The effects of curcumin on the liver and remote organs after hepatic ischemia reperfusion injury formed with Pringle manoeuvre in rats.

BACKGROUND: We aimed to investigate the effects of curcumin on ischemia/ reperfusion (IR) injury of the liver and distant organs resulting from liver blood flow arrest. MATERIALS AND METHODS: Totally 40 rats, divided into four groups, each included 10 rats were used. Group I as only laparatomy, Group II laparatomy and curcumin application, Group III hepatic IR; and Group IV as hepatic IR and curcumin application group. Ischemia was generated by hepatoduedonal ligament clamping for 30 minutes and then reperfusion is started. Curcumin capsules were opened and appropriate dose had been created within weighing scales. After calculations, the powder was diluted with saline. Fifteen minutes before the ischemia, curcumin was applied via oral gavage. Blood samples were taken from the animals for biochemical analysis at 60th minutes of the experiment in the first and second groups; 30 minutes after beginning reperfusion in the third and forth groups. Simultaneously, liver, lung and kidney tissues were sampled for biochemical and histopathological examinations. RESULTS: Plasma malondialdehyde levels were found to be higher (p < 0.001), but total antioxidant activity values were not different in IR group compared with IR + curcumin group (p > 0.05). Biochemical and histopathological evaluation of tissue samples revealed that there were no differences in total antioxidant activity, total oxidant activity and histopathologic scores in IR + curcumin group compared with values of IR group (p > 0.05). CONCLUSIONS: Curcumin did not reduce the effects of hepatic ischemia reperfusion injury on the liver and distant organs including kidneys and lungs significantly.

The effects of ellagic acid on the liver and remote organs' oxidative stress and structure after hepatic ischemia reperfusion injury caused by pringle maneuver in rats.

INTRODUCTION: We aimed to investigate the possible protective effects of ellagic acid (EA) on the liver and remote organs against the hepatic ischemia-reperfusion injury. METHODS: Forty Wistar-Albino rats were divided into four groups each containing 10 rats. Group I with laparotomy only, Group II with laparatomy and ellagic acid application, Group III with hepatic ischemia-reperfusion and Group IV with hepatic ischemia-reperfusion and ellagic acid application. Hepatic ischemia was induced by pringle's manoeuvre for 30 minutes followed by 30 minutes reperfusion period. After induction of ischemia, EA was applied via oral gavage at a dose of 85 mg/kg. Blood samples were taken from the animals for biochemical analysis at 60th minute of the experiment in all groups. Simultaneously, liver, lung and kidney tissues were sampled for biochemical analyses and histopathological examinations. RESULTS: The administration of EA reduced serum malonyldialdehid levels (p<0.05) and liver's oxidative stress index compared with the non-use EA groups (p0.05). The use of EA did not exert significant protective effects against the effects of liver ischemia-reperfusion injury on the kidney and lung. CONCLUSION: In our experiments ellagic acid reduced the liver oxidative stress induced by ischemia-reperfusion injury. However, no significant histological improvement was found with EA. There were no significant protective effects on the remote organ injuries induced by ischemia-reperfusion (Tab. 3, Fig. 7, Ref. 37).

Protective effects of thymoquinone on vancomycin-induced nephrotoxicity in rats.

AIM: Oxidative stress has been implicated as a potential responsible mechanism in the pathogenesis of vancomycin (VCM)-induced renal toxicity. Therefore, we aimed to investigate the protective effect of thymoquinone (TQ) against VCM-induced nephrotoxicity by tissue oxidant/antioxidant parameters and histological changes in rats. MATERIALS AND METHODS: Wistar albino rats were randomly separated into four groups consisting of seven rats per group. The groups had normal saline (control group), VCM, VCM and TQ and TQ, respectively. VCM was injected intraperitoneally at a dose of 200 mg/kg and continued at 12-h intervals for 7 days. TQ was injected intraperitoneally at a dose of 10 mg/kg and continued at 24 h intervals for 8 days. Animals were killed and blood samples were analyzed for the levels of serum blood urea nitrogen (BUN) and creatinine (Cr). Kidney specimens were analyzed for levels of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) as well as for histopathological changes. RESULTS: We found that the levels of serum BUN, Cr and kidney tissue MDA were increased in the VCM group. Activities of SOD and GSH-Px in kidney tissue were decreased. TQ administration ameliorated significantly these changes. CONCLUSION: These results indicate that the TQ produces a protective mechanism against VCM-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.

Oxidative stress and antioxidant defense in plasma after repeated bouts of supramaximal exercise: the effect of coenzyme Q10.

