Effects of hemorrhagic shock and retransfusion on catalase and superoxide dismutase activities in rabbits.

The effects of hemorrhagic shock and retransfusion on the activities of two endogenous antioxidant enzymes, catalase and superoxide dismutase, were studied in male New Zealand white rabbits. Following instrumentation and stabilization, blood was withdrawn to reduce mean arterial pressure to 35 mmHg (SHOCK). After 60 min of shock, the warmed autologous blood was infused and the animals were allowed to recover for an additional 30 min (RETRANS). CONTROL animals were instrumented but not bled or transfused. A 60 min period of hemorrhagic shock had no significant effect on tissue or plasma activities of catalase or superoxide dismutase. However, transfusion following hemorrhagic shock resulted in an increase in catalase activity of nearly two-fold in the liver and five-fold in the small intestine. In contrast, superoxide dismutase activity remained unchanged after retransfusion in other tissues and in plasma. These results indicate that superoxide dismutase and catalase activities may be preserved or even induced following transfusion for hemorrhagic shock.     

The effect of platelet activating factor antagonist (BN 52021) on acute experimental pancreatitis with reference to multiorgan oxidative stress

Summary Acute hemorrhagic pancreatitis was induced in Wistar rats using a retrograde intraductal injection of 5% Na-taurocholate. Rats were treated with platelet-activating factor receptor (PAF) antagonist—BN 52021 (5 mg/kg) and sacrificed at 1 and 3 h after induction of acute pancreatitis. Malondialdehyde and sulfhydryl groups concentration were measured in pancreatic, lung, and liver tissue as a parameters of oxidant-antioxidant balance. We have shown that BN 52021 exerts only partial protecting effect against Na-TC-induced AP in rats. The positive effects of BN 52021 were expressed by: (1) Significant reduction of hyperamylasemia accompanied by lower malondialdehyde accumulation in pancreatic tissue; (2) Prevention of sulfl hydryl groups depletion in lung tissue; (3) Diminution of necrotic and inflammatory changes in pancreatic tissue; and (4) Improvement of survival rate. We suggest that these effects may depend on the inhibition of PAF-mediated activation and oxidant generation by phagocytes.     

Oxidative stress in distant organs and the effects of allopurinol during experimental acute pancreatitis.

BACKGROUND: The present study was aimed at an assessment of the role of oxygen-derived free radicals in the development of local and systemic manifestations of L-arginine (Arg)-induced acute pancreatitis and at an evaluation of the protective effect of the xanthine oxidase inhibitor allopurinol. METHODS: Acute pancreatitis was induced in male Wistar rats by injecting 2 x 250 mg/100 g body weight of Arg intraperitoneally at an interval of 1 h, as a 20% solution in 0.15 M NaCl. Control rats received the same quantity of glycine. In a third group, 200 mg/kg of allopurinol was administered subcutaneously 30 min before the first Arg injection. Rats were killed at 6, 12, 24, or 48 h following Arg administration. Acute pancreatitis was confirmed by a serum amylase level elevation and typical inflammatory features were observed microscopically. Tissue concentrations of malonyl dialdehyde (MDA), superoxide dismutase (Mn- and Cu,Zn-SOD), glutathione peroxidase (GPx), and catalase were measured in the pancreas, liver, and kidney. RESULTS: The tissue concentration of MDA was significantly elevated in each organ. The activities of Mn-SOD, Cu,Zn-SOD, GPx, and catalase were quickly depleted in the pancreas and kidney, whereas only the Mn-SOD and GPx activities were reduced in the liver after the onset of pancreatitis. Histologic examination revealed acinar cell necrosis in the pancreas, but only mild alterations in the liver and kidney. Allopurinol pretreatment prevented the generation of reactive oxygen metabolites in the pancreas and reduced their formation in the kidney. CONCLUSION: Oxygen-derived free radicals are generated in the pancreas, liver, and kidney at an early stage of Arg-induced acute pancreatitis. The liver and the kidney, but not the pancreas, are able to defend against oxidative stress. The prophylactic application of allopurinol significantly restrains the generation of free radicals in pancreas and kidney.     

