Oxidation damage zone formed in creep fatigue crack growth of GH4169 alloy at 650℃

In the creep fatigue crack growth of GH4169 alloy,oxidation is a prominent damage source,which is mainly manifested as the oxidation damage zone in front of crack tip.In order to investigate the property of the oxidation damage zone formed in the creep fatigue crack growth,crack growth tests of directly aged GH4169 alloy were conducted at 650℃ in air under various load conditions.Interrupted tests were performed to observe the damage characteristics at crack tip.Block tests were systematically executed to quantify the dependency of oxidation damage zone size on load and holding time.The crack propagation of the GH4169 alloy has a close relationship with grain boundary oxidation at 650℃.An oxidation damage zone in front of crack tip includes intergranular microcracks and oxidised but uncracked grain boundaries.Its size has been calculated from transient crack growth rate and described as a function of maximum stress intensity factor and holding time.Based on oxidation damage zone size,a novel model has been developed to predict the creep fatigue crack growth rate of the GH4169 alloy at 650℃.

Reduction of the oxidative damage to H_(2)O_(2)-induced HepG2 cells via the Nrf2 signalling pathway by plant flavonoids Quercetin and Hyperoside

Hyperoside and quercetin are similar in molecular structures.In this study,the antioxidant regulatory targets of hyperoside and quercetin are mainly in the nuclear factor(erythroid-2-derived)-related factor 2(Nrf2)pathway predicted by network pharmacology.And the antioxidant effect and mechanism of hyperoside and quercetin were measured and compared in H_(2)O_(2)-induced Hep G2 cells and Caenorhabditis elegans.The findings indicated that quercetin was more effective than hyperoside in reducing oxidative damage,which was proved by improved cell viability,decreased reactive oxygen species(ROS)production,decreased cellular apoptosis,and alleviated mitochondrial damage.In addition,quercetin was more efficient than hyperoside in enhancing the expression of Nrf2-associated m RNAs,increasing the activities of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),and catalase(CAT),and reducing the cellular malondialdehyde(MDA)content.Quercetin was superior to hyperoside in prolonging the lifespan of worms,decreasing the accumulation of lipofuscin,inhibiting ROS production,and increasing the proportion of skn-1 in the nucleus.With the Nrf2 inhibitor ML385,we verified that quercetin and hyperoside primarily protected the cells against oxidative damage via the Nrf2 signalling pathway.Furthermore,molecular docking and dynamics simulations demonstrated that the quercetin-Kelch-like ECH-associated protein 1(Keap1)complex was more stable than the hyperoside-Keap1 complex.The stable structure of the complex might hinder the binding of Nrf2 and Keap1 to release Nrf2 and facilitate its entry into the nucleus to play an antioxidant role.Overall,quercetin had a better antioxidant than hyperoside.

Roles of Aqueous Extract of Marigold on Arsenic-Induced Oxidative Damage in Pancreatic Islet β-Cells

Roles of Marigold extracts (ME) on arsenic trioxide (ATO)-induced oxidative damage to pancreatic β-cells need to be further elucidated. In this study, NIT-1 cells were treated with different concentrations of and/or ATO, following by the cell viability was detected by CCK8 assay. Then, intracellular reactive oxygen species (ROS) levels, lipid peroxide (MDA) contents and superoxide dismutase (SOD) activity were measured with a fluorescence probe method and colorimetric assay, respectively. The apoptosis rate and morphology was detected and observed with hoechst 33,258 staining assay. The mRNA levels and protein expressions of nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were measured by real-time fluorescence quantitative polymerase chain reaction and protein immunoblotting assay, respectively. Our results indicated that Co-treatment with ME and ATO exacerbated the cell viability decreasing reduced by ATO, while the addition of ME after ATO treatment effectively promote the recovery of ATO reduced survival rates. The ATO group increased apoptosis (P P β-cells by modulating the activation of the Nrf2 signaling pathway.

Oxidative stress and lipid peroxidation products:effect of pinealectomy or exogenous melatonin injections on biomarkers of tissue damage during acute pancreatitis

BACKGROUND:Melatonin (N-acetyl-5-methoxytripta-mine) is a free radical scavenger and a strong antioxidant,secreted by the pineal gland.In this study,we evaluated the effects of decreasing and increasing serum melatonin levels on malonyldialdehyde (MDA),superoxide dismutase (SOD),and reduced glutathione (GSH) levels in pancreatic tissue from rats with experimental acute pancreatitis.METHODS:Experimental acute pancreatitis was induced in three groups of Wistar albino rats (10 animals per group) by pancreatic ductal ligation.The first group had only acute pancreatitis and served as the control.Surgical pinealectomy was added to acute pancreatitis in the second group,removing the source of endogenous melatonin (low melatonin levels group).The third group was given 0.1 ml daily intraperitoneal injections of 20 mg/ml melatonin solution for one week (high melatonin levels group).The effects of melatonin levels were evaluated by comparison of the levels of MDA,SOD,and GS in pancreatic tissue.RESULT:We found that intraperitoneal melatonin injections decreased the levels of MDA and increased the levels of SOD and GSH in pancreatic tissue.CONCLUSION:Exogenous melatonin has a preventive effect on lipid peroxidation and oxidative damage in acute pancreatitis.

