Some toxic effects of molybdenum in adult male albino rats

Ammonium molybdate is an essential trace element in plants, animals and humans, as it is present as a cofactor for some enzymes; also, it is an environmental pollutant. Thirty adult male albino rats were used to investigate the adverse effects of ammonium molybdate on the liver, kidneys, spleen and lungs of adult male albino rats. Therty adult male rats were equally divided into 3 groups. The rats of the 1[st] group were left without treatment and used as a negative control group for measuring the basic parameters. The rats of the 2[nd] group were daily intragastrically administered 2 ml normal saline [vehicle of molybdenum] for each rat for 30 days and were used as a positive control group. The rats of the 3rd group were daily intragastrically administered ammonium molybdate in a dose of 136 mg /kg body weight in 2 ml of normal saline [1/5 of the LD50] for each rat for 30 days. At the end of the study, blood samples were collected from the retro-orbital plexus of each anethetized rat in all groups for measuring levels of liver enzymes [ALT, AST, Aikaline phosphatase], total bilirubin, urea and createnine; then the rats were sacrificed, and specimens from the livers kidneys, spleens and lungs of all rats were collected for histopathological examination. The levels of liver enzymes, bilirubin, urea and createnine of the rats of the 3[rd] group [ammonium molybdate group] were statistically significantly elevated compared to those of the negative control group [P <0.001]. Histopathological examination of the rats of the 3rd group showed, moderate liver damage consisting of scattered necrotic areas, inflammatory infiltrates and congested central vein, In the Kidneys, there were degeneration of the epithelium of the convoluted tubules appeared as cloudy swelling and congestion. There were also cellular infiltrates. Histopathological examination of the spleen showed reactive follicular hyperplasia with areas of necrosis and congestion reflecting congested splenomegally. The lungs revealed diffuse haemorrhage and mononuclear inflammatory cellular infiltration in the interstitial tissue with congested dilated vessels. It can be concluded that ammonium molybdate could produce toxic effects on the liver, kidneys, spleen and lungs of adult male albino rats

Nephrotoxic effects of celecoxib on adult male albino rats

Nonsteroidal anti-inflammatory drugs are widely used for a variety of indications, including acute pain, arthritic pain, and headache. The long-term use of these agents is often limited by unwanted adverse effects, such as gastritis and renal dysfunction. In an effort to decrease the adverse effects while retaining pain-relieving properties, the selective cyclo-oxygenase [COX]-2 inhibitors were developed. The aim of the present study was to evaluate the nephrotoxic hazards of celecoxib and also to evaluate the extent of recovery that occur after discontinuation of this drug during a follow up period .The study was conducted on 50 adult male albino rats weighing approximately [150-200 gm] and divided into 3 groups; group I [negative control group]: consisted of 15 rats, each rat was given no medications to evaluate the basic parameters; group II [positive control group [Gum acacia group]]: consisted of 15 rats, each rat was gavaged with 2 mL of Gum acacia suspension once daily for 6 weeks and group III [celecoxib group]: consisted of 20 rats, each rat was gavaged with 14,4 mg celecoxib/rat once daily for 6 weeks. Twenty four hours after the last dose of celecoxib, 15 rats from each control group and 10 rats from the celecoxib group were used. The kidneys of the rats of these groups were investigated histopathologically by light microscope and biochemically by measuring blood urea nitrogen and serum creatinine, sodium and potassium levels. The remaining rats of celecoxib group were left for another 6 weeks without drug, administration for follow up. At the end of this period the. rats were examined as mentioned above. The main findings of the present study were as follow: group 1 [negative control group], and group II [positive control group], showed no abnormal findings without a statistically significant difference between them so we used the results of the negative control group to compare it with those of celecoxib group. As regard biochemical changes, there was an increase in blood urea nitrogen and serum creatinine, sodium and potassium levels in the rats of celecoxib group with a statistically significant difference when compared with the negative control group [P<0.001]. Six weeks after discontinuation of celecoxib administration, the above mentioned biochemical changes improved and showed a statistically significant difference when compared with the results obtained 24 hours after the last dose of celecoxib, but the level of improvement didn't reach to the control level and gave a significant difference when compared with the negative control group. This means that, these parameters improved but didn't return to the level' of the control, which was supported by the histopathological results. As regard histopathological study of celecoxib group, microscopical examination of the kidneys showed severe affection of the kidneys in the form of renal papillary necrosis and acute and chronic tubulo-interstitial nephritis with interstitial oedema and inflammatory cell infiltrate. After 6 weeks of follow-up, histopathological examination of the kidney in the celecoxib group showed incomplete recovery. It could, be concluded that celecoxib is nephrotoxic and its toxic effects were partially reversible after its discontinuation

