Does vitamin D have any role in the improvement of diabetic peripheral neuropathy in type 1 diabetic patients?

AIM: The aim of this study was to evaluate the relationship between diabetic peripheral neuropathy (DPN) and vitamin D, nerve growth factor (NGF) and oxidative stress markers in patients with type 1 diabetes. METHODS: Ninety-six patients with type 1 diabetes were included in the study. All patients were evaluated for DPN with Michigan Neuropathy Screening Instrument. Fasting blood glucose, HbA1c, lipid parameters, 25 (OH) D3, NGF, total oxidant status, total antioxidant status and oxidative stress index were measured. RESULTS: Twenty-six patients (27 %) had DPN (group 1) and 70 patients did not have neuropathy (group 2). When the groups were evaluated with respect to general demographic characteristics, no differences were detected. Mean age, duration of diabetes and retinopathy were found significantly higher in patients who had neuropathy. Glomerular filtration rate levels were significantly lower in the neuropathy group. Between the groups, 25 (OH) vitamin D levels were significantly lower in the neuropathy group, while there were no differences in NGF levels or in oxidative stress markers. Michigan neuropathy examination score was positively correlated with age, and diabetes duration was negatively correlated with 25 (OH) vitamin D levels. In addition, 25 (OH) vitamin D was positively correlated with NGF. In the logistic regression analysis to determine the independent variables that will affect the development of neuropathy, duration of diabetes was detected as the only factor (p = 0.039, OR = 1.071). CONCLUSION: It seems that the most important risk factor for the development of neuropathy in type 1 diabetic patients is disease duration.

Evalution of Serum Lipid Profiles in Turkish Children Aged Two to Eighteen Years.

OBJECTIVE: The purpose of this study was to evaluate dyslipidaemia in children according to age, gender, percentiles, mother's education level, breastfeeding duration and areas of residence. METHODS: A total of 285 children (137 girls; 148 boys), aged between two and 18 years, were enrolled in this cross-sectional, epidemiologic study. Lipid profiles were assessed and its relation with sociodemographic features was evaluated. RESULTS: Dyslipidaemia prevalence was 37.4% (n = 107). High very low-density lipoprotein cholesterol (VLDL-C) and low high-density lipoprotein cholesterol (HDL-C) levels are related with percentiles of the children (p = 0.006, p = 0.03, respectively). Gender was a significant factor for VLDL-C, which was higher in girls than boys (p = 0.04). Total cholesterol levels were high in 14 children (4.9%); 72 of the study group (25.3%) had high triglyceride levels; HDL-C levels were low in 52 children (18.2%). CONCLUSION: All the parameters of dyslipidaemia are not so high in our region. However, as early detection of dyslipidaemia should begin in childhood, we should perform periodic checks to prevent cardiovascular risks.

The effects of PDE5 inhibitory drugs on renal ischemia/reperfusion injury in rats.

The aim of the present study was to evaluate the effects of phosphodiesterase type 5 (PDE5) inhibitory drugs, Tadalafil and Sildenafil, on inducible NOS (iNOS), endothelial NOS (eNOS) and p53 genes expressions and apoptosis in ischemia/reperfusion (I/R) induced oxidative injury in rat renal tissue. Eighty Sprague-Dawley rats (300-350 g) were divided into four groups. In ischemia/reperfusion group, rats were subjected to renal ischemia by clamping the left pedicle for 60 min, and then reperfused for 90 min. On the other hand, in other two groups the rats were individually pretreated with Tadalafil and Sildenafil 1 h before the induction of ischemia. Malondialdehyde (MDA) is determined in renal tissue homogenates by high-performance liquid chromatography, the number of apoptotic cell were calculated by TUNEL method and p53 and eNOS expression were detected with immunohistochemistry. On the other hand, myeloperoxidase (MPO) levels were measured by spectrophotometric method and the mRNA level of iNOS in renal tissue was determined by Real-time PCR (RT-PCR). Our results indicate that MDA and MPO levels were increased in the I/R group than those in the control group. Both Tadalafil and Sildenafil treatment decreased the MDA levels in ischemia/reperfusion group, whereas this effect was more potent with Sildenafil. RT-PCR results showed that, iNOS gen expression increased in the I/R group, but decreased in the PDE5 inhibitory drugs treated group. Apoptotic cells, eNOS levels and p53 positive cells were also decreased in PDE5 inhibitory drugs treated group. We suggest that Tadalafil and Sildenafil have beneficial effects against I/R related renal tissue injury and this protective effect is clearer for Sildenafil than Tadalafil.