Effect of intraarterial active oxygen species on the rat pancreas.

To explore the role of active oxygen species in the development and progression of acute pancreatitis, we studied the direct toxic effect on the rat pancreas of active oxygen species: superoxide anions generated by xanthine/xanthine oxidase (X/XO), and hydrogen peroxide (H2O2). After a continuous injection of X (10(-3)M, 0.9 ml/hour)/XO (1 U/ml, 0.3 ml/hour) into the celiac artery supplying the pancreas, hemorrhages and extensive edema developed in the pancreas. The amylase and lipase concentrations in the peritoneal fluid rose to 10.3 and 13.8 times the control values, respectively. The subsequent infusion of superoxide dismutase (SOD, 3600 U/hour) into the external jugular vein completely suppressed hemorrhages, and reduced edema and the amylase and lipase concentrations in the peritoneal fluid. After continuous injection of H2O2 (100 microM, 1.2 ml/hour), via the celiac artery, marked hemorrhages and edema appeared in the pancreas, and the amylase and lipase concentrations in the peritoneal fluid were 11.1 and 17.3 times higher than the control values, respectively. These abnormalities were significantly suppressed by the intravenous infusion of catalase (10 mg/kg/hour) or gabexate mesilate (10 mg/kg/hour). These results indicate that active oxygen species have a direct toxic effect on the pancreas and that free radicals may play an important role in the development of acute pancreatitis.     

Effect of antioxidant treatment in rats with acute hemorrhagic pancreatitis

The purpose of this study was to evaluate the effect of free radical ablation therapy in acute hemorrhagic pancreatitis. Acute pancreatitis was induced in 64 rats by retrograde injection of 5% sodium taurocholate. Thirty animals were pretreated with 100,000 units/kg/hr of superoxide dismutase (SOD) and 400,000 units/kg catalase within the first 3 hr. After 0.5, 3.5, and 12 hr of observation time, serum enzymes and the tissue content of conjugated dienes, malondialdehyde, reduced and oxidized glutathione, as well as ATP, ADP and AMP were measured. In addition, tissue samples were examined by light microscopy. Untreated rats (N=34) developed within 12 hr an acute hemorrhagic necrotizing pancreatitis with a concomitant increase in serum enzyme levels and a decrease in reduced glutathione and ATP. Within the 12-hr observation period, 57% of the animals died. Scavenger treatment improved the tissue damage and attenuated the increase of the serum enzyme levels and the decrease in reduced glutathione and ATP. Moreover, the lethality rate was significantly lower. Oxygen radicals seem to be instrumental for the development of acute hemorrhagic pancreatitis. Thereby, antioxidant treatment reduces tissue damage, biochemical alterations and extrapancreatic complications, thus improving the final outcome.     

Effects of octreotide in acute hemorrhagic necrotizing pancreatitis in rats

BACKGROUND AND AIM: Octreotide is considered to reduce exocrine pancreatic secretion in acute hemorrhagic necrotizing pancreatitis decreasing pancreatic autodigestion. The aim of this study was to determine whether octreotide also has antioxidative effects in acute pancreatitis. Additionally time and dose of application were of interest. METHOD: Ninety male Sprague-Dawley rats were randomized into six groups (n = 15). Group 1 underwent a laparotomy, and animals in groups 2-6 received intraductal glycodeoxycholic acid followed by intravenous cerulein. Groups 3 and 4 were injected with 0.5 mg octreotide, while groups 5 and 6 received continuous intravenous infusion of 0.05 mg octreotide/h for 10 h. Treatment was initiated 6 hours after induction of pancreatitis (IP) in groups 3 and 5, and 14 h after IP in groups 4 and 6. At 24 h after IP all animals were killed and each pancreas was analyzed histopathologically. In addition, levels of pancreatic lipid peroxidation protective enzymes glutathione-peroxidase (GSH-Px) and superoxide dismutase (SOD) as well as lipid peroxidation via thiobarbituric acid reactive substances (TBARS) were determined. RESULTS: Early bolus application of octreotide reduced severity of histopathological changes in acute pancreatitis and decreased lipid peroxidation in pancreatic tissue samples; however, late bolus application and continuous intravenous infusion did not influence pancreatitis or lipid peroxidation. CONCLUSION: Octreotide seems to have a dose- and time-dependent effect on histopathology and lipid peroxidation in a model of pancreatitis in rats.     