Differential effects of vitamin E supplementation on cardiovascular risk factors and on cardiac vulnerability to ischemia and reperfusion in rats

The present study was performed to examine the effects of vitamin E on hemodynamics, electrocardiogram [ECG] pattern, plasma levels of lipid profile, enzymes reflecting myocardial cell integrity creatine kinase [CK] and lactate dehydrogenase [LDH] and rate of lipid peroxidation as well as on myocardial performance after ischemia-reperfusion injury in isolated rat hearts. Vitamin E-treated rats were injected with vitamin E in a dose of 4 mg/100g body weight [b.w.] daily, for 6 consecutive days. Control rats were treated with vitamin E-solvent, daily, for the same duration. Then, rats were sacrificed, and the isolated heart were subjected to 30 min. ischemia followed by 30 min period of reperfusion. The present study demonstrated that administration of vitamin E in normal rats did not produce any appreciable hemodynamic effects as regards heart rate [HR], mean arterial pressure [MAP,], and pressure rate product[PRP]. The ECG pattern showed no arrhythmias or ischemic changes compared to control group. Concerning changes in plasma lipid profile, vitamin E-treated rats showed significant reduction in both total cholesterol [TC], and low density lipoprotein-cholesterol [LDL-C] Moreover, high density lipoprotein-cholesterol / total cholesterol [HDL-C/TC] was significantly elevated, in contrast to a non significant decrease in both low density lipoprotein-cholesterol/ total cholesterol [LDL-C /TC] and LDL-C /HDL-C ratios, when compared with controls. Myocardial cellular integrity, estimated by the plasma level of CK and LDH, was preserved by the administration of vitamin E, revealed evidently by the significant decrease in CK and LDH release in plasma of rats treated with vitamin E as compared to control rats. Moreover, the plasma level of malondialdehyde, as an index for the degree of lipid peroxidation, was significantly reduced. The preischemic, baseline activity of the isolated hearts obtained from rats treated with vitamin E, revealed non significant changes in myocardial inotropy except for prolongation of half relaxation time. Also there was a significant reduction in both heart rate and LDH release in the coronary effluent, while there was a non significant change in tile coronary flow rate. The results of the isolated hearts subjected to reperfusion following 30 minutes ischemic period, showed that vitamin E decreased the detrimental effect of reperfusion on the inotropic activity observed in the control group, evident by superior recovery of postischemic reperfusion myocardial functions. Manifested by elevated peak developed tension, and tension generation per unit time, concomitant with shortening of time to peak tension, and half relaxation time, along the reperfusion period. In addition, the percentage recovery of the heart rate was better during the whole reperfusion period but the difference was statistically significant only at 15-minute of reperfusion, and as well myocardial flow rate percentage .showed significant superior recovery in vitamin E-treated rat hearts. Moreover, there was a significant reduction in both CK and LDH release in the coronary effluent of vitamin E treated rat hearts, compared to control hearts. It could be concluded that vitamin E administration has a favorable potential against the risk of atherosclerosis and lipid peroxidation and as well it may attenuate the detrimental effects of postischemic reperfusion on the myocardial contractility