Positive inotropic, positive chronotropic and coronary vasodilatory effects of rat amylin: mechanisms of amylin-induced positive inotropy.

Even though there are a few studies dealing with the cardiac effects of amylin, the mechanisms of amylin-induced positive inotropy are not known well. Therefore, we investigated the possible signaling pathways underlying the amylin-induced positive inotropy and compared the cardiac effects of rat amylin (rAmylin) and human amylin (hAmylin).Isolated rat hearts were perfused under constant flow condition and rAmylin or hAmylin was infused to the hearts. Coronary perfusion pressure, heart rate, left ventricular developed pressure and the maximum rate of increase of left ventricular pressure (+dP/dtmax) and the maximum rate of pressure decrease of left ventricle (-dP/dtmin) were measured.rAmylin at concentrations of 1, 10 or 100 nM markedly decreased coronary perfusion pressure, but increased heart rate, left ventricular developed pressure, +dP/dtmax and -dP/dtmin. The infusion of H-89 (50 µM), a protein kinase A (PKA) inhibitor did not change the rAmylin (100 nM)-induced positive inotropic effect. Both diltiazem (1 µM), an L-type Ca2+ channel blocker and ryanodine (10 nM), a sarcoplasmic reticulum (SR) Ca2+ release channel opener completely suppressed the rAmylin-induced positive inotropic effect, but staurosporine (100 nM), a potent protein kinase C (PKC) inhibitor suppressed it partially. hAmylin (1, 10 and 100 nM) had no significant effect on coronary perfusion pressure, heart rate and developed pressure, +dP/dtmax and -dP/dtmin.We concluded that rAmylin might have been produced vasodilatory, positive chronotropic and positive inotropic effects on rat hearts. Ca2+ entry via L-type Ca2+ channels, activation of PKC and Ca2+ release from SR through ryanodine-sensitive Ca2+ channels may be involved in this positive inotropic effect. hAmylin may not produce any significant effect on perfusion pressure, heart rate and contractility in isolated, perfused rat hearts.

NMDA receptor blockage with 2-amino-5-phosphonovaleric acid improves oxidative stress after spinal cord trauma in rats.

STUDY DESIGN: 2-amino-5-phosphonovaleric acid (APV) is an N-methyl-D-aspartate (NMDA) receptor blocker and has neuroprotective properties. This study is aimed at evaluating the effect of APV treatment on oxidative status after spinal cord injury (SCI). METHODS: The experiment was carried out on the following five groups: Group 1: sham operated, non-traumatized; Group 2: with injured spinal cord, no treatment; Group 3: with SCI, injected with 100 microg kg(-1) APV; Group 4: with SCI, injected with 200 microg kg(-1) APV; and Group 5: with SCI, injected with 400 microg kg(-1) APV. SCI was inflicted by epidural compression with a cerebral vascular clip after T9-11 laminectomy. The experiments were completed after 12 h of trauma. Spinal cords were excised for evaluation of superoxide dismutase (SOD), catalase, reduced glutathione (GSH) and malonyldialdehyde (MDA) levels. RESULTS: After SCI, SOD and GSH levels decreased and the MDA level increased significantly. APV treatment decreased the MDA level and increased SOD, catalase and GSH levels. The maximum decrease in MDA was detected in the group treated with 100 microg kg(-1) APV compared with the other groups. The GSH level was significantly increased in the group treated with 200 microg kg(-1) APV. The SOD level was significantly increased in the group treated with 200 microg kg(-1) APV. CONCLUSION: The results of this study have shown that APV treatment creates a dose-dependent antioxidant effect in rats with SCI and may be used for the treatment of SCIs.

Protective effects of doxycycline in ischemia/reperfusion injury on kidney.