Oxidative stress in distant organs and the effects of allopurinol during experimental acute pancreatitis

Summary Background. The present study was aimed at an assessment of the role of oxygen-derived free radicals in the development of local and systemic manifestations of l-arginine (Arg)-induced acute pancreatitis and at an evaluation of the protective effect of the xanthine oxidase inhibitor allopurinol. Methods. Acute pancreatitis was induced in male Wistar rats by injecting 2×250 mg/100 g body weight of Arg intraperitoneally at an interval of 1 h, as a 20% solution in 0.15 M NaCl. Control rats received the same quantity of glycine. In a third group, 200 mg/kg of allopurinol was administered subcutaneously 30 min before the first Arg injection. Rats were killed at 6, 12, 24, or 48 h following Arg administration. Acute pancreatitis was confirmed by a serum amylase level elevation and typical inflammatory features were observed microscopically. Tissue concentrations of malonyl dialdehyde (MDA), superoxide dismutase (Mn- and Cu,Zn-SOD), glutathione peroxidase (GPx), and catalase were measured in the pancreas, liver, and kidney. Results. The tissue concentration of MDA was significantly elevated in each organ. The activities of Mn-SOD, Cu,Zn-SOD, GPx, and catalase were quickly depleted in the pancreas and kidney, whereas only the Mn-SOD and GPx activities were reduced in the liver after the onset of pancreatitis. Histologic examination revealed acinar cell necrosis in the pancreas, but only mild alterations in the liver and kidney. Allopurinol pretreatment prevented the generation of reactive oxygen metabolites in the pancreas and reduced their formation in the kidney. Conclusion. Oxygen-derived free radicals are generated in the pancreas, liver, and kidney at an early stage of Arg-induced acute pancreatitis. The liver and the kidney, but not the pancreas, are able to defend against oxidative stress. The prophylactic application of allopurinol significantly restrains the generation of free radicals in pancreas and kidney.     

Oxygen radicals mediate depletion of pancreatic sulfhydryl compounds in rats with cerulein-induced acute pancreatitis

Acute edematous pancreatitis was induced in conscious rats by intravenous infusion of cerulein at a supramaximal dose of 7.5 micrograms/kg/h during 6 h. The most important finding of our study was a marked decrease in the protein and non-protein content of sulfhydryl groups parallel to an evident elevation in the malondialdehyde concentration in pancreatic tissue. The presented data suggest that in cerulein-induced acute pancreatitis in rats, oxygen radicals mediate increased peroxidation reactions which are accompanied by depletion of nonenzymatic sulfhydryl-containing free radical scavengers. The above phenomenon contributes to a disturbance in thiol metabolism resulting in serious diminution of pancreatic protein sulfhydryl compounds.     

Effect of short-term ketogenic diet on redox status of human blood

The present study investigated the effect of a ketogenic diet on the blood redox status of healthy female subjects. Twenty healthy females with mean body mass index of 21.45 +/- 2.05 kg/m(2) were provided a low-carbohydrate (55 +/- 6 g; 13% total energy), high-fat (138 +/- 16 g; 74% total energy), calorie-restricted (-465 +/- 115 kcal/d) diet. The followings were tested prior to and after 14 days consumption of the diet: Whole body, body weight and total body fat; blood, complete blood count, red blood cells, white blood cells, hemoglobin, and hematocrit; plasma, 3-beta-hydroxybutyrate, total antioxidative status, and uric acid; red blood cells, total sulfhydryl content, malondialdehyde, superoxide dismutase activity, and catalase activity. After 14 days, weight loss was significant whereas no changes were detected in body fat. No alterations were observed in blood count or morphology. 3-beta-hydroxybutyrate, total antioxidative status, uric acid, and sulfhydryl content were significantly increased. There were no alterations in malondialdehyde, or superoxide dismutase or catalase activity. The present study demonstrates that 14 days of a ketogenic diet elevates blood antioxidative capacity and does not induce oxidative stress in healthy subjects.     

