Superoxide dismutase prevents development of adenocarcinoma in a rat model of Barrett's esophagus

AIM： To test whether antioxidant treatment could prevent the progression of Barrett＇s esophagus to adenocarcinoma. METHODS： In a rat model of gastroduodenoesophageal reflux by esophagojejunal anastomosis with gastric preservation, groups of 6-10 rats were randomized to receive treatment with superoxide dismutase （SOD） or vehicle and followed up for 4 too. Rat＇s esophagus was assessed by histological analysis, superoxide anion and peroxinitrite generation, SOD levels and DNA oxidative damage. RESULTS： All rats undergoing esophagojejunostomy developed extensive esophageal mucosal ulceration and inflammation by mo 4. The process was associated with a progressive presence of intestinal metaplasia beyond the anastomotic area （9% 1st mo and 50% 4th too） （94% at the anastomotic level） and adenocarcinoma （11% 1^ST mo and 60% 4th too）. These changes were associated with superoxide anion and peroxinitrite mucosal generation, an early and significant increase of DNA oxidative damage and a significant decrease in SOD levels （P〈0.05）. Exogenous administration of SOD decreased mucosal superoxide levels, increased mucosal SOD levels and reduced the risk of developing intestinal metaplasia beyond the anastomotic area （odds ratio = 0.326; 95%CI： 0.108-0.981; P = 0.046）, and esophageal adenocarcinoma （odds ratio = 0.243; 95%CI： 0.073-0.804; P = 0.021）. CONCLUSION： Superoxide dismutase prevents the progression of esophagitis to Barrett＇s esophagus and adenocarcinoma in this rat model of gastrointestinal reflux, supporting a role of antioxidants in the chemoprevention of esophageal adenocarcinoma.

Glutathione peroxidase, superoxide dismutase and catalase activities in children with chronic hepatitis

The advantages of measuring hepatic oxidative status in liver biopsy are that it helps in diagnosis of hepatic dysfunction, reflects the degree of deterioration in the liver tissues, and helps to determine the severity of hepatic injury. We aimed to study the oxidative stress state in children with chronic hepatitis by using indirect approach in which antioxidant enzymes such as glutathione peroxidase (GPX), superoxide dismutase (SOD) and catalase (CAT) are determined in the liver tissue. The present study included 21 children and adolescents (12 males, 9 females) suffering from chronic hepatitis. Patients were selected from the Hepatology Clinic, New Children’s Hospital, Cairo University from November 2006 till 2009 and compared with a group of 7 children who happened to have incidental normal liver biopsy. Children with chronic hepatitis had mean age 8.12 ± 1.15 years. It was further subdivided into 2 subgroups: chronic viral heaptitis (n = 13) and cryptogenic hepatitis (n = 8). GPX, SOD and CAT levels were measured in fresh liver tissue (cell free homogenates) using ELISA. In chronic hepatitis group;there was a significant increase in the hepatic GPX activity (38.59 ± 35.82 nmol/min/ml) as compared to the control group (10.62 ± 6.68 nmol/min/ml). Also a significant correlation was observed between SOD and both ALT (r = 0.87, p < 0.05) and AST (r = 0.74, p < 0.05). GPX correlated with ALT (r = 0.80, p < 0.05) level in the chronic viral hepatitis subgroup. Our findings suggest that oxidative stress could play a role in the pathogenesis of chronic hepatitis. These preliminary results are encouraging to conduct more extensive clinical studies combining antioxidant therapy with various treatments.