Renal ischemia and reperfusion injury is the major cause of acute renal failure and may also be involved in the development and progression of some forms of chronic kidney disease. The aim of this study was to evaluate whether doxycycline, a member of the tetracycline family of antibiotics, protects kidney tissue or not. 36 Sprague-Dawley rats (200-250 g) were used. The animals were divided into three groups: control, ischemia/reperfusion and ischemia/reperfusion+doxycycline group. Rats were subjected to renal ischemia by clamping the left pedicle for 1 h, and then reperfused for 1 h. The ischemia/reperfusion+doxycycline group were pretreated intraperitoneally with doxycycline suspension (10 mg/kg) 2 h before the induction of ischemia. Our results indicate that malondialdehyde, matrix-metalloproteinase-2, interleukin-2, interleukin-6, interleukin-10, interleukin 1-beta and tumor necrosis factor-alpha levels were significantly higher in the ischemia/reperfusion group than those in the control group. Doxycycline administration significantly decreased these parameters. Tissue inhibitor of metalloproteinases-1 levels also increased after ischemia/reperfusion and decreased with doxycycline pretreatment, but these changes were not significantly different. Glutathione levels significantly decreased after ischemia/reperfusion injury when compared with the control group and doxycycline pretreatment significantly increased glutathione levels when compared with the ischemia/reperfusion group. Apoptotic cells and p53 positive cells were significantly decreased in doxycycline treated group. These results suggest that doxycycline reduces renal oxidative injury and facilitates repair. Doxycycline may play a role in a renoprotective therapeutic regimen.

Protective effects of doxycycline in ischemia/reperfusion injury on kidney

Renal ischemia and reperfusion injury is the major cause of acute renal failure andmay also be involved in the development and progression of some forms of chronickidney disease. The aim of this study was to evaluate whether doxycycline, a memberof the tetracycline family of antibiotics, protects kidney tissue or not. 36 Sprague-Dawley rats (200-250 g) were used. The animals were divided into three groups: control,ischemia/reperfusion and ischemia/reperfusion+doxycycline group. Rats weresubjected to renal ischemia by clamping the left pedicle for 1 h, and then reperfusedfor 1 h. The ischemia/reperfusion+doxycycline group were pretreated intraperitoneallywith doxycycline suspension (10 mg/kg) 2 h before the induction ofischemia. Our results indicate that malondialdehyde, matrix-metalloproteinase-2,interleukin-2, interleukin-6, interleukin-10, interleukin 1-beta and tumor necrosisfactor-alpha levels were significantly higher in the ischemia/reperfusion group thanthose in the control group. Doxycycline administration significantly decreased theseparameters. Tissue inhibitor of metalloproteinases-1 levels also increased afterischemia/reperfusion and decreased with doxycycline pretreatment, but thesechanges were not significantly different. Glutathione levels significantly decreasedafter ischemia/reperfusion injury when compared with the control group and doxycyclinepretreatment significantly increased glutathione levels when compared withthe ischemia/reperfusion group. Apoptotic cells and p53 positive cells were significantlydecreased in doxycycline treated group. These results suggest that doxycyclinereduces renal oxidative injury and facilitates repair. Doxycycline may play a role in arenoprotective therapeutic regimen(AU)

Obstructive sleep apnoea, glucose tolerance and liver steatosis in obese women.

In this study of obstructive sleep apnoea (OSA), glucose tolerance and liver steatosis in females from an obesity unit, 45 patients (mean age 46.8 years, mean body mass index 39.4 kg/m(2), all non-diabetic and alcohol abstainers) underwent nocturnal polysomnography, a 2 h oral glucose tolerance test and abdominal ultrasonography. OSA, defined as an apnoea-hypopnoea index (AHI) of > or = 10 events/h, was present in 20 patients (44%). Impaired glucose tolerance (IGT) was found in eight patients (40%) with OSA and three patients (12%) without OSA; there was a positive linear relationship between AHI and post-load glucose levels. On multivariate logistic regression analysis, IGT was predicted by OSA independently of age, waist circumference, systolic blood pressure and current smoking. Liver steatosis was present in 37 women (82.2%), of whom six had grade III steatosis. Of the variables tested, IGT was the only predictor of grade III steatosis. In conclusion, OSA is an independent predictor of IGT which, in turn, is associated with severe liver steatosis in an obesity unit-based sample of women.

