The Influence of Hyperbaric Oxygen Treatment on the Healing of Experimental Defects Filled with Different Bone Graft Substitutes

To assess potential effects of hyperbaric oxygen (HBOT) on artificial bone grafts, β - Tricalcium phosphate (β-TCP) and calcium phosphate coated bovine bone (CPCBB) substitutes were applied to standard bone defects in rat tibiae. The control defects were left empty. Half of the animals received 60 minutes of 2.4 atmosphere absolute (ATA) of HBOT. Rats were sacrificed at one, two and four weeks. Bone healing was assessed histologically and histomorphometrically using light microscopy. The periosteum over the bone defects was examined ultrastructurally. Cardiac blood was collected to determine the serum osteocalcin levels. The HBOT increased new bone formation in the unfilled controls and β-TCP groups and significantly decreased cartilage matrix and fibrous tissue formations in all groups. Active osteoblasts and highly organized collagen fibrils were prominent in the periosteum of β-TCP and control groups. Serum osteocalcin levels also increased with HBOT. The healing of defects filled with CPCBB was similar to the controls and it did not respond to HBOT. These findings suggested that the HBOT had beneficial effects on the healing of unfilled bone defects and those filled with β-TCP bone substitute but not with CPCBB, indicating a material-specific influence pattern of HBOT

Morphologic changes and lipid peroxidation in renal tissues of young rats following intestinal ischemia-reperfusion

Intestinal ischemia-reperfusion (IIR) is a complex phenomenon causing local and remote tissue destruction, and even multiple-organ failure. To examine the hypothesis that IIR affects renal function, 21-day-old male Sprague-Dawley rats underwent 45 min superior mesenteric artery occlusion and control rats were subjected to a sham laparotomy. After 2 and 24 h and 1 week of reperfusion, blood was sampled for urea and the kidneys were harvested for lipid peroxidation and histologic examination. Malondialdehyde (MDA) levels as an indicator of lipid peroxidation were significantly increased in renal tissue after 2 h of reperfusion, and this finding was in accordance with serum urea levels (SU) and endothelial injury. However, at 24 h of reperfusion MDA and SU had returned to normal. These data were supported by electron-microscopic studies suggesting reversibility of the changes. It is concluded that IIR leads to renal injury and that free radicals may be responsible for this injury

Effects of valsartan on stress-induced changes of serum vascular endothelial growth factor and nitric oxide in mice

This study investigated the effects of renin- angiotensin system ( RAS) blockade on stress- induced changes of serum vascular endothelial growth factor ( VEGF) and nitric oxide ( NO) in mice. Chronic stress increased the serum NO levels significantly compared to control group ( p =.0172). Valsartan, an angiotensin II receptor antagonist, alone, did not make significant difference versus control group. In chronic stress + valsartan group, serum NO levels decreased nonsignificantly compared to chronic stress group. There was a nonsignificant increase in serum VEGF levels after chronic stress. Valsartan alone or with chronic stress did not significantly affect the serum VEGF levels. In conclusion, there was no correlation between NO and VEGF changes during the stress response. In this respect, there may be other mechanisms to explain the stress- induced NO increase

Changes in Prooxidant-Antioxidant Balance in Tissues of Rats Following Long-term Hyperglycemic Status

Introduction. Reactive oxygen species play an important role in the pathogenesis of organ damage in diabetes mellitus. Streptozotosin (STZ) is a commonly employed compound to produce diabetes mellitus and these animals exhibit most of diabetic complications. Methods. In our study, diabetes was induced by a single intraperitoneal injection of STZ at a dose of 50 mg/kg in rats and they were killed 12 weeks after STZ. Endogenous lipid peroxide levels, enzymatic and non-enzymatic antioxidants were measured in liver, heart, kidney, brain, and testis tissues to investigate the effect of long-term hyperglycemic state. The susceptibility of diabetic tissues to oxidative stress was also examined in in vitro oxidizing system containing ascorbic acid and iron. Results. We found that prooxidant and antioxidant balance has changed in favor of prooxidation in the tissues of diabetic rats. The susceptibility of liver to oxidative stress increased; however, this susceptibility did not change in heart, kidney, brain, and testis of diabetic rats. Conclusion. Our results indicate that long-term hyperglycemic state disturbs hepatic prooxidant-antioxidant balance at an earlier period and more pronouncedly than other tissues