Serum manganese superoxide dismutase and thioredoxin are potential prognostic markers for hepatitis C virus-related hepatocellular carcinoma

AIM:To evaluate the clinical significance of oxidative stress markers in patients with hepatitis C virus(HCV)related hepatocellular carcinoma(HCC).METHODS:Sixty-four consecutive patients who were admitted to Kagoshima University Medical and Dental Hospital were enrolled in this retrospective study.All patients had chronic liver disease(CLD) due to infection with HCV.Thirty patients with HCV-related HCC,34 with HCV-related CLD without HCC(non-HCC),and 20 healthy volunteers(HVs) were enrolled.Possible associations between serum manganese superoxide dismutase(MnSOD) and thioredoxin(TRX) levels and clinical parameters or patient prognosis were analyzed over a mean follow-up period of 31.7 mo.RESULTS:The serum MnSOD levels were significantly higher in patients with HCV-related HCC than in patients without HCC(P = 0.03) or HVs(P < 0.001).Similarly,serum TRX levels were also significantly higher in patients with HCV-related HCC than in patients without HCC(P = 0.04) or HVs(P < 0.01).However,serum levels of MnSOD and TRX were not correlated in patients with HCC.Among patients with HCC,the overall survival rate(OSR) was lower in patients with MnSOD levels ≥ 110 ng/mL than in patients with levels < 110 ng/mL(P = 0.01),and the OSR tended to be lower in patients with TRX levels < 80 ng/mL(P = 0.05).In addition,patient prognosis with HCC was poorest with serum MnSOD levels ≥ 110 ng/mL and serum TRX levels < 80 ng/mL.Furthermore,a multivariate analysis using a Cox proportional hazard model and serum levels of five factors(MnSOD,prothrombin time,serum albumin,serum α-fetoprotein(AFP),and serum des-γ-carboxy prothrombin) revealed that MnSOD levels ≥ 110 ng/mL(risk ratio:4.12,95% confidential interval:1.22-13.88,P = 0.02) and AFP levels ≥ 40 ng/mL(risk ratio:6.75;95% confidential interval:1.70-26.85,P < 0.01) were independent risk factors associated with a poor patient prognosis.CONCLUSION:Serum MnSOD and TRX levels are potential clinical biomarkers that predict patient prognosis in HCV-related HCC.

Effects of low molecular weight heparin-superoxide dismutase conjugate on serum levels of nitric oxide,glutathione peroxidase,and myeloperoxidase in a gerbil model of cerebral ischemia/reperfusion injury

BACKGROUND： Several studies have demonstrated that low molecular weight heparin-superoxide dismutase （LMWH-SOD） conjugate may exhibit good neuroprotective effects on cerebral ischemia/reperfusion injury though anticoagulation, decreasing blood viscosity, having anti-inflammatory activity, and scavenging oxygen free radicals. OBJECTIVE： To investigate the intervention effects of LMWH-SOD conjugate on serum levels of nitric oxide （NO）, glutathione peroxidase （GSH-Px）, and myeloperoxidase （MPO） following cerebral ischemia/reperfusion injury. DESIGN, TIME AND SETTING： A randomized, controlled, and neurobiochemical experiment was performed at the Institute of Biochemical Pharmacy, School of Pharmaceutical Sciences, Shandong University between April and July 2004. MATERIALS： A total of 60 Mongolian gerbils of either gender were included in this study. Total cerebral ischemia/reperfusion injury was induced in 50 gerbils by occluding bilateral common carotid arteries. The remaining 10 gerbils received a sham-operation （sham-operated group）. Kits of SOD, NO, and MPO were sourced from Nanjing Jiancheng Bioengineering Institute, China. LMWH, SOD, and LMWH-SOD conjugates were provided by Institute of Biochemistry and Biotechnique, Shandong University, China. METHODS： Fifty successful gerbil models of total cerebral ischemia/reperfusion injury were evenly randomized to five groups： physiological saline, LMWH-SOD, SOD, LMWH ＋ SOD, and LMWH. At 2 minutes prior to ischemia, 0.5 mL/65 g physiological saline, 20 000 U/kg LMWH-SOD conjugate, 20 000 U/kg SOD, a mixture of SOD （20 000 U/kg） and LMWH （LMWH dose calculated according to weight ratio, LMWH： SOD = 23.6：51）, and LMWH （dose as in the LMWH ＋ SOD group） were administered through the femoral artery in each above-mentioned group, respectively. MAIN OUTCOME MEASURES： Serum levels of NO, MPO, and GSH-Px. RESULTS： Compared with 10 sham-operated gerbils, the cerebral ischemia/reperfusion injury gerbils exhibited decreased serum levels of GSH-Px and increased serum levels of NO and MPO （P 〈 0.01）. The serum level of GSH-Px was significantly upregulated in all groups, in particular in the LMWH-SOD group （P 〈 0.01）, compared with the physiological saline group （P 〈 0.05-0.01）. Following medical treatment, serum levels of NO and MPO were significantly downregulated in all groups, in particular in the LMWH-SOD group （P 〈 0.01）. Serum levels of GSH-Px, NO, and MPO in the LMWH-SOD group were close to those in the sham-operated group （P 〉 0.05）. CONCLUSION： In cerebral ischemia/reperfusion injury, LMWH-SOD conjugate exhibits stronger neuroprotective effects on free radical scavenging, inflammation inhibition, and cytotoxicity inhibition than simple or combined application of LMWH and SOD by downregulating NO and MPO levels and upregulating the GSH-Px level.