Epidermal growth factor increases tissue antioxidant enzyme activities in ethanol-induced gastric injury in rat

The aim of the present study is to investigate whether the antioxidant mechanisms are involved in epidermal growth factor (EGF)-mediated protection from ethanol-induced gastric damage. Twenty four female Sprague-Dawley rats were assigned into 3 groups; control (C) group (n=8) was given physiologic saline by gavage; ethanol (E) group (n=8) was given 1 ml of 80% ethanol (v/v) in distilled water by gavage and EGF group (n=8) was given EGF (100 mg/kg-body wt.) intraperitonealy half an hour before the administration of ethanol. The protein carbonyl content was significantly higher in the E group than the C group (p<0.01). On the other hand, EGF decreased the protein carbonyl content in the EGF group (p<0.01). Gastric myeloperoxidase activity increased significantly after the administration of ethanol (p<0.01). The administration of EGF decreased significantly the myeloperoxidase activity (p<0.01). Although ethanol caused a slight decrease in the catalase activity, no statistical significance was observed between groups E and C. The catalase activity increased significantly after EGF treatment (p<0.01). The superoxide dismutase activity decreased significantly in the E group when compared to the C group (p<0.05) while it was found to be increased significantly in the EGF group in comparison with the E group (p<0.01). In summary, the present results indicate that the gastroprotective effect of EGF in the experimental lesions induced by ethanol could be attributed to its property such as to augment the antioxidant enzyme activities (AU)

Se investiga si los mecanismos antioxidantes están implicados en la protección del factor de crecimiento epidérmico (EGF) sobre el daño gástrico inducido por el alcohol. Veinticuatro ratas hembra se dividieron en tres grupos: las del grupo control (C) recibieron solución salina por vía intragástrica; las del grupo etanol (E) recibieron 1 ml de etanol al 80% (v/v) en agua destilada por la misma vía y a las del grupo EGF se les administró i.p. EGF (100 mg/Kg w.w.) media hora antes del etanol. El contenido en grupos carbonil de las proteínas y la actividad mieloperoxidasa gástrica aumentó significativamente en el grupo E, mientras que disminuyó en el grupo EGF. Aunque el etanol provocó una ligera disminución de la actividad catalasa, no hubo diferencias significativas entre los grupos C y E, pero aumentó por la administración de EGF. La actividad superóxido dismutasa disminuyó en el grupo E respecto del grupo C y resultó incrementada en el grupo EGF respecto del grupo E. En suma, los resultados indican que el efecto gastroprotector del EGF en las lesiones experimentales inducidas por el etanol podrían atribuirse a su efecto estimulador sobre la actividad de enzimas antioxidantes (AU)

Epidermal growth factor increases tissue antioxidant enzyme activities in ethanol-induced gastric injury in rat.

The aim of the present study is to investigate whether the antioxidant mechanisms are involved in epidermal growth factor (EGF)-mediated protection from ethanol-induced gastric damage. Twenty four female Sprague-Dawley rats were assigned into 3 groups; control (C) group (n=8) was given physiologic saline by gavage; ethanol (E) group (n=8) was given 1 ml of 80% ethanol (v/v) in distilled water by gavage and EGF group (n=8) was given EGF (100 mg/kg-body wt.) intraperitonealy half an hour before the administration of ethanol. The protein carbonyl content was significantly higher in the E group than the C group (p<0.01). On the other hand, EGF decreased the protein carbonyl content in the EGF group (p<0.01). Gastric myeloperoxidase activity increased significantly after the administration of ethanol (p<0.01). The administration of EGF decreased significantly the myeloperoxidase activity (p<0.01). Although ethanol caused a slight decrease in the catalase activity, no statistical significance was observed between groups E and C. The catalase activity increased significantly after EGF treatment (p<0.01). The superoxide dismutase activity decreased significantly in the E group when compared to the C group (p<0.05) while it was found to be increased significantly in the EGF group in comparison with the E group (p<0.01). In summary, the present results indicate that the gastroprotective effect of EGF in the experimental lesions induced by ethanol could be attributed to its property such as to augment the antioxidant enzyme activities.

Cardioprotection with resveratrol pretreatment: improved beneficial effects over standard treatment in rat hearts after global ischemia.