Free oxygen radical-induced acute pancreatitis. A light and electron microscopic study

BACKGROUND/AIMS: To date direct toxic effects of free oxygen radicals in vivo on pancreatic parenchyma have not been studied thoroughly. We aimed to study: 1) the detailed histopathological changes induced by free oxygen radicals in pancreas; and 2) the preventive effect of intraductal catalase in H2O2-induced acute pancreatitis. METHODOLOGY: Wistar Albine rats were randomized into six groups. 1) First experiment: Bile-pancreatic duct was cannulated close to the liver and perfused through the duodenum with (i) normal saline solution, (ii) iron sulfate (FeSO4), (iii) hydrogen peroxide (H2O2), (iv) hydrogen peroxide and iron sulfate simultaneously. 2) Second experiment: Bile pancreatic duct was perfused either with H2O2 or H2O2 + catalase. Serum amylase and pancreas malondialdehyde levels were measured in both experiments after 3 hours of perfusion period. Tissue samples were obtained for histopathological examinations. RESULTS: 1) First experiment: Intraductal perfusion of FeSO4 or H2O2 or H2O2 + FeSO4 induced acute edematous pancreatitis with focal parenchymal necrosis. At the ultrastructural level, intracytoplasmic formation of vacuoles. fusion of the vacuoles and zymogen granules, and autophagosomes containing cellular organelles were found. Serum amylase and pancreas malondialdehyde levels, and morphological score were significantly higher in these groups than control group (p < 0.001). 2) Second experiment: Catalase perfusion simultaneously with H2O2 decreased the serum amylase and pancreas malondialdehyde levels, and morphological score significantly (p < 0.001) and prevented the desquamation of the columnar epithelium and development of gross edema but not parenchymal necrosis. CONCLUSIONS: Intraductal perfusion of FeSO4 or H2O2 or H2O2 + FeSO4-induced acute pancreatitis with marked light and electronmicroscopic changes. Intraductal perfusion of catalase and H2O2 simultaneously did not prevent or lessen the parenchymal necrosis. These findings have suggested that another mechanism of injury may also play a role in parenchymal injury in oxygen radical-induced acute pancreatitis.     

Antioxidant activity of chito-oligosaccharides on pancreatic islet cells in streptozotocin-induced diabetes in rats

AIM： To investigate the antioxidant activity of chitooligosaccharides （COSs） on pancreatic islet cells in diabetic rats induced by streptozotocin.
METHODS： The antioxidant effect of COSs on pancreatic islet cells was detected under optical microscopy and with colorimetric assay and gel electrophoresis. The activities of glutathione peroxidase and superoxide dismutase, total antioxidant capacity, and content of malondialdehyde in serum and tissue slices of pancreas were examined after 60 d to determine the effect of COSs in streptozotocin-induced diabetes in rats.
RESULTS： COSs can prohibit the apoptosis of pancreatic islet cells. All concentrations of COSs can improve the capability of total antioxidant capacity and activity of superoxide dismutase and decrease the content of malondialdehyde drastically. Morphological investigation in the pancreas showed that COSs have resulted in the reduction of islets, loss of pancreatic cells, and nuclear pyknosis of pancreatic cells.
CONCLUSION： COSs possess various biological activities and can be used in the treatment of diabetes mellitus.     

Effect of a specific synthetic inhibitor of neutrophil elastase (ONO-5046) on the course of acute hemorrhagic pancreatitis in dogs