GroESL protects superoxide dismutase (SOD)— Deficient cells against oxidative stress and is a chaperone for SOD

Superoxide dismutase (SOD)-deficient Escherichia coli OX326Acells are protected against chemically-induced oxidative stress by expression of the chaperonin GroESL. This protection is equivalent to expression of superoxide dismutase even though GroESL has no inherent SOD activity. Co-overexpression of GroESL and SOD in the same cells results in higher protein yields of SOD and greater metallation of SOD when compared with expression of SOD alone. Greater metallation results in the higher specific activity of SOD that is observed in heat shock, and is not due to increased synthesis of SOD mRNA or protein.

Superoxide Dismutase: Therapeutic Targets in SOD Related Pathology

There are growing evidences on the role of adaptive mechanisms of all cell types in pathological processes: atherosclerosis, ischemic attack, bacterial infections, etc. All kinds of these processes involve as main mechanism oxidative stress. Aerobic organisms use oxygen in processes that accidentally or deliberately generate aggressive species for the biologic components in the form of radicals. Radicals were looked initially as “harmful” molecules and this is true for large quantities but in small or even moderate amounts these molecules prove to have a physiological role. Reactive species are highly reactive and as a consequence are short living species. Their impact is supposed to be limited in the proximity area of their formation. Instead recent evidences indicate their implications in cellular signaling suggesting that individual chemical properties of reactive species make a difference in their biological role. This paper presents superoxide, nitric oxide and peroxide radical generation under cellular changing conditions, the adapting behavior of the enzymes that synthesize and remove them as well as some therapeutic target in superoxide related pathology.

Experience of Using the Recombinant Human Superoxide Dismutase Drug in Neurological and Ophthalmological Practice

Recsod? has been used for treating epilepsy and ophthalmological disease. Oxidative stress has been demonstrated to be a pathogenic chain of these diseases. Parameters of pro- and antioxidant systems were studied in all the patients treated. Recsod? drug was shown to produce positive effect in all the patients. Improvement of patients’ clinical condition correlated with an increase in antioxidant activities. Antioxidants, in particular, the recombinant human SOD drug, proved to be effective in treatment of some neurological and ophthalmological diseases.

Hypidone hydrochloride(YL-0919)ameliorates functional deficits after traumatic brain injury in mice by activating the sigma-1 receptor for antioxidation