OBJECTIVE: The major objective of the present study is to evaluate the potential role of resveratrol (RVT), a natural antioxidant found in grapes and red wine, in protecting the myocardium from the deleterious effects of ischemia-reperfusion (I/R) injury using isolated rat hearts. METHODS: Langendorff perfused isolated rat hearts were subjected to 60 min of global ischemia following 60 min of reperfusion. RVT was given according to chronic pretreatment and/or acute treatment protocols. Animals received RVT at the dose of 20 mg/kg via an intragastric tube for 14 days before the experiment and/or at the infusion concentration of 10 microM for 30 min before the onset of ischemia. The myocardial postischemic recovery was compared using hemodynamic data (peak systolic pressure, end diastolic pressure, and +dP/dtmax), coronary flow, biochemical parameters (LDH, CK-MB, cTnI, myoglobin) from coronary effluent, and oxidative stress markers (MDA, GSH, carbonyl) from heart tissue homogenates in each group. RESULTS: RVT pretreatment and treatment protocols have provided increased preservation in myocardial recovery following global ischemia compared to a non-treated group. Furthermore, the ischemic damage of myocardium was significantly lower in chronic pretreated rats than in the acutely treated group. In contrast, no significant difference was observed in cardioprotective effects of RVT between the only pretreated group, and both the pretreated and treated group throughout reperfusion. CONCLUSION: The findings from this study indicate that RVT has potent cardioprotective properties against I/R injury in rat hearts. The study also highlighted that the administration of RVT, as pretreatment, has amplified the beneficial effects over the standard treatment.

The effect of verapamil on the prevention of ischemia/reperfusion injury in the experimental retroperitoneoscopic donor nephrectomy model.

BACKGROUND: This study investigated the effect of intravenous administration of verapamil in prevention of the injury caused by free oxygen radicals generated in a rabbit retroperitoneoscopic donor nephrectomy model. METHODS: Twenty-four adult New Zealand rabbits were divided into four groups. In group I, balloon dissection of the left retroperitoneal space was performed. In group II, CO2 at 10 mmHg was applied for 3 hours after the balloon dissection. In group III, laparotomy was performed, the left renal pedicle was clamped for 3 min, and the clamp was removed 5 min before nephrectomy. In group IV, 2 min before the attempt 0.2 mg/kg verapamil was given intravenously, and the same procedure was employed as in group III. Nephrectomy was performed after each experiment. The concentrations of malonyl dialdehyde (MDA), reduced glutathione (GSH), and protein carbonyl content were measured in renal tissue samples as markers of oxidative stress. RESULTS: Pneumoretroperitoneum (Prp) promoted oxidative stress in renal tissues, with an increase of MDA and protein carbonyl content. The verapamil- pretreated group (group IV) showed statistical significantly lower values of MDA and protein carbonyl content when compared with group II and III (p < 0.05), whereas tissue GSH concentrations were unchanged in all groups. CONCLUSIONS: Our study showed that Prp causes increased oxidative stress in renal tissue. Warm ischemia lasting 3 min did not exert an additive effect on Prp-associated oxidative stress. Verapamil reduces the oxidative stress markers caused by Prp.

Effect of leptin on renal ischemia-reperfusion damage in rats.

Tumor necrosis factor-alpha (TNF-alpha) has been established as an important mediator in renal ischemia-reperfusion (I/R) injury. Leptin, a product of the ob gene, has been known to exhibit cytoprotective effects on renal tissue, but its effect on renal tissue TNF-alpha level after renal I/R injury in rats remains unknown. The purpose of the study was to evaluate the effects of leptin on renal tissue TNF-alpha, malondialdehyde (MDA), protein carbonyls (PCs) and total sulfydryl group (SH) levels, and plasma nitrite levels after renal I/R injury in rats. The animals were divided into three groups: control, I/R and I/R+leptin. Rats were subjected to renal ischemia by clamping the left pedicle for 45 min, and then reperfused for 1 h. The I/R+leptin group was pretreated intraperitoneally with leptin (10 microg/kg) 30 min before the induction of ischemia. Our results indicate that MDA, TNF-alpha levels, and PCs were significantly higher in the I/R group than those in the control group (p < 0.05). The administration of leptin decreased these parameters (p < 0.05) significantly. The SH level was observed to significantly decrease after I/R injury when compared to the control group (p < 0.05). Leptin treatment significantly increased tissue SH and plasma nitrite levels when compared to the I/R group (p < 0.05). Plasma nitrite levels did not change significantly in I/R when compared to the control. These results suggest that leptin could exert a protective effect on I/R induced renal damage by decreasing TNF-alpha levels and increasing nitrite level.

