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

Low Serum Glutathione Peroxidase Activity Is Associated with Increased Cardiovascular Mortality in Individuals with Low HDLc’s

Background Since oxidized LDL is thought to initiate atherosclerosis and the serum glutathione peroxidase (GPx3) reduces oxidized lipids, we investigated whether high GPx3 activity reduces cardiovascular disease (CVD) mortality. Methods We determined GPx3 in stored samples from the Minnesota Heart Survey of 130 participants who after 5 to 12 years of follow-up had died of CVD and 240 controls. Participants were 26 to 85 years old and predominantly white. In a nested case-control, study we performed logistic regressions to calculate odds ratios (OR) adjusted for age, sex, baseline year, body mass index, smoking, alcohol intake, physical activity, total and HDL cholesterols, systolic blood pressure, serum glucose and gamma glutamyltransferase (GTT) activity. The referent was the quartile with the highest GPx3 activity (quartile 4). Results OR’s for CVD mortality for increasing quartiles of GPx3 were 2.37, 2.14, 1.83 and 1.00 (P for trend 0.02). This inverse correlation was confined to those with HDLc’s below the median (P for interaction, 0.006). The OR’s for increasing quartiles of GPx3 in this group were 6.08, 5.00, 3.64 and 1.00 (P for trend, 0.002). Conclusions Individuals with both low HDLc and GPx3 activity are at markedly increased risk for death from CVD

Short term effects of a low-carbohydrate diet in overweight and obese subjects with low HDL-C levels

<p>Abstract</p> <p>Background</p> <p>The aim of this study was to evaluate short-term effects of a low-carbohydrate diet in overweight and obese subjects with low HDL-C levels.</p> <p>Methods</p> <p>Overweight (BMI between 25-30 kg/m²) or obese (BMI over 30 kg/m²) subjects with low HDL-C levels (men with HDL-C <1.03, women <1.29 mmol/l) were invited to the study. A 1400 kcal 75-gram carbohydrate (CHO) diet was given to women and an 1800 kcal 100-gram CHO diet was given to men for four weeks. The distribution of daily energy of the prescribed diet was 21-22% from CHO, 26-29% from protein and 49-53% from fat. Subjects completed a three-day dietary intake record before each visit. Anthropometric indices, body fat ratio, blood lipids, glucose and insulin were measured. Baseline and week-four results were compared with a Wilcoxon signed ranks test.</p> <p>Results</p> <p>Twenty-five women and 18 men participated. Basal median LDL-C level of men was 3.11 and basal median LDL-C level of women was 3.00 mmol/l. After four weeks of a low-carbohydrate diet, the median energy intake decreased from 1901 to 1307 kcal/day, daily energy from carbohydrate from 55% to 33%, body weight from 87.7 to 83.0 kg and HDL-C increased from 0.83 to 0.96 mmol/l in men (p < 0.002, for all). After four weeks of a low-carbohydrate diet, the median energy intake tended to decrease (from 1463 to 1243 kcal, p = 0.052), daily energy from carbohydrate decreased from 53% to 30% (p < 0.001) and body weight decreased from 73.2 to 70.8 kg (p < 0.001) in women, but HDL-C did not significantly change (from 1.03 to 1.01 mmol/l, p = 0.165). There were significant decreases in body mass index, waist circumference, body fat ratio, systolic blood pressure, total cholesterol, triglyceride and insulin levels in all subjects.</p> <p>Conclusions</p> <p>HDL-C levels increased significantly with energy restriction, carbohydrate restriction and weight loss in men. HDL-C levels didn't change in women in whom there was no significant energy restriction but a significant carbohydrate restriction and a relatively small but significant weight loss. Our results suggest that both energy and carbohydrate restriction should be considered in overweight and obese subjects with low HDL-C levels, especially when LDL-C levels are not elevated.</p

Protective Role of Taurine against Arsenic-Induced Mitochondria-Dependent Hepatic Apoptosis via the Inhibition of PKCδ-JNK Pathway

BACKGROUND: Oxidative stress-mediated hepatotoxic effect of arsenic (As) is mainly due to the depletion of glutathione (GSH) in liver. Taurine, on the other hand, enhances intracellular production of GSH. Little is known about the mechanism of the beneficial role of taurine in As-induced hepatic pathophysiology. Therefore, in the present study we investigated its beneficial role in As-induced hepatic cell death via mitochondria-mediated pathway. METHODOLOGY/PRINCIPAL FINDINGS: Rats were exposed to NaAsO(2) (2 mg/kg body weight for 6 months) and the hepatic tissue was used for oxidative stress measurements. In addition, the pathophysiologic effect of NaAsO(2) (10 microM) on hepatocytes was evaluated by determining cell viability, mitochondrial membrane potential and ROS generation. As caused mitochondrial injury by increased oxidative stress and reciprocal regulation of Bcl-2, Bcl-xL/Bad, Bax, Bim in association with increased level of Apaf-1, activation of caspase 9/3, cleavage of PARP protein and ultimately led to apoptotic cell death. In addition, As markedly increased JNK and p38 phosphorylation with minimal disturbance of ERK. Pre-exposure of hepatocytes to a JNK inhibitor SP600125 prevented As-induced caspase-3 activation, ROS production and loss in cell viability. Pre-exposure of hepatocytes to a p38 inhibitor SB2035, on the other hand, had practically no effect on these events. Besides, As activated PKCdelta and pre-treatment of hepatocytes with its inhibitor, rottlerin, suppressed the activation of JNK indicating that PKCdelta is involved in As-induced JNK activation and mitochondrial dependent apoptosis. Oral administration of taurine (50 mg/kg body weight for 2 weeks) both pre and post to NaAsO(2) exposure or incubation of the hepatocytes with taurine (25 mM) were found to be effective in counteracting As-induced oxidative stress and apoptosis. CONCLUSIONS/SIGNIFICANCE: Results indicate that taurine treatment improved As-induced hepatic damages by inhibiting PKCdelta-JNK signalling pathways. Therefore taurine supplementation could provide a new approach for the reduction of hepatic complication due to arsenic poisoning

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