Traumatic brain injury involves complex pathophysiological mechanisms,among which oxidative stress significantly contributes to the occurrence of secondary injury.In this study,we evaluated hypidone hydrochloride(YL-0919),a self-developed antidepressant with selective sigma-1 receptor agonist properties,and its associated mechanisms and targets in traumatic brain injury.Behavioral experiments to assess functional deficits were followed by assessment of neuronal damage through histological analyses and examination of blood-brain barrier permeability and brain edema.Next,we investigated the antioxidative effects of YL-0919 by assessing the levels of traditional markers of oxidative stress in vivo in mice and in vitro in HT22 cells.Finally,the targeted action of YL-0919 was verified by employing a sigma-1 receptor antagonist(BD-1047).Our findings demonstrated that YL-0919 markedly improved deficits in motor function and spatial cognition on day 3 post traumatic brain injury,while also decreasing neuronal mortality and reversing blood-brain barrier disruption and brain edema.Furthermore,YL-0919 effectively combated oxidative stress both in vivo and in vitro.The protective effects of YL-0919 were partially inhibited by BD-1047.These results indicated that YL-0919 relieved impairments in motor and spatial cognition by restraining oxidative stress,a neuroprotective effect that was partially reversed by the sigma-1 receptor antagonist BD-1047.YL-0919 may have potential as a new treatment for traumatic brain injury.

Green tea polyphenols protect spinal cord neurons against hydrogen peroxide-induced oxidative stress

Green tea polyphenols are strong antioxidants and can reduce free radical damage. To investigate their neuroprotective potential, we induced oxidative damage in spinal cord neurons using hydrogen peroxide, and applied different concentrations （50-200μg,/mL） of green tea polyphenol to the cell medium for 24 hours. Measurements of superoxide dismutase activity, malondialdehyde content, and expression of apoptosis-related genes and proteins revealed that green tea polyphenol effectively alleviated oxidative stress. Our results indicate that green tea polyphenols play a protective role in spinal cord neurons under oxidative stress.

Effect of Nitric Oxide on Esophageal Cancer Cell Line TE-1

Objective To investigate the radiosensitizing effect of nitric oxide(NO) combined with radiation on esophageal cancer cell line TE-1.Methods Methyl thiazolyl tetrazolium(MTT) assay was used to assess the effects of NO and radiation on TE-1 cells regarding inhibition of cell proliferation.Flow cytometry was used to examine the effect of NO and radiation on cell apoptosis and cycle.Reverse transcription polymerase chine reaction and Western blot were used to evaluete the effect of NO on mRNA and protein expression of manganese superoxide dismutase(MnSOD).Results NO inhibited the proliferation of TE-1 cells while significantly enhancing their radiosensitivity.The application of NO combined with radiation significantly increased the apoptosis rate and G2/M phase proportion of TE-1 cells,with substantial decreases in the MnSOD mRNA and protein expression levels.Conclusions NO reduces the MnSOD mRNA and protein expression levels by affecting TE-1 cell cycle,further inhibiting the apoptosis of esophageal cancer cells and enhancing the killing effect of radiation on esophageal cancer cells.

Action of Gaseous Nitric Oxide on Some Physical and Chemical Parameters of Human Blood Samples

We studied the metabolic changes induced by gaseous nitric oxide in whole blood samples in vitro. Blood samples were collected from healthy donors (Nizhny Novgorod station of blood transfusion). We carried out the direct bubbling of blood samples (n = 14) with gaseous flow with NO in a special appliance. We modeled standard conditions using the apparatus “Plazon” (concentration NO 800 mcg/l). Middle power of gas flow was used. The blood sparging time was 2 min, and exposition time lasted 3 min. Every blood sample volume was 5 ml. All the parameters were controlled before and after blood processing with NO. We tested lactate dehydrogenase activity in direct and reverse reactions spectrometrically by G. A. Kochetov’s method. Aldehyde dehydrogenase activity was examined by B. M. Kershnhots’s and E. V. Serkina’s methods, superoxide dismutase—by T. V. Sirota’s technology. Total protein level was examined by modified Louri’s method. The concentration of lactate was tested with the automatic analyzer “SuperGL Ambulance”. The indices of acidbase balance and blood gases partial pressure were estimated with special analyzer “ABL-77”. Additional control of energy metabolism changes was accomplished with derivative parameters, such as coefficient of energy reaction balance and coefficient of substrate provision. Different changes of blood physical and chemical parameters are induced by NO-processing which was fixed in our experiments. There is an inhibition of erythrocytes energy metabolism, decreasing of plasma antioxidant reserves, moderate ionic disorders and of acid-base misbalance in blood samples in vitro. Besides, according to the indirect signs, the used regimen of NO-processing mainly affected erythrocytes, and stipulated methemoglobin formation. These data testify that the used dose of gaseous nitric oxide is too high for investigated human blood. In our opinion, registered negative effects of free NO may be eliminated by bound nitric oxide use (first of all in its natural form—dinitrosyl-iron complexes).