The effect of different intraabdominal pressures on lipid peroxidation and protein oxidation status during laparoscopic cholecystectomy.

BACKGROUND: This prospective, randomized, and controlled study was designed to investigate the effects of different intraabdominal pressures (IAPs) on lipid peroxidation and protein oxidation status during laparoscopic cholecystectomy (LC). METHODS: Twenty-four patients (12 men, 12 women) who underwent LC at either 10 or 15 mmHg of IAP were randomized into two groups. Repeated blood samples were collected to measure thiobarbituric acid reactive substances (TBARS) levels to assess lipid peroxidation and protein carbonyl content and protein sulfhydryl groups to assess protein oxidation status. RESULTS: Serum protein carbonyls and TBARS levels were found to be increased immediately after desufflation in both study groups when compared to the preoperative levels. On the other hand, protein sulfhydryl levels were found to be decreased in both study groups. Although increases in protein carbonyls and TBARS levels were more prominent in patients who underwent LC at 15 mmHg of IAP, this difference was not statistically significant between both groups. CONCLUSIONS: The results suggest that both 15 and 10 mmHg of LAP could lead to an increased oxidative stress response during LC, but no difference was found between the groups.

Ischemic preconditioning decreases laparoscopy-induced oxidative stress in small intestine.

BACKGROUND/AIMS: Laparoscopy is advantageous but its adverse effects have not yet been completely elucidated. Pneumoperitoneum performed to facilitate laparoscopy causes the organ perfusion decrease such as in the intestine. Oxidative stress reflects the tissue injury related to ischemia and reperfusion. We previously showed that laparoscopy causes oxidative stress in intestinal tissues. To assess whether the preconditioning phenomenon could be taken advantage of during laparoscopy we designed this randomized, controlled, experimental study with blind outcome assessment. We evaluated the effect of preconditioning, including sequential periods of pneumoperitoneum and desufflation on laparoscopy-induced tissue injury of small bowel with the help of two important markers of oxidative stress, thiobarbituric acid reactive substances and reduced glutathione. METHODOLOGY: Forty Sprague-Dawley male rats were used. After anesthesia, an intraperitoneal catheter was inserted. Pneumoperitoneum was created in all except controls, by CO2 insufflation under a pressure of 15 mmHg. The rats were randomized into the groups below: Group P was subjected to 60 minutes of pneumoperitoneum; Group P/D was subjected to 60 minutes of pneumoperitoneum followed by 45 minutes of desufflation; Group IP + P was subjected to 10 minutes of pneumoperitoneum, 10 minutes of desufflation and 60 minutes of pneumoperitoneum; Group IP + P/D was subjected to 10 minutes of pneumoperitoneum, 10 minutes of desufflation, 60 minutes of pneumoperitoneum and 45 minutes of desufflation; Group C (Control) was subjected to a sham operation, without pneumoperitoneum. Small bowel tissue malondialdehyde and reduced glutathione activities were measured, as applicable, by investigators blinded to the study design. The results were decoded and statistically analyzed with Kruskal-Wallis test. Mann-Whitney U test was used to compare the paired groups. p < 0.05 was considered significant. RESULTS: Small bowel tissue malondialdehyde levels were increased, whereas glutathione values were decreased in Groups P and P/D, as compared to Groups PRE/P and PRE/P/D; the latter two groups had results similar to the Control Group. CONCLUSIONS: Laparoscopic preconditioning may reduce the oxidative injury in intestine following laparoscopic procedures.

A comparison of the oxidative stress response and antioxidant capacity of open and laparoscopic hernia repairs.