VCAM1 (T-1591C and T-833C) and E-selectin S128R polymorphisms are not risk factors for Hashimoto’s thyroiditis

Aim: The etiopathogenesis of Hashimoto’s thyroiditis (HT)  has not been clearly elucidated although the role of chronical inflammation and endothelial dysfunction has been established.   Adhesion molecules such as vascular cell adhesion molecule1 (VCAM1) and E-selectin are secreted from vascular endothelium and promote accummulation of leukocytes in damaged endothelial areas.  This study examined the possible association of VCAM1 (T-1591C and T-833C) and E-selectin S128R single nucleotide polymorphisms (SNPs) with the occurence of HT for the first time. Methods: VCAM1 (T-1591C and T-833C), and E-selectin S128R SNPs in DNA from peripheral blood leukocytes of 189 patients with HT and 247 healthy controls were investigated by real-time PCR combined with melting curve analysis using fluorescence-labeled hybridization probes. Results: We did not find significant differences in the distributions of studied polymorphisms   between patients with HT and healthy controls. Conclusions: The results of present study suggest that VCAM1 (T-1591C and T-833C) and E-selectin S128R SNPs may not be risk factors for HT. For all that; further studies with a larger cohort, analyzing other polymorphisms in VCAM1 and E-selectin genes are necessary to support our observations

Artichoke Leaf Extract reduces Oxidative Stress and Lipoprotein Dyshomeostasis in Rats Fed on High Cholesterol Diet

Hypercholesterolemia and lipid peroxidation play complementary role in atherosclerosis. Artichoke leaf extract (ALE) is rich in natural antioxidants and has a cholesterol-reducing effect. However, there is no study investigating the effect of ALE on lipid levels and lipid peroxidation in experimental hypercholesterolemic conditions. Rats were fed on 4% (w/w) cholesterol and 1% (w/w) cholic acid supplemented diet for 1 month. ALE (1.5 g/kg/day) was given by gavage during the last 2 weeks. Serum lipid composition, malondialdehyde (MDA) and diene conjugate (DC) levels and plasma antioxidant activity (AOA) were measured. In addition, endogenous DC and copper-induced MDA levels were determined in apo B-containing lipoproteins (LDL+VLDL fraction). Serum cholesterol and triglyceride levels and the ratio of cholesterol to HDL-cholesterol decreased due to ALE treatment in rats fed on HC diet. Significant decreases in serum MDA and DC levels and increases in plasma AOA were detected in serum in ALE-treated hypercholesterolemic rats. Endogenous DC and copper-induced MDA levels were also lower in LDL+VLDL fraction due to ALE-treatment in hypercholesterolemic rats. Our results indicate that ALE may be useful for the prevention of hypercholesterolemia-induced pro-oxidant state in LDL+VLDL fraction and the reduction of increased serum cholesterol and triglyceride levels. Copyright (C) 2009 John Wiley & Sons, Ltd

Increased susceptibility of serum and apo-B-containing lipoproteins to peroxidation in aged rats

Oxidative modifications of apo-B-containing lipoproteins (LDL+VLDL) appear to play a role in atherogenesis. Increased atherosclerosis is one of the major causes of morbidity and mortality during ageing. The aim of this study was to investigate the susceptibility of serum and LDL+VLDL to lipid peroxidation in 12 young (6 months) and 12 old (22 months) rats. Serum endogenous malondialdehyde (MDA) and diene conjugate (DC) levels were found to be increased by 24.9% and 30.0% respectively, in old rats. In addition, 2,2'-azobis-(2-amidino-propane) hydrochloride (AAPH)-induced lipid peroxide levels were increased in serum of old rats. Although serum vitamin E levels were significantly increased (27.4%), there was a significant decrease in cholesterol-adjusted vitamin E levels (14.3%) in old rats. Serum vitamin C and total sulphydryl levels were found to be decreased by 25.5% and 22.7% respectively. The ferric reducing ability of plasma (FRAP) was also lower (15.9%) in old rats. Endogenous DC and copper-induced MDA levels were significantly higher (65.1% and 26.7% respectively) in LDL+VLDL fractions obtained from EDTA-plasma by dextrane sulphate and MgCl2 solution in old rats. The propagation rate and maximal amount of DC increased, but the lag phase and t(max) were shortened in LDL+VLDL fractions of old rats. Our results clearly indicate that the susceptibility of whole serum and LDL+VLDL fractions to lipid peroxidation is increased in aged rats