Impact of metal oxide nanoparticles on cotton(Gossypium hirsutum L.):a physiological perspective

Cotton production substantiated a crucial part in the escalating economic development of many countries.To realize the increasing global demand for cotton,the emphasis should be laid on to improve cotton fiber growth and production.The bioengineered transgenic cotton proved expedient in resolving inadequacies of conventional cotton,but still required improvements to encounter heightened demand of textile industries.One possible solution pertaining to this has been provided by nanoscience in the form of metal or metal oxide nanoparticles.These metal oxide nanoparticles have easy access to the various parts of cotton plants through its transportation system,and thus significantly influence several parameters relative to the growth and production of cotton fiber.This review summarizes the distribution and accumulation of metal oxide nanoparticles in cotton plant and its impact on different plant growth-promoting factors,which resulted in the improved cotton yields.

Oxidative Stress in Collegiate Cross Country Skiers in Mid- and Post-Seasons

Purpose: The oxidative stress (OS) hypothesis of overtraining syndrome argues that increased production of free radicals through exercise cause muscle fatigue and damage resulting in lower athletic performance. Several studies have investigated OS immediately before and after exercise bouts in a training macrocycle. Our study aimed to compare OS of endurance athletes between a competition macrocycle and the immediate post-season recovery macrocycle. In addition, we aimed to identify athletes who experienced an unexplainable drop in athletic performance during the competition season in order to compare their OS to those who experienced no drop in performance. Methods: Fifteen members of the University of Alaska Fairbanks cross country ski team volunteered for this study. Blood samples were taken in early February (“mid-season”) and late April (“post-season”). Participants completed questionnaires regarding physical activity and athletic performance at the time of the blood draws. Plasma was analyzed for 4-hydroxynonenal (HNE), nitrotyrosine, nitric oxide (NOX), and superoxide dismutase (SOD). Significance was determined by Wilcoxon and Mann-Whitney tests. Results: Participants displayed significantly higher (p Conclusion: Signs of oxidative stress and mitigation during the post-season recovery macrocycle were higher in athletes who reported experiencing a drop in athletic performance during the competition season macrocycle.

芒果苷对大鼠骨髓间充质干细胞氧化应激损伤的保护作用

背景:间充质干细胞移植治疗脊髓损伤有一定效果,但仍存在局部氧化应激环境导致移植细胞存活率低、细胞移植效率不佳等问题。目的:探究芒果苷在氧化应激状态下对骨髓间充质干细胞的保护作用。方法:取第3代大鼠骨髓间充质干细胞,按浓度梯度0,20,40,80,160μmol/L加入芒果苷孵育2 h,然后加入含400μmol/L H_(2)O_(2)的无血清L-DMEM培养基及相应浓度的芒果苷继续培养12 h及24 h,以常规培养的大鼠骨髓间充质干细胞为正常对照组。MTT法检测各组细胞存活情况,按照试剂盒操作方法检测细胞培养液中超氧化物歧化酶、丙二醛及过氧化氢酶水平。结果与结论:与正常对照组相比,H_(2)O_(2)组细胞的存活能力显著降低(P<0.01),超氧化物歧化酶、过氧化氢酶水平显著降低(P<0.01),丙二醛水平显著升高(P<0.01);与H_(2)O_(2)组相比,芒果苷组细胞的存活能力显著升高(P<0.01),超氧化物歧化酶、过氧化氢酶水平显著升高(P<0.01),丙二醛水平显著降低(P<0.01)。芒果苷在20μmol/L浓度以上表现出浓度依赖性的抗氧化应激保护活性,且在160μmol/L以下无细胞毒性。结果表明,抗氧化剂芒果苷可增加骨髓间充质干细胞的抗氧化活性,为骨髓间充质干细胞移植提供一种新的预处理策略。