BACKGROUND: Free radical-induced lipid peroxidation that is associated with a decrease in the antioxidant status of plasma occurs in many kinds of surgical procedures. In this study, we aimed to investigate markers of oxidative stress--malondialdehyde (as thiobarbituric acid reactive substances), protein carbonyls, and protein sulfhydryls--in patients undergoing Lichtenstein tension-free hernioplasty (LH) or laparoscopic preperitoneal hernia (LPPH) repair. METHODS: Seventeen patients with unilateral inguinal hernia and no complications or recurrence were included in this study. Ten were randomized to undergo LH and seven to LPPH repair. Heparinized blood samples were taken to measure the levels of oxidative stress markers in the patients undergoing hernia repair. Levels of malondialdehyde, protein carbonyls, and protein sulfhydryls were measured preoperatively and at 6 and 24 hours postoperatively in all patients. RESULTS: Both types of hernia repair caused a significant increase in the oxidative stress response and a decrease in antioxidant activity. Plasma levels of malondialdehyde and carbonyls (indicators of oxidant activity) were significantly higher in the LH than in the LPPH repair group (P<.05), and plasma sulfhydryl levels (indicators of antioxidant activity) were significantly lower in the LH than in the LPPH group (P<.05). In both groups, significant differences were also found between the preoperative levels and the postoperative levels 6 and 24 hours (P<.05). CONCLUSIONS: These data demonstrate that both LH and LPPH repair cause a significant increase in markers of oxidative stress; however, the oxidative stress response associated with LH is greater than that associated with LPPH repair.

Can preconditioning reduce laparoscopy-induced tissue injury?

BACKGROUND: Pneumoperitoneum (P) created to facilitate laparoscopy (L) is associated with splanchnic perfusion, ischemia/reperfusion (I/R) injury, and oxidative stress. In this randomized controlled experimental study with blind outcome assessment, we evaluated the effect of preconditioning (PRE) on L-induced I/R injury. METHODS: The subjects were 40 Sprague-Dawley male rats. P was created in all except controls, using carbondioxide (CO2) insufflation under a pressure of 15 mmHg. PRE consisted of 10 min of P, followed by 10 min of deflation (D). The rats were randomized to the following groups: Group P was subjected to 60 min of P. Group P/D was subjected to 60 min of P, followed by 45 min of D. Group PRE/P was subjected to PRE, followed by 60 min of P. Group PRE/P/D was subjected to PRE, followed by 60 min of P and 45 min of D. Group C (control) was subjected to a sham operation, without P. Its anesthesia time was equal to that for group PRE/P/D. At the end of the experiments, the rats were killed; blood, liver, and kidney samples were then obtained and coded. Plasma alanine aminotransferase (ALT) and malondialdehyde (MDA), as well as homogenized tissue MDA levels and glutathione (GSH) activities, were measured; tissue samples were assessed for histopathological evidence of injury; all assessments were done by investigators blinded to the study design. The results were decoded and analyzed statistically with the Kruskal-Wallis and Mann Whitney tests. A p <0.05 was considered significant. RESULTS: Plasma ALT as well as plasma, liver, and kidney MDA levels and liver and kidney injury scores were increased, whereas liver and kidney GSH values were decreased in groups P and P/D, as compared to group C. Rats subjected to PRE before P had plasma ALT, kidney MDA, and kidney and liver GSH levels comparable to controls; their kidney and liver injury scores were higher than controls but significantly lower than nonpreconditioned animals. PRE enabled decreased plasma, kidney, and liver MDA as well as increased kidney GSH if applied before P; its efficacy on oxidative stress was limited to providing decreased kidney MDA and increased kidney GSH if applied before P/D. However, PRE significantly attenuated kidney and liver injury after P as well as P/D. CONCLUSION: PRE consisting of 10 min of P followed by 10 min of D decreases the oxidative stress induced by sustained P in the plasma, liver, and kidney. PRE significantly limits liver and kidney injury after prolonged P and P/D. After further studies to define its ideal timing, PRE before L incorporating P may have clinical relevance, especially for elderly patients or those with impaired hepatic and/or renal function or perfusion.

Beneficial effects of quercetin on oxidative stress induced by ultraviolet A.

