative real time PCR in all groups. Compared to control group, nicotine increased the concentrations of TBARS and nitric oxide significantly. However, Vit. C or Se supplementation with nicotine caused a significant decrease in these concentrations. SOD and CAT activities of nicotine group decreased significantly compared to control group. Treatment with Vit. C or Se plays a significant role in elevation of SOD and CAT activities. In splenic tissues, nicotine significantly decreases the protein levels and the mRNA expression of P53 and increases the protein levels of Bcl2 and its expression. Administration of Vit. C. to nicotine-treated rats completely reversed the decrease in P53 levels and its mRNA expression and the increase in Bcl2 levels and its mRNA expression to the control values. In contrast, Se administration did not induce any significant changes in these genes levels or expressions compared to nicotine group. CONCLUSION Vit. C supplementation to nicotine treated rats was more effective than selenium in attenuation of nicotine-induced oxidative stress, p53 and Bcl2 expression in rat spleen tissues.

Comparative study of the effect of verapamil and vitamin D on iron overload-induced oxidative stress and cardiac structural changes in adult male rats

The present study was designed to compare the effect of verapamil and vitamin D on the expression of the voltage-dependent LTCC alpha 1c subunit (Cav1.2) and thereby on iron overload-induced cardiac dysfunction in adult male rat. Forty rats were randomly divided into four groups. Control group received the vehicle, iron overload group received ferrous sulfate intraperitoneally (IP) for 4 weeks, iron overload+verapamil received ferrous sulfate and verapamil IP concurrently for 4 weeks and iron overload+vitamin D group received ferrous sulfate IP and vitamin D3 orally concurrently for 4 weeks. Serum ferritin, total antioxidant capacity (TAC), total peroxide (TP) and cardiac iron and calcium were determined. Oxidative stress index (OSI) was calculated. Histopathological studies using H&E, Masson trichrome and Prussian blue stains and immunohistochemical studies using Cav1.2 antibody were also carried out. Administration of ferrous sulfate induced a significant increase in serum ferritin, OSI, cardiac iron and calcium contents. Moreover, cardiomyocytes were degenerated and the expression of Cav1.2 protein was increased in iron overload group as compared to control. Verapamil decreased ferrous sulfate-induced increase in serum ferritin, OSI and cardiac iron deposition. In addition, verapamil improved myocardial degeneration and decreased the expression of Cav1.2 protein. In contrast, vitamin D produced insignificant changes in ferrous sulfate-induced increase in cardiac iron content, myocardial degeneration and the expression of Cav1.2 protein. These results indicate that verapamil has a protective effect against iron overload-induced cardiac dysfunction, oxidative stress and structural changes, while vitamin D has an insignificant effect on these parameters.

Cardio protective effects of Nigella sativa oil on lead induced cardio toxicity: Anti inflammatory and antioxidant mechanism

The present study aimed to evaluate cardio-protective effect of Nigella sativa oil (NSO) on lead induced cardio toxicity. Forty five albino adult rats were randomly divided into 3 groups: control lead (Pb) group that received lead acetate (20 mg/kg/day) 3 times weekly for 8 weeks and PB + NSO group (rats pretreated with Nigella sativa oil (4 ml/kg) orally for 1 h before administration of lead acetate (given as in Pb group). Myocardial injury was assessed by laboratory and pathological studies, and heart rate was recorded in all animals. Lead intake resulted in significant increases in cardiac high-sensitivity C-reactive protein (hs-CRP), interlukin-6 (IL-6), E-selectin, troponin I, malondialdehyde (MDA) and serum creatine kinase-MB (CK-MB). The cardiac apelin, superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione (GSH) levels significantly decreased in Pb group compared to the control. Currently, heart rate and ST segment increased significantly after lead intake. Heart lesions as a result of lead treatment were in the form of hemorrhage, myocardial necrosis, mononuclear cell infiltration and fibrosis. Immuno histochemical results of the heart revealed positive cyclooxyenase-2 (Cox-2) expressions in Pb-treated group. NSO administration produced significant normalization of the physiological parameters as well as restored the histological structure and decreased the COX-2 expression of the heart compared to Pb group. In conclusion, NSO intake has cardio protective potential through its ability to decrease pro inflammatory cytokines, oxidative stress and cardiac tissue damage in lead-induced cardio toxicity. Key words: Nigella sativa oil, lead acetate, cardio toxicity, inflammation.