In acute pancreatitis, particularly in severe cases, polymorphonuclear neutrophil (PMN) elastase induces tissue damage in remote organs such as the lung, as well in the pancreas itself. Therefore, we examined the therapeutic effect of a specific synthetic inhibitor of PMN elastase (ONO-5046: Ono Pharmaceuticals, Osaka, Japan) on the lung, liver, and kidney, as well as pancreas, in severe hemorrhagic pancreatitis in dogs. Acute hemorrhagic pancreatitis was induced by the injection of a mixture of autologous bile and porcine trypsin into the main pancreatic duct. Lipopolysaccharide (LPS) was administered intravenously as a septic challenge. Two animal groups were used. In one group, continuous infusion of ONO-5046 was started prior to the injection of LPS (ONO group). In the other group (control), saline was infused instead. At the end of the experiment (330 min after the injection of bile and trypsin), the pancreas revealed severe hemorrhagic pancreatitis, and a large amount of bloody ascites had accumulated in the peritoneal cavity. The white blood cell count was markedly reduced in response to the induction of pancreatitis, and was decreased further by the septic attack, irrespective of the administration of ONO-5046, although the count increased again in the ONO group. Serum levels of amylase and α₂-macroglobulin-trypsin complex increased similarly in both groups following administration of bile and trypsin. Serum Ca levels decreased in both groups. At the end of the experiment, the wet weight of the lung was slightly higher in the control group (without ONO-5046). Microscopically, the pancreas showed severe hemorrhage accompanied by extensive interstitial edema in both groups. The lung and liver demonstrated mild infiltration of inflammatory cells in the interstitium in both groups, although the inflammatory change in the liver was slightly milder in the ONO group. These findings indicate that severe hemorrhagic pancreatitis cannot be alleviated by the administration of a specific inhibitor of PMN elastase alone, although this may lessen damage to remote organs such as the liver and lung. The white blood cell count decreased markedly after the induction of acute pancreatitis, and much more after a septic challenge. This seems to be closely related to the accumulation of bloody ascites in the peritoneal cavity.     

肺缺血再灌注损伤中氧化应激与Fas/FasL系统的关系

目的探讨肺缺血再灌注损伤中氧化应激与Fas/FasL系统的关系。方法采用在体兔单侧肺缺血再灌注损伤模型,日本大耳白兔40只,随机分为对照组,缺血再灌注1h、3h和5h组,每组10只。对比观察各组血浆超氧化物歧化酶活性、丙二醛含量和一氧化氮水平,以及肺组织细胞凋亡指数及Fas/FasL mRNA定位表达。结果缺血再灌注组肺组织凋亡指数明显高于对照组(P<0.01);再灌注后Fas、FasL mRNA在肺血管内皮细胞、肺泡上皮细胞及支气管上皮细胞等呈阳性表达,明显强于对照组(P<0.01);丙二醛含量随再灌注时间延长逐渐增加(P<0.01),而超氧化物歧化酶活性与一氧化氮则随再灌注时间延长有所降低(P<0.01)。结论肺缺血再灌注损伤期间,氧化应激参与Fas/FasL系统的激活。     

Parenteral superoxide dismutase plus catalase diminishes pancreatic edema in sodium taurocholate-induced pancreatitis in the rat

Scavengers of toxic oxygen reduction products have been reported to reduce the inflammatory reaction in some models of pancreatitis. In a blinded study, the effect of parenteral pretreatment with superoxide dismutase plus catalase was compared with placebo on pancreatitis induced in rats by infusion of 0.25% or 2% sodium taurocholate into the hepatopancreatic duct. The degree of inflammation was assessed by macroscopic examination of the pancreas, dry/wet weight ratios of pancreatic specimens, amylase activity in plasma and peritoneal exudate, the weight of the exudate, and its content of total protein. All parameters were indicative of a more severe inflammation in rats given the higher concentration of sodium taurocholate. The only significant effect of the superoxide dismutase plus catalase treatment was a moderate reduction of the dry/wet weight ratio, i.e., pancreatic edema, in rats given 2% sodium taurocholate. Our results indicate that toxic oxygen reduction products, available for interception by parenterally administered superoxide dismutase plus catalase, are of only minor importance in the pathogenesis of sodium taurocholate-induced pancreatitis in the rat.     

Activity of Superoxide Dismutase, Catalase, Glutathione Peroxidase, and Glutathione Reductase in Different Stages of Colorectal Carcinoma

Background

Reactive oxygen species are involved in the pathogenesis of colorectal carcinoma. Clarification of oxidative/antioxidant specificities of different stages of colorectal carcinoma is of special importance.

Aim

To determine oxidative/antioxidant status in plasma of patients with different stages of colorectal carcinoma using malondialdehyde concentration, superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activities and distribution of superoxide dismutase isoforms.