Cells exposed to ultraviolet A (UVA) radiation can induce the production of reactive oxygen species (ROS) that may damage cellular elements. By contrast, antioxidants can reduce production of ROS. To assess these cellular events in a model system, rats were divided into three groups comprising control (C), ultraviolet exposed (UV), and ultraviolet exposed and quercetin-treated (UV + Q). UV and UV + Q group rats were irradiated 4 h/day with UVA radiation (1.25 mW/cm2) for 9 days. In the UV + Q group rats quercetin (50 mg/kg body weight) was administered intraperitoneally before irradiation. The levels of malondialdehyde (MDA) were increased significantly following irradiation (P < 0.001). In the UV + Q group MDA levels declined significantly compared with the UV group (P < 0.001). With respect to levels of glutathione (GSH), no statistically significant changes were found between the control and the UV group. The GSH levels in the UV + Q group were slightly higher than those of the control and UV groups, but not significantly so. The enzyme activities of glutathione peroxidase, glutathione reductase, catalase and superoxide dismutase decreased significantly after irradiation (P < 0.001). In the UV + Q group all of these enzyme activities were found to be considerably higher than those in the UV group (P < 0.001). This study demonstrates that exposure of rats to UVA leads to oxidative stress as reflected by increased MDA levels and reduced enzymatic antioxidant levels. It also shows that quercetin may be useful in reducing or preventing photobiologic damage.

The effect of nitric oxide on ischemia-reperfusion injury in rat liver.

A dual role for nitric oxide (NO) in ischemia-reperfusion (I/R) injury is still controversial. This study aims to investigate the role of NO in rat hepatic reperfusion injury. Ischemia was induced by total occlusion of hepatic artery and portal vein for 30 min, then the tissue was reperfused for 30 min. The animals in the L-NAME group (n=10) received N(G)nitro-L-arginine methyl ester (L-NAME) (15 mg/kg) intraperitoneally 60 min before ischemia. The ischemia group (n=10) was given an equal volume of saline solution. The control group comprised eight healthy rats which were not exposed to ischemia or reperfusion. An indicator of hepatic injury, plasma alanine amino transferase (ALT) enzyme activities, were increased in the L-NAME group as compared with the ischemia group (p<0.001). The level of serum nitrite, an index of NO production, and hepatic reduced glutathione (GSH) concentration were lower in the L-NAME group than in the ischemia group (p<0.001, p<0.01, respectively). Hepatic levels of malondialdehyde (MDA) and conjugated dienes (CD) were significantly increased in the L-NAME group as compared to the ischemia group (p<0.05, p<0.001, respectively). Our results confirm that L-NAME, an inhibitor of the enzyme NO synthase, increased the lipid peroxidation and possibly tissue injury, due to the inhibition of cytoprotective effects of NO in a rat hepatic I/R model.

The effect of alpha-tocopherol and pentoxyfilline on ischemia-reperfusion induced liver injury in rats.

BACKGROUND/AIM: In the present study our purpose was to investigate the effect of pentoxyfilline, that plays a role in microcirculation and tissue oxygenation, alone and in combination with an antioxidant vitamin E on tissue damage in the rat liver induced by ischemia-reperfusion. METHODOLOGY: Thirty-one albino rats were divided into four groups. Rats in group I (n= 7), group II (n= 8) and group III (n= 8) were given, respectively, pentoxyfilline (25 mg/kg), pentoxyfilline and vitamin E in combination (25 mg/kg and 50 mg/kg, respectively) and equal volume of saline solution intraperitoneally for 7 days. Rats in group IV (n= 8) served as controls and received no treatment. On day 7 ischemia was induced by cross-clamping the hepatic artery, portal vein and left branch of the biliary duct for 30 minutes. Malondialdehyde (MDA) and catalase activity were assessed in tissue sample, and the level of ALT was measured in serum obtained after reperfusion for 30 minutes. Histological examination of tissue sample was also carried out. RESULTS: There was no significant difference in ALT level between three study groups. Group I and group II had significant lower MDA and catalase levels than those of group III. The results of histopathologic examination in group I and group II were better than that of group III. CONCLUSION: Our findings suggested that the treatment of pentoxyfilline alone and in combination with vitamin E decreased liver damage induced by ischemia-reperfusion and that the effect of latter was more effective but the difference between the two treatment patterns was not statistically significant.