The aim of this study is to evaluate the influences of short-term treatment with levosimendan (chemical formula: C 14 H 12 N 6 O) on oxidative stress and some trace element levels in renal tissues of healthy rats. A total of 20 male Wistar-albino rats were randomly divided into two groups, each consisting of 10 rats. Animals in the first group were not treated with levosimendan and served as control. Animals in the second group were injected intraperitoneally with 12 mg/kg levosimendan and served as levosimendan group. Animals in both the groups were killed 3 days after the treatment, and their kidneys were harvested for the determination of tissue oxidant/antioxidant statues and trace element levels in renal tissues. The tissue malondialdehyde level was significantly (p < 0.001) lower in levosimendan group than in controls. The protective enzyme activities such as superoxide dismutase, catalase, and glutathione peroxidase and antioxidant glutathione level were significantly (p < 0.001) higher in levosimendan group than in controls. It was concluded that levosimendan reduced oxidative stress by avoiding lipid peroxidation and production of reactive oxygen species, and overactivating and/or increasing the protective antioxidant enzyme levels in renal tissues of rats. It is supposed that this experimental study provides beneficial data for clinicians in the management of renal tissue damage related to obstruction and/or ischemia.

This study aimed to investigate the possible protective effect of paricalcitol on experimental amikacin-induced nephrotoxicity model in rats. Wistar albino rats (n ¼ 32) were allocated into four equal groups of eight each, the control (Group C), paricalcitol (Group P), amikacin-induced nephrotoxicity (Group A), and paricalcitol-treated amikacin-induced nephrotoxicity (Group A þ P) groups. Paricalcitol was given intra-peritoneally at a dose of 0.4 lg/kg/d for 5 consecutive days prior to induction of amikacin-induced nephrotoxicity. Intra-peritoneal amikacin (1.2 g/kg) was used to induce nephrotoxicity at day 4. Renal function parameters, oxidative stress biomarkers, oxidative DNA damage (8-hydroxy-2 0 -deoxyguanosine/deoxyguanosine ratio), kidney histology, and vascular endothelial growth factor (VEGF) immunoexpression were determined. Group A þ P had lower mean fractional sodium excretion (p < 0.001) as well as higher creatinine clearance (p ¼ 0.026) than the amikacin group (Group A). Renal tissue malondialdehyde levels (p ¼ 0.035) and serum 8-hydroxy-2 0 -deoxyguanosine/deoxyguanosine ratio (8-OHdG/dG ratio) (p < 0.001) were significantly lower; superoxide dismutase (p ¼ 0.024) and glutathione peroxidase (p ¼ 0.007) activities of renal tissue were significantly higher in group A þ P than in group A. The mean scores of tubular necrosis (p ¼ 0.024), proteinaceous casts (p ¼ 0.038), medullary congestion (p ¼ 0.035), and VEGF immunoexpression (p ¼ 0.018) were also lower in group A þ P when compared with group A. This study demonstrates the protective effect of paricalcitol in the prevention of amikacin-induced nephrotoxicity in an experimental model. Furthermore, it is the first study to demonstrate that paricalcitol improves oxidative DNA damage in an experimental acute kidney injury model. ARTICLE HISTORY

More than 600 chemicals can cause damage in liver, one of which is carbon tetrachloride (CCl₄). Hepatoprotective agents could prevent tissue damage and reduce morbidity and mortality rates; such agents may include alternative or folkloric treatments. We investigated sesame (Sesamum indicum L.) for its hepatoprotective effect in CCl₄-induced experimental liver damage. To this end, 0.8 mg/kg of sesame fixed oil was provided intraperitoneally to rats whose livers were damaged by CCl₄. Tissue and blood samples were taken at the end of the experiments and evaluated histologically and biochemically. Ballooning degenerations and an increase in lipid droplets in liver parenchyma and increases in serum alanine transaminase, aspartate transaminase, and bilirubin were found in the CCl₄ group. Biochemical and histopathological findings in the sesame fixed oil treated group were not significantly different from the CCl₄ group. Sesame did not show a hepatoprotective effect in CCl₄-induced liver toxicity.

The aim of this study was to investigate the effects of radiofrequency radiation emitted from Wi-Fi systems and mobile phones on cord blood and placenta. The study included 149 pregnant women who were divided in subgroups: unexposed (control), mobile phone exposed, Wi-Fi exposed and mobile phone plus Wi-Fi exposed groups. Immediately after birth, placenta and cord blood samples were collected and protein carbonyl (PCO), malondialdehyde (MDA), total oxidant status (TOS), total antioxidant status, 8-hydroxy-2 0-deoxyguanosine (8-OHdG) levels and DNA single strand breaks were analysed. The results of the study showed an increase in 8-OHdG, MDA, PCO and TOS in cord blood and placenta in the group exposed to mobile phones during gestation. However, the group exposed to Wi-Fi did not show alterations in the studied oxidative stress parameters. On the other hand, tail intensity and tail moment of DNA in the mobile phone exposure groups were higher than those in the control and Wi-Fi exposure groups. In conclusion, the results of this study indicated that mobile phone exposure during pregnancy could have an important potential to cause oxidative stress and DNA damage in cord blood and placenta. The results of this study also indicated that combined effects of Wi-Fi plus mobile phone exposure have a higher potential to cause synergistic harmful effects.

This experiment was designed to investigate the effect of levosimendan injection on lipid peroxidation product malondialdehyde (MDA) and antioxidant glutathione (GSH) levels, and activities of antioxidant enzymes in myocardium of rats. Twenty male Wistar-albino rats were divided randomly into 2 study groups, each consisting of 10 rats. The animals in the first group were not treated with drug and served as control. It was found that the MDA and GSH levels decreased in levosimendan injected group. Superoxide dismutase, glutathione peroxidase, catalase and carbonic anhydrase enzyme activities were lower in levosimendan injected group than controls. It was concluded that lower tissue free radical level caused by levosimendan injection led to a lower antioxidant enzymes synthesis in the body and a decrease in the antioxidant enzyme activity and free radical scavenger level in myocardium of rat.