AIM: The purpose was to determine the changes of oxidative stress and antioxidant markers in plasma after repeated bouts of supramaximal exercise and the effects of coenzyme Q10 supplementation on these changes. METHODS: This randomized, double blind, crossover study was composed of two 8-week periods of supplementation with either 100 mg.day(-1) CoQ10 or placebo. Fifteen healthy and sedentary men participated in the study. Five Wingate tests with 2 min rest between tests were performed. Blood samples were collected at rest, immediately after, 15 and 60 min after the fifth Wingate test for oxidative stress (malondialdehyde, nitric oxide, xanthine oxidase and adenosine deaminase) and antioxidant (superoxide dismutase, glutathione peroxidase and uric acid) markers. RESULTS: At baseline exercise session, malondialdehyde increased 15 and 60 min after the exercise compared to the rest and immediately after the exercise. Malondialdehyde at rest, immediately after and 60 min after the exercise decreased with coenzyme Q10 supplementation when compared to baseline. At baseline exercise session, uric acid increased 15 and 60 min after the exercise when compared to the rest. In conclusion, lipid peroxidation and antioxidant defense increase after repeated short-term supramaximal exercise. CONCLUSION: Coenzyme Q10 supplementation partially prevents the increase in lipid peroxidation after repeated short-term supramaximal exercise.

C677T polymorphism of the methylenetetrahydrofolate reductase gene does not affect folic acid, vitamin B12, and homocysteine serum levels in Turkish children with neural tube defects.

Association between neural tube defects (NTDs) and C677T polymorphism of the methylenetetrahydrofolate reductase (MTHFR) gene was suspected, because the MTHFR gene codes for a key enzyme in folate metabolism. Its deficiency usually leads to significant reductions in plasma concentrations of folate, vitamin B(12) and methionine, whereas homocysteine levels are increased. We examined folate, vitamin B(12) and homocysteine serum concentrations and polymorphism of the C677T MTHFR gene in Turkish children with neural tube defects. Thirty-three children with NTDs, 26 mothers and 48 healthy individuals were studied. C677T MTHFR polymorphism was determined by melting curve analyses (LightCycler). The levels of folate, vitamin B(12) and homocysteine serum concentrations in NTDs were evaluated and compared, along with information concerning alleles of the MTHFR gene. C677T allele frequencies in NTD children and their mothers were similar to those found in controls. Serum folate and vitamin B(12) concentrations were significantly higher in NTD children than that of controls. Serum homocysteine concentrations were not significantly higher in NTD children and mothers. We concluded that C677T MTHFR gene polymorphism does not affect folic acid, vitamin B(12) and homocysteine metabolism in Turkish children with NTDs. C677T polymorphism of the MTHFR gene cannot be regarded as a major risk factor for NTDs in Turkish children.

Neuroprotective effects of Nigella sativa on experimental spinal cord injury in rats.

The aim of this study was to investigate the possible beneficial effects of Nigella sativa (NS) in comparison to methylprednisolone on experimental spinal cord injury (SCI) in rats. SCI was performed by placing an aneurysm clip extradurally at the level of T11-12. Rats were neurologically tested over 24 h after trauma and spinal cord tissue samples were harvested for both biochemical and histopathological evaluation. The neurological scores of rats were not found to be different in SCI groups. SCI significantly increased the spinal cord tissue malondialdehyde (MDA) and protein carbonyl (PC) levels, however SCI decreased superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) enzyme activities compared to the control. Methylprednisolone and NS treatment decreased tissue MDA and PC levels and prevented inhibition of SOD, GSH-Px and CAT enzymes in the tissues. The most significant results were obtained when NS was given. In SCI and placebo groups, the neurons of spinal cord tissue became extensively dark and degenerated with picnotic nuclei. The morphology of neurons in methylprednisolone and NS-treated groups were well protected, however, not as well as the neurons of the control group. The number of neurons in the spinal cord tissue of the SCI and placebo groups was significantly less than the control, laminectomy, methylprednisolone and NS-treated groups. In conclusion, NS treatment might be beneficial in spinal cord tissue damage, and therefore shows potential for clinical implications.

Cytotoxic effects of dental desensitizers on human gingival fibroblasts.

The purpose of this study was to evaluate the effects of three different desensitizers on the cell viability and morphology of human gingival fibroblasts (HGF). Human gingival tissues were obtained from individuals who have clinically, healthy periodontium. HGF were grown at 37 degrees C in humidified atmosphere of 5% CO2 in Dulbecco's modified eagle's medium, supplemented with glutamine, penicillin, streptomycin, and 10% fetal bovine serum. The cells were treated with different concentrations (0.1, 0.3, and 0.5 microL/mL) of desensitizers (Gluma Desensitizer, Seal&Protect, and MicroPrime). After 24- and 48-h exposure to the desensitizer solutions, the viable cells were examined using a hemocytometer. To monitor HGF viability, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl tetrazolium bromide (MTT) colorimetric assay was used and cell morphology was also observed at 48 h. Following exposure to concentrations of 0.1 microL/mL of test materials for 24 h, cell survival rates for Gluma Desensitizer (106%) and Micro Prime (62%) were not significantly different from the control, while it was significant for Seal&Protect (50%). Growing cells were significantly inhibited by all tested materials for 48 h (p < 0.05) in survival rates of 51, 47, and 31%, respectively. On the basis of the MTT assay, the cytotoxic effect of MicroPrime was more prominent, especially at high concentrations, than does Gluma Desensitizer and Seal&Protect. After exposure to Seal&Protect and MicroPrime, HGF became retracted, rounded in appearance and had loss of normal organization, leading to enlargement of intercellular space when compared with Gluma Desensitizer. As a conclusion, taking the limitations of an in vitro experiment into consideration, the cytotoxic effects were varied, depending on the chemical composition and exposure periods of the tested desensitizers.