In this experimental study, 68 adult Wistar rats made the subject of the study. Administration of vitamin E and C, in an individual manner, can have some more favorable effects on urea, creatinine and nitrite level in GM nephrotoxicity than their coadministration. On the other hand, there is a gender difference, in response to vitamin E and C in which male gender responded more favorably to the antioxidant vitamins.

Backgrounds: The prevalence of metabolic syndrome (MetS) is increasing in developing countries that affects the liver in a variety of ways. This study was designed to investigate the protective role of eugenol on liver damage caused by fructose-induced MetS. Materials and Methods: Thirty male Wistar rats were randomly divided into five groups: 1: tap water (control), 2: fructose, 3: fructose + eugenol solvent, 4: fructose + eugenol 50 mg/kg, and 5: fructose + eugenol 100 mg/kg. At the end of the experiment, blood samples were taken for measurement fast blood glucose (FBG), serum glutamic-oxaloacetic transaminase (SGOT), serum glutamic pyruvate transaminase (SGPT), low-density lipoprotein, high-density lipoprotein, cholesterol, and triglyceride. Results: FBG significantly increased in Group 2 compared to Group 1 (P < 0.001); however, it significantly decreased in Groups 4 and 5 compared to Group 2 (P < 0.05). SGOT and SGPT levels significantly increased in Group 2 compared to the control group (P < 0.001). However, SGOT and SGPT levels significantly decreased in Groups 4 and 5. Malondialdehyde (MDA) and liver tissue damage score (LTDS) significantly increased in Group 2 compared with the control group (P < 0.01), whereas MDA and LTDS decreased in Groups 4 and 5 compared to Group 2 (P < 0.05). Conclusion: Eugenol may ameliorate liver damage in a rat model of fructose-induced MetS, and these protective effects may in part be mediated by improving antioxidant status and reducing oxidative stress and lipid peroxidation. It may also reduce hepatic inflammation and fat accumulation as well as fibrosis of liver cells.

Background: Nephrotoxicity is the most known side effect of gentamicin. In addition, renin angiotensin system (RAS) plays an important role in the pathogenesis of renal injury and nephrotoxicity. Hypomagnesaemia is other complication of gentamicin. Previous studies reported that magnesium plays an important role in cell enzymatic functions, reducing lipid peroxidation. Objectives: We investigated the role of losartan and magnesium sulfate (MgSO4 ) on gentamicin nephrotoxicity. Materials and Methods: In this study, rats randomly assigned to five groups. The first group, received saline, the second group received gentamicin 80 mg/kg/d, intraperitoneally (ip), and the third group, received a regular dose of losartan, 10 mg/kg/d + gentamicin 80 mg/kg/d. The fourth group received MgSO4 , 80 mg/kg/d + gentamicin 80 mg/kg/d. The fifth group obtained a continuous dose of gentamicin 80 mg/kg/d + losartan 10 mg/kg/d + MgSO4 80 mg/kg/d simultaneously. Nine days after administration of drugs, blood samples were collected from the heart. The level of urea, creatinine (Cr), malondialdehyde (MDA) and nitrite were measured in the animal serum and homogenized kidney tissue. Results: Gentamicin increased serum urea and Cr levels. The administration of losartan and MgSO4 lonely and combination of them, significantly reduced the levels of serum urea and Cr. Losartan alone and combination of losartan and MgSO4 compared with gentamicin, significantly decreased kidney MDA level too. Decrease of kidney nitrite level by gentamicin was compensated by the administration of losartan, MgSO4 alone or their combination. Additionally, losartan and MgSO4 alone and their combination together significantly reduced renal damage. Conclusions: The results of this study indicated that administration of losartan and MgSO4 individually and their combination decreased kidney nephrotoxicity and improved renal function. This effect is probably related to the improvement of antioxidant status and renal blood flow.

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Introduction: Metabolic syndrome consists of a group of abnormities which is involved with chronic kidney disease and nephropathy. Eugenol is an important phenolic component, which is present in many plants’ essential oils such as cloves oil with antioxidant effects. Objectives: Our study planned to demonstrate eugenol’s effects over nephrotoxicity derived from metabolic syndrome. Materials and Methods: Thirty-five male Wistar rats were picked accidentally and then divided into five groups including 1) tap water; 2) water with fructose10%; 3) water with fructose + sweet almond oil and administered intraperitoneally; 4) water with fructose+ eugenol 50 mg/kg/d and administered intraperitoneally; 5) water with fructose+ eugenol 100 mg/kg/d administered intraperitoneally. This regime lasted for 60 days, and at the beginning of day 31st, injections started for 30 days. Assessment of serum, urine and renal parameters (in homogenized kidney tissue) were conducted in the last step. Results: The results argued that the induction of metabolic syndrome following renal injury has significantly increased serum blood urea nitrogen (BUN) and creatinine (Cr) levels in the fructose group. Consumption of eugenol resulted in a significant reduction in the level of these two biochemical factors (P < 0.05). The renal level of malondialdehyde (MDA) increased in the fructose group while treatment with a dose of 50 eugenol decreasing its level (P < 0.05). Proteinuria and kidney tissue damage score (KTDS) increased in the fructose group compared with the tap water group (P < 0.001). It is noteworthy that treatment with eugenol did not affect the level of proteinuria and KTDS with any of the used doses. Conclusion: Our results indicated the improvement of renal functioning and decrease in lipid peroxidation, although eugenol doses used in this study did not reduce proteinuria and KTDS.