Antioxidative mechanism of Lycium barbarum polysaccharides promotes repair and regeneration following cavernous nerve injury

Polysaccharides extracted from Lycium barbarum exhibit antioxidant properties.We hypothesized that these polysaccharides resist oxidative stress-induced neuronal damage following cavernous nerve injury.In this study,rat models were intragastrically administered Lycium barbarum polysaccharides for 2 weeks at 1,7,and 14 days after cavernous nerve injury.Serum superoxide dismutase and glutathione peroxidase activities significantly increased at 1 and 2 weeks post-injury.Serum malondialdehyde levels decreased at 2 and 4 weeks.At 12 weeks,peak intracavernous pressure,the number of myelinated axons and nicotinamide adenine dinucleotide phosphate-diaphorase-positive nerve fibers,levels of phospho-endothelial nitric oxide synthase protein and 3-nitrotyrosine were higher in rats administered at 1 day post-injury compared with rats administered at 7 and 14 days post-injury.These findings suggest that application of Lycium barbarum polysaccharides following cavernous nerve crush injury effectively promotes nerve regeneration and erectile functional recovery.This neuroregenerative effect was most effective in rats orally administered Lycium barbarum polysaccharides at 1 day after cavernous nerve crush injury.

Panax notoginseng saponin attenuates hypoxia/reoxygenation-induced oxidative stress in cortical neurons

The present study monitored the effect of 2, 10, and 50 mg/L of Panax notoginseng saponin exposure following hypoxia-reoxygenation injury in fetal rat cortical neurons. Results showed that varying doses of Panax notoginseng saponin significantly enhanced the cell viability of neurons, reduced malondialdehyde content, increased superoxide dismutase activity, inhibited mRNA and protein expression of inducible and neuronal nitric oxide synthase, and decreased the release of nitric oxide in hypoxia/reoxygenation injured cells. In particular, 50 mg/L of Panax notoginseng saponin was the most effective dose. These findings suggest that Panax notoginseng saponin can attenuate neuronal oxidative stress injury caused by hypoxia/reoxygenation in a dose-dependent manner.

Epalrestat protects against diabetic peripheral neuropathy by alleviating oxidative stress and inhibiting polyol pathway

Epalrestat is a noncompetitive and reversible aldose reductase inhibitor used for the treatment of diabetic neuropathy. This study assumed that epalrestat had a protective effect on diabetic peripheral nerve injury by suppressing the expression of aldose reductase in peripheral nerves of diabetes mellitus rats. The high-fat and high-carbohydrate model rats were established by intraperitoneal injection of streptozotocin. Peripheral neuropathy occurred in these rats after sustaining high blood glucose for 8 weeks. At 12 weeks after streptozotocin injection, rats were intragastrically administered epalrestat 100 mg/kg daily for 6 weeks. Transmission electron microscope revealed that the injuries to myelinated nerve fibers, non-myelinated nerve fibers and Schwann cells of rat sciatic nerves had reduced compared to rats without epalrestat administuation. Western blot assay and immunohistochemical results demonstrated that after intervention with epalrestat, the activities of antioxidant enzymes such as superoxide dismutase, catalase and glutathione peroxidase gradually increased, but aldose reductase protein expression gradually diminished. Results confirmed that epalrestat could protect against diabetic peripheral neuropathy by relieving oxidative stress and suppressing the polyol pathway.

