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Association of increased oxidative stress (OS) with the pathophysiology of renal stone formation has not been explored greatly in the field of urolithiasis. In this prospective case–control study, we measured 24-h urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels in patients with urolithiasis and compared them with matched healthy controls. We also measured 24-h urinary uric acid, calcium, oxalate, and citrate levels in patients with renal stone disease and studied their relation with urinary 8-OHdG levels. Seventy-five cases of renal stone disease and 75 well-matched controls were included. Median 24-h urinary 8-OHdG levels were significantly higher in cases compared to controls (7.6 vs. 3.7 µg/g of creatinine; p < 0.000). Receiver-operating curve (ROC) analysis for 8-OHdG between cases and controls revealed an area under the curve of 0.90. At 8-OHdG (µg/g of creatinine) value of 5 or more, a sensitivity and a specificity of 84% each were obtained. A positive correlation between 8-OHdG (µg/g of creatinine) and 24-h urinary oxalate level was noted (r = 0.461, p = 0.000). No correlation between 8-OHdG (µg/g of creatinine) and other variables was noted. On multivariate linear regression analysis, we noted 24-h urinary oxalate levels to be an independent predictor of urinary 8-OHdG levels. OS is significantly higher in patients with renal stone diseases compared to healthy controls. Urinary oxalate levels were significantly correlated with urinary 8-OHdG levels. [ABSTRACT FROM AUTHOR]

The biomedical applications of the noble metal nanoparticles have been the field of interest, especially in cancer therapy. In this paper, the synthesis of spherical silver and gold nanoparticles and their apoptotic activity against breast cancer cells is reported. The chemicals reduction method is used to synthesize nanoparticles. Two different types of surfactants i.e., citrate and polyvinylpyrrolidone were used as a reducing and capping agent. The synthesized nanoparticles have been characterized using X-ray diffraction, ultraviolet-visible absorption spectroscopy, dynamic light scattering, zeta potential and transmission electron microscopy. The synthesized nanoparticles have crystalline phase with average size in the range of 25-30 nm and possess negative surface charge. In vitro studies of nanoparticles against breast cancer cells (MCF-7), were performed. The results show the significant cytotoxicity of nanoparticles against the cancer cell line and found to be mediated by DNA damage. [ABSTRACT FROM AUTHOR]

To evaluate the effect of different doses of Manuka honey in experimentally induced inflammatory bowel disease in rats. Adult Wistar rats of either sex were used ( n = 30). Colitis was induced by a single intracolonic administration of TNBS dissolved in 35% ethanol. The rats ( n = 30) were divided into five groups ( n = 6) and were treated with vehicle (ethanol), TNBS, Manuka honey (5 g/kg, p.o.), Manuka honey (10 g/kg, p.o.) or sulfasalazine (360 mg/kg, p.o.) body weight for 14 days. After completion of treatment, the animals were killed and the following parameters were assessed: morphological score, histological score and different antioxidant parameters. Manuka honey at different doses provided protection against TNBS-induced colonic damage. There was significant protection with Manuka honey 5 g/kg as well as with 10 g/kg body weight compared with the control ( p < 0.001). All the treated groups showed reduced colonic inflammation and all the biochemical parameters were significantly reduced compared with the control in the Manuka honey treated groups ( p < 0.001). Manuka honey at different doses restored lipid peroxidation as well as improved antioxidant parameters. Morphological and histological scores were significantly reduced in the low dose Manuka honey treated group ( p < 0.001). In the inflammatory model of colitis, oral administration of Manuka honey 5 g/kg and Manuka honey 10 g/kg body weight significantly reduced the colonic inflammation. The present study indicates that Manuka honey is efficacious in the TNBS-induced rat colitis model, but these results require further confirmation in human studies. Copyright © 2008 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the effect of low-dose ( Materials and methods: Male Balb/c mice, 5 – 6 weeks of age, were divided into irradiated and non-irradiated groups. Whole body irradiation was done with ?-rays from a 60 Co source at doses of 10, 25 and 50 cGy (48.78 cGy/min). Lipid peroxidation and antioxidant status were measured in the liver and the lungs at 4, 12 and 24 h after irradiation. Results: Lipid peroxidation increased by 1.38 and 2.0 fold in lung and liver respectively at 12 h after exposure to 25 cGy. Whole body exposure to 25 and 50 cGy significantly ( p < 0.05) increased the hepatic reduced glutathione at 4 h. Reduced glutathione continued to rise until 12 h and returned to the basal level at 24 h, whereas in the lungs it remained elevated until 24 h at 10 and 25 cGy. Antioxidant enzymes activities for superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase increased by 1.22, 1.13, 1.22 and 1.11 fold respectively ( p < 0.05) in the liver at 4 h after exposure to 50 cGy and remained elevated at almost the same level up to 12 h after exposure. Surprisingly these antioxidant defense enzymes remained unaltered in the lung at the above radiation doses. Conclusions: Low-dose whole body ?-irradiation differentially modulates the antioxidant defense system in the liver and lungs of mice. The induction of endogenous glutathione, immediately after exposure to low-dose ?-irradiation, may be beneficial in protecting the cells from reactive oxygen species (ROS) induced oxidative stress. [ABSTRACT FROM AUTHOR]

Background and aim: One of the active combustion product of cigarette smoke, Benzo[a]pyrenes, role in pulmonary cancer is clearly understood. However, its role in gastrointestinal cancer including colon cancer is not clearly understood. Methods: In this study, benzo(a)pyrenes was treated to colon cells to evaluate its role in cell viability, cellular ROS, and gene expression of various PLA2 isoforms was evaluated by FACS and PCR. The identified PLA2 was silenced at the gene level to evaluate its role in cell viability and ROS generation. Results: B(a)P treatment at 1 µg/mL for 48 h to HCT-15 male colon cells significantly reduced the cell viability without affecting HT-29 female colon cells. Higher doses and longer treatment duration with B(a)P showed that female colon cells were highly sensitive than male colon cells. Annexin-V/PI staining for preapoptotic detection showed that B(a)P treatment increased the apoptosis in both the cell types in a concentration and time-dependent manner. The cytosolic ROS (cROS) and superoxide radical (SOR) formation in the female colon cells was significantly higher than male colon cells unlike the mitochondrial ROS (mtROS) production which was significantly higher in male colon cells. Treatment with B(a)P significantly upregulated the IID and IVA PLA2 isoform groups in HCT-15 male colon cells, whereas IB was upregulated in HT-29 female colon cells among the various PLA2 isozyme gene studied (IB, IID, III, IVA, IVB, IVC, VI, X, aiPLA2 and iPLA2). Gene silencing experiments targeting PLA2 IID and IVA in the HCT-15 male colon cells and IB in HT-29 female colon cells showed no effect with B(a)P treatment on the cell proliferation, apoptosis, membrane integrity and free radicals (ROS, mtROS, and SOR) generation. Conclusion: Targeting specific PLA2 isozymes in a cell-specific manner abolished the B(a)P-induced PLA2-mediated oxidative damage–related signaling pathways. [ABSTRACT FROM AUTHOR]