Methods

Lipid peroxidation and antioxidant enzymes activity were estimated using spectrophotometric methods. Reverse zymography was applied for characterization of superoxide dismutase isoforms.

Results

Lipid peroxidation is increased in all groups compared to the control, but without differences between different stages of colorectal carcinoma. Total superoxide dismutase activity is lower in all colorectal carcinoma groups than in control, and there is a significant increase in tumor stage IV when compared with tumor stage II. Manganese superoxide dismutase isoform is dominant in all groups and its relative activities are significantly higher than activities of a copper/zinc isoform. Total peroxidase potential reflected in catalase and glutathione peroxidase activity is increased when compared to the control, but without any significant differences between colorectal carcinoma groups. Glutathione reductase activity is lower in all colorectal carcinoma groups than in control, and a significant decrease in glutathione reductase activity was obtained between patients in tumor stage II and III compared to tumor stage IV.

Conclusions

Colorectal carcinoma is characterized by increased oxidative stress and antioxidant disbalance. Progression of disease is followed by an increase in redox disbalance.     

Melatonin reduces apoptosis and necrosis induced by ischemia/reperfusion injury of the pancreas

The pancreas is highly susceptible to the oxidative stress induced by ischemia/reperfusion (IR) injury leading to the generation of acute pancreatitis. Melatonin has been shown to be useful in the prevention of the damage by ischemia-reperfusion in liver, brain, myocardium, gut and kidney. The aim of the study was to evaluate the cytoprotective properties of melatonin against injury induced by IR in pancreas. The obstruction of gastro-duodenal and inferior splenic arteries induced pancreatic IR in male Wistar rats. Melatonin was intraperitoneally administered before or/and after IR injury. The animals were killed at 24 and 48 hr after reperfusion and there were evaluated parameters of oxidative stress (lipoperoxides, superoxide dismutase, catalase, glutathione peroxidase and reduced glutathione), glandular endocrine and exocrine function (lipase, amylase, insulin) and cell injury (apoptosis and necrosis). The IR induced a marked enhancement of oxidative stress and impaired pancreatic function. The histological analysis showed that IR induced acute pancreatitis with the accumulation of inflammatory infiltrate, disruption of tissue structure, cell necrosis and hemorrhage. Melatonin administration before or after pancreatic IR prevented all tissue markers of oxidative stress, biochemical and histological signs of apoptosis and necrosis, and restored glandular function. No histological signs of pancreatitis were observed 48 hr after reperfusion in 80% of the animals treated with melatonin, with only a mild edematous pancreatitis being observed in the remaining rats. Preventive or therapeutic administration of melatonin protected against the induction of oxidative stress and tissue injury, and restored cell function in experimental pancreatic IR in rats.     

Oxidative stress in rodent closed duodenal loop pancreatitis

Summary Conclusions Production of excited oxygen species is earlier in the liver than in the pancreas and could contribute to damage in a reflux model. Treatment with SOD could attenuate 59% light emission in pancreas, but did not modify serum enzyme levels or pancreatic edema, resulting as an insufficient isolated therapy. Unexpectedly, it was found an increased plasma antioxidant capacity that was related to total bilirubin levels, and declined at late stages probably denoting other circulating antioxidant consumption. Background Oxidative stress has been shown to play a role in different models of acute pancreatitis, although it has not been studied in the severe necrohemorrhagic model produced by closed duodenal loop pancreatitis. Methods We studied Sprague Dawley female rats in two groups: a closed duodenal loop pancreatitis group and a control, sham-operated group. In order to evidence the oxygen excited species production,in situ spontaneous chemiluminescence from living and naturally perfused pancreas and liver was measured at 0, 0.5, 1.5, 3, 6, 12, and 24 h after the duodenal ligature. Blood pancreatic amylase and aminotransferases levels were determined as expression of tissue damage in pancreas and liver. At the same time, plasma antioxidant capacity was measured by the peroxyl radical trapping capability of plasma samples compared to that of Trolox (synthetic analog of vitamin E), and results are expressed as Trolox equivalence. Bovine superoxide dismutase (SOD) was administered to attenuate oxygen free radicals activity at the beginning of the peroxidation chain and also as a therapeutic tool. Results The experimental procedure induced a severe pancreatitis, as evidenced by pancreatic enzymes that rose markedly in the early hours of disease and remained heightened throughout the experiment. The results show early light emission from the liver at 3 h and peak levels at 12 h, whereas in the pancreas, luminescence increased at 6 h and doubled later at 12 h, both returning to control levels at 24 h.     