Oxidative stress related enzymes in response to chromium(VI) toxicity in Oxya chinensis (Orthoptera: Acridoidae)

The toxic effects of Cr（Vl） on antioxidant enzymes of Oxya chinensis（Orthoptera： Acridoidae） were determined. Changes in the activities of the antioxidant enzymes superoxide dismutase（SOD）, catalase（CAT）, and guaiacol peroxidase（GPx） were measured in O. chinensis insects injected with Cr（VI）. Fifth-nymphs of O. chinensis insects were injected with Cr（VI） with different concentrations （0, 75, 150, 225, 300, 375, 450 mg/kg of body weight）. The results showed that Cr（VI） led to the change of SOD, CAT, and GPx activities at different concentrations, which revealed that： （1） The oxidative stress of SOD increased with the increase of Cr （VI） concentration. （2） With the increase of Cr （VI） concentrations, CAT activities for females increased at lower concentrations, but decreased at higher concentration range, which indicated that antioxidant system of O. chinensis was not influenced by the presence of Cr （VI）. A very similar response to Cr（VI） effect for males indicated that Cr（VI） concentrations were not high enough to damage O. chinensis in terms of CAT. （3） The GPx activity for females increased in all treatments, which revealed that the damage power of Cr（VI） was increased with the increase of Cr（Vi） concentrations in terms of GPx, but the effect was not so remarkable. There was not a consistent trend of GPx activities for males in all treatments of Cr（VI）. Cr（VI）-induced changes in antioxidant enzymes were different for SOD, CAT and GPx, of which the tendency was that activities generally changed with increase of concentrations of Cr（VI） suggesting SOD, CAT, and GPx could serve as indices of oxidative stress to some extent.

Effects and Clinical Significance of Pentoxifylline on the Oxidative Stress of Rats with Diabetic Nephropathy

Diabetic nephropathy（DN） is a common and serious clinical complication of diabetes and presently there are no effective ways to prevent its occurrence and progression. Recent studies show that pentoxifylline（PTX） can improve renal hemodynamics, reduce urinary protein excretion, and alleviate or delay renal failure in DN patients. In this study, we focused on the anti-oxidative stress effect of PTX on alleviating renal damages of DN using rat models. DN rats were established with injection of streptozotocin. Blood glucose, urinary protein excretion, serum cystatin C, renal biopsy, superoxide dismutase（SOD） and malondialdehyde（MDA） in serum and renal homogenate and renal nitrotyrosine levels were analyzed before and 12 weeks after the treatment of PTX. Before treatment, all the DN rats had elevated blood glucose, increased urinary protein excretion and elevated serum cystatin C. Morphologically, DN rats exhibited renal tissue damages, including swelling and fusions of foot processes of podocytes under electron microscope. Masson staining revealed blue collagen deposition in glomeruli and renal interstitium. With treatment of PTX, symptoms and renal pathological changes of DN rats were alleviated. Furthermore, the MDA levels were increased and the SOD levels were decreased in the serum and kidneys of DN rats, and these changes were reversed by PTX. The expression of nitrotyrosine was up-regulated in DN rat model and down-regulated by PTX, indicating that PTX was able to inhibit oxidative reactions in DN rats. PTX could alleviate renal damage in DN, which may be attributable to its anti-oxidative stress activity.

Shielding of the geomagnetic field reduces hydrogen peroxide production in human neuroblastoma cell and inhibits the activity of CuZn superoxide dismutase

Accumulative evidence has shown the adverse effects of a geomagnetic field shielded condition, so called a hypomagnetic field （HMF）, on the metabolic processes and oxidative stress in animals and cells. However, the underlying mechanism remains unclear. In this study, we evaluate the role of HMF on the regulation of cellular reactive oxygen species （ROS） in human neuroblastoma SH-SY5Y cells. We found that HMF exposure led to ROS decrease, and that restoring the decrease by additional H2O2 rescued the HMF-enhanced cell proliferation. The measurements on ROS related indexes, including total anti-oxidant capacity, H2O2 and superoxide anion levels, and superoxide dismutase （SOD） activity and expres- sion, indicated that the HMF reduced H2O2 production and inhibited the activity of CuZn-SOD. Moreover, the HMF accelerated the denaturation of CuZn-SOD as well as enhanced aggregation of CuZn-SOD protein, in vitro. Our findings indicate that CuZn-SOD is able to response to the HMF stress and suggest it a mediator of the HMF effect.