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Purpose: This study aimed to determine the possible effects of single-dose intravitreal bevacizumab on nitric oxide (NO) levels in serum and remote organs and to reveal one of the possible mechanisms in the pathophysiology of hypertension., Methods: Thirty-eight adult New Zealand albino rabbits were divided into a control group (no injection was performed, killed on day 28 of the study), group 1 (killed on day 1 of the study), group 2 (killed on day 7 of the study), group 3 (killed on day 14 of the study), and group 4 (killed on day 28 of the study). The right eyes of the animals in groups 1-4 received an intravitreal single injection of 1.25 mg (0.05 ml) bevacizumab (Avastin), and their brain, heart, liver, kidney, and blood samples were collected. NO levels were evaluated in the serum and organ homogenates. Kidney tissues were assessed by electron microscopy., Results: Serum, brain, kidney, and liver NO levels significantly decreased in groups 2, 3, and 4 as compared with the control group (P<0.05). In addition, heart NO levels significantly decreased in groups 3 and 4 compared with the control group (P<0.05). There were no electron microscopic changes in the kidneys of either group., Conclusions: This study demonstrated that single intravitreal injection of bevacizumab decreased NO levels in serum, brain, heart, liver, and kidneys. In addition, there were no electron microscopic changes in the kidneys.

The effect of cobalt(II) chloride (CoCl2) and CoCl2 with ascorbic acid (AA) on components of the antioxidant defense system and lipid oxidative damage were studied in controls and streptozotocin-induced diabetic rat livers. Three days after injection, rats received either 0.5 mM CoCl2 or 0.5 mM CoCl2 with a combination of 1 g/L AA in drinking water up to 6 wk. The elevated blood glucose levels in diabetic rats were about 12% restored by oral administration of CoCl2 (0.05 mM) and were significant reduced (46%) following AA addition (1 g/L) to CoCl2. Cobalt therapy effectively decreased the increased activities of catalase (CAT), superoxide dismutase (SOD), and thiobarbituric acid reactant substances (TBARS) but could not restore the increased glutathione peroxidase (GSH-Px) in the liver of diabetic rats. Our findings suggest that cobalt therapy may prove effective in improving the impaired antioxidant status during the early state of diabetes, and ascorbic acid supplementation at this dose potentiates the effectiveness of cobalt action.

Purpose: The increased consumption of high-fructose corn syrup (HFCS) may contribute to the worldwide epidemic of fatty liver. In this study, we have investigated whether HFCS intake (20 % beverages) influences lipid synthesis and accumulation in conjunction with insulin receptor substrate-1/2 (IRS-1; IRS-2), endothelial nitric oxide synthase (eNOS), sirtuin 1 (SIRT1) and inducible NOS (iNOS) expressions in liver of rats. Resveratrol was tested for its potential efficacy on changes induced by HFCS. Methods: Animals were randomly divided into four groups as control, resveratrol, HFCS and resveratrol plus HFCS (resveratrol + HFCS). HFCS was given as 20 % solutions in drinking water. Feeding of all rats was maintained by a standard diet that enriched with or without resveratrol for 12 weeks. Results: Dietary HFCS increased triglyceride content and caused mild microvesicular steatosis in association with up-regulation of fatty acid synthase and sterol regulatory element binding protein (SREBP)-1c in liver of rats. Moreover, HFCS feeding impaired hepatic expression levels of IRS-1, eNOS and SIRT1 mRNA/proteins, but did not change iNOS level. Resveratrol promoted IRS, eNOS and SIRT1, whereas suppressed SREBP-1c expression in rats fed with HFCS. Conclusions: Resveratrol supplementation considerably restored hepatic changes induced by HFCS. The improvement of hepatic insulin signaling and activation of SIRT1 by resveratrol may be associated with decreased triglyceride content and expression levels of the lipogenic genes of the liver. [ABSTRACT FROM AUTHOR]

The liver has long been identified as a target organ of arsenic exposure. Arsenic is a potent environmental toxicant and its accumulation in the liver causes hepatotoxicity. In our study, the investigation of effects of melatonin on arsenic-induced liver damage in rats was planned. In our study, 27 male rats were divided into three groups: control (saline, 5 ml/kg/day, intragastrically), arsenic (sodium arsenite, 5 mg/kg/day, intragastrically), and arsenic+melatonin (sodium arsenite, 5 mg/kg/day, intragastrically and melatonin, 25 mg/kg/day, intraperitoneally) group. At the end of 15 days, the rats were weighed and sacrificed then liver tissues were collected. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidise (GSH-Px) activities as well as malondialdehyde (MDA) levels were determined by spectrophotometry. The amount of arsenic in liver tissue was analyzed by Inductively Coupled Plasma/Optical Emission Spectrometer (ICP-OES). There were no significant differences in respect to weights of rats among the groups. Arsenic significantly decreased the enzyme activities of SOD, CAT, and GSH-Px as well as increased the levels of MDA in liver tissues. Melatonin treatments significantly increased of reduced SOD, CAT, and GSH-Px enzyme activities and decreased the elevated tissue MDA levels in liver tissues. The amount of arsenic in liver tissues significantly increased in arsenic group. There were no significant differences in respect to the amount of arsenic in liver tissues between the arsenic group and melatonin group. These data suggested that melatonin has beneficial effects against arsenic-induced liver damage by decreasing oxidative stress and lipid peroxidation. [ABSTRACT FROM AUTHOR]