Folic acid protects against experimental prenatal nicotine–induced cardiac injury by decreasing inflammatory changes, serum TNF and COX-2 expression

Nicotine administration has been shown to increase the risk for cardiovascular diseases and death. The present study was designed to investigate the impact of nicotine administration on serum level tumor necrosis factor and cycloxygenase -2 (COX-2) expression mediated cardiac injury in rat off springs, and the possible protective effect of folic acid. Eighteen pregnant female rats were randomly divided into three groups, six animals each. Control group received the vehicle, nicotine group received a dose of nicotine 0.1 mg/kg body weight, daily with subcutaneous injection from day 3 of gestation until weaning on postnatal day 21. Nicotine treated group received daily oral supplementation with folic acid 200 mg/kg body weight by intragastric tube prior to injection of nicotine. In serum of the pups, levels of tumor necrosis factor (TNF), nitric oxide (NO), total antioxidant capacity (TAC) and malondialdehyde (MDA) were measured. Histopathological studies of cardiac tissues using hematoxylin-eosin (H&E) were carried out. The expression of COX-2 was evaluated using immunohistochemistry. Serum TNF and MDA were significantly increased, while serum NO and TAC were significantly decreased in nicotine group. Moreover, nicotine-exposed rats showed complete lysis of cardiac myocytes, marked cytoplasmic vacuolation of myocytes, muscle fibers show loss of striation and increased COX-2 expression. Concomitant folic acid administration resulted in a significant alleviation of biochemical and structural alteration-induced by nicotine. In conclusion, folic acid has a protective role against nicotine induced cardiac injury by reduction of COX-2 expression, decreasing TNF production and lipid peroxidation mediated cell injury.

The Impact of Vitamin E Supplementation on Urinary Bladder Contractility in Streptozotocin-Induced Diabetic Rats

Background : To determine whether vitamin E protects streptozotocin-induced diabetic rats from diabetic urinary bladder dysfunction and discover its possible mechanism. Materials and Methods : A total of 40 rats were randomly divided into four groups: a control group (A), a diabetic group (B), a group given vitamin Eonly (C), and a diabetic group given vitamin E therapy for 8 weeks (D). Diabetes was induced in the rats by 65 mg/kg streptozosin (STZ) via an intraperitoneal (i.p.) injection. Vitamin E was given in a dose of 50 mg/kg/day i.p. Under urethane anaesthesia (1.2 g/kg) subcutaneously and decapitation, contractile responses to carbachol of detrusor strips in all groups were studied in vitro . The levels of nitrite, nitrate, malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were detected in bladder tissues homogenates. Apoptosis studies were performed by detection of the levels of caspase 3 and cell death detection. Results : The bladder weights were significantly increased ( p <0.001) in diabetic groups compared to the other studied groups. Contractile responses to carbachol increased in the diabetic group more than in the other groups (p<0.001). Vitamin E improved the contractile responses of group D and improved them but still significantly higher than those of control group (p < 0.05). Vitamin E treatment decreased the tissue MDA, nitrite, nitrate and GSH levels of group D which were significantly higher in group B than A and C groups (p<0.001). All enzyme activities of group B were significantly lower than those of the other groups, although they increased significantly in group D but still lower than those of A and C groups. However, no significant differences were detected between the levels of GPx and SOD of group D and those of A and C groups. Conclusions : These data suggest that vitamin E supplementation may be beneficial in delaying the progression of diabetic dysfunction in experimental animal model. Keywords: Vitamin E, Bladder contractitliy, Diabetes, Rats