Administration of hyaluronic acid and chondroitin-4-sulfate limits endogenous antioxidant depletion and reduces cell damage in experimental acute pancreatitis

Several reports have described a loss of endogenous antioxidants and molecular oxidative damage during acute pancreatitis. Since hyaluronic acid and chondroitin-4-sulfate possess antioxidant properties, the effect of the administration of these glycosaminoglycans in a cerulein-induced acute pancreatitis in rats was investigated. Cerulein administration produced pancreatic edema and a marked increase in serum lipase and amylase activity; induced a severe depletion of reduced glutathione, catalase, and superoxide dismutase levels; primed lipid peroxidation; and promoted neutrophil intervention. Intraperitoneal pretreatment of rats with hyaluronic acid or chondroitin-4-sulfate or with both compounds ameliorated pancreatic cell conditions; restored the endogenous antioxidants reduced glutathione, catalase and superoxide dismutase; limited cell membrane peroxidation; and reduced neutrophil activation. Our data confirm the antioxidant activity of these 2 glycosaminoglycans.     

Lipid peroxidation, some extracellular antioxidants, and antioxidant enzymes in serum of patients with rheumatoid arthritis

The aims of our study were to assess whether the increased oxidative stress in inflamed joints is reflected by serum lipid peroxidation and also to check alterations in the levels of extracellular antioxidants and antioxidant enzyme activities in patients with rheumatoid arthritis. Serum malondialdehyde and ceruloplasmin levels and the activity of CuZn superoxide dismutase were higher, while transferrin levels and the activities of glutathione peroxidase and catalase were lower in patients (n = 37) than in healthy controls (n = 30). Disease activity score correlated positively with serum malondialdehyde level and CuZn superoxide dismutase activity. Probably, superoxide radicals in serum could be dismutated to produce hydrogen peroxide by increased CuZn superoxide dismutase activity, but hydrogen peroxide could not have been detoxified due to decreased activities of serum glutathione peroxidase and catalase. Hydrogen peroxide possibly converted to hydroxyl radical by iron due to lower transferrin level might have led to increased serum lipid peroxidation in patients with rheumatoid arthritis.     

Treino de Força Reduz Stress Oxidativo Cardíaco e Renal em Ratos com Hipertensão Renovascular

BackgroundStrength training has beneficial effects on kidney disease, in addition to helping improve antioxidant defenses in healthy animals.ObjectiveTo verify if strength training reduces oxidative damage to the heart and contralateral kidney caused by the renovascular hypertension induction surgery, as well as to evaluate alterations in the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) endogenous antioxidant enzymes.MethodsEighteen male rats were divided into three groups (n=6/group): sham, hypertensive, and trained hypertensive. The animals were induced to renovascular hypertension through left renal artery ligation. Strength training was initiated four weeks after the induction of renovascular hypertension, continued for a 12-weeks period, and was performed at 70% of 1RM. After the training period, the animals were euthanized and the right kidney and heart were removed for quantitation of hydroperoxides, malondialdehyde and sulfhydryl groups, which are markers of oxidative damage. In addition, the activity of SOD, CAT, and GPx antioxidant enzymes was also measured. The adopted significance level was 5% (p < 0.05).ResultsAfter strength training, a reduction in oxidative damage to lipids and proteins was observed, as could be seen by reducing hydroperoxides and total sulfhydryl levels, respectively. Furthermore, an increased activity of superoxide dismutase, catalase, and glutathione peroxidase antioxidant enzymes was observed.ConclusionStrength training is able to potentially reduce oxidative damage by increasing the activity of antioxidant enzymes. (Arq Bras Cardiol. 2021; 116(1):4-11)