Estrogen inhibits lipid peroxidation after hypoxic-ischemic brain damage in neonatal rats

Sprague-Dawley neonatal rats within 7 days after birth were used in this study. The left common carotid artery was occluded and rats were housed in an 8% O2 environment for 2 hours to establish a hypoxic-ischemic brain damage model. 17β-estradiol （1 × 10-5 M） was injected into the rat abdominal cavity after the model was successfully established. The left hemisphere was obtained at 12, 24, 48, 72 hours after operation. Results showed that malondialdehyde content in the left brain of neonatal rats gradually increased as modeling time prolonged, while malondialdehyde content of 17β-estrodial-treated rats significantly declined by 24 hours, reached lowest levels at 48 hours, and then peaked at 72 hours after injury. Nicotinamide-adenine dinucleotide phosphate histochemical staining showed the nitric oxide synthase-positive cells and fibers dyed blue/violet and were mainly distributed in the cortex, hippocampus and medial septal nuclei. The number of nitric oxide synthase-positive cells peaked at 48 hours and significantly decreased after 17β-estrodial treatment. Our experimental findings indicate that estrogen plays a protective role following hypoxic-ischemic brain damage by alleviating lipid peroxidation through reducing the expression of nitric oxide synthase and the content of malondialdehyde.

Novel C_(sf)/SiBCN composites prepared by densifying C_(sf)/MA-SiBCN with the PIP process:Oxidation behavior and damage mechanism

To improve the oxidation resistance of short carbon fiber(C_(sf))-reinforced mechanically alloyed SiBCN(MA-SiBCN)(C_(sf)/MA-SiBCN)composites,dense amorphous C_(sf)/SiBCN composites containing both MA-SiBCN and polymer-derived ceramics SiBCN(PDCs-SiBCN)were prepared by repeated polymer infiltration and pyrolysis(PIP)of layered C_(sf)/MA-SiBCN composites at 1100℃,and the oxidation behavior and damage mechanism of the as-prepared C_(sf)/SiBCN at 1300–1600℃ were compared and discussed with those of C_(sf)/MA-SiBCN.The C_(sf)/MA-SiBCN composites resist oxidation attack up to 1400℃ but fail at 1500℃ due to the collapse of the porous framework,while the PIP-densified C_(sf)/SiBCN composites are resistant to static air up to 1600℃.During oxidation,oxygen diffuses through preexisting pores and the pores left by oxidation of carbon fibers and pyrolytic carbon(PyC)to the interior of the matrix.Owing to the oxidative coupling effect of the MA-SiBCN and PDCs-SiBCN matrices,a relatively continuous and dense oxide layer is formed on the sample surface,and the interfacial region between the oxide layer and the matrix of the as-prepared composite contains an amorphous glassy structure mainly consisting of Si and O and an incompletely oxidized but partially crystallized matrix,which is primarily responsible for improving the oxidation resistance.

The action mechanism by which C1q/tumor necrosis factor-related protein-6 alleviates cerebral ischemia/reperfusion injury in diabetic mice

Studies have shown that C1q/tumor necrosis factor-related protein-6 (CTRP6) can alleviate renal ischemia/reperfusion injury in mice. However, its role in the brain remains poorly understood. To investigate the role of CTRP6 in cerebral ischemia/reperfusion injury associated with diabetes mellitus, a diabetes mellitus mouse model of cerebral ischemia/reperfusion injury was established by occlusion of the middle cerebral artery. To overexpress CTRP6 in the brain, an adeno-associated virus carrying CTRP6 was injected into the lateral ventricle. The result was that oxygen injury and inflammation in brain tissue were clearly attenuated, and the number of neurons was greatly reduced. In vitro experiments showed that CTRP6 knockout exacerbated oxidative damage, inflammatory reaction, and apoptosis in cerebral cortical neurons in high glucose hypoxia-simulated diabetic cerebral ischemia/reperfusion injury. CTRP6 overexpression enhanced the sirtuin-1 signaling pathway in diabetic brains after ischemia/reperfusion injury. To investigate the mechanism underlying these effects, we examined mice with depletion of brain tissue-specific sirtuin-1. CTRP6-like protection was achieved by activating the sirtuin-1 signaling pathway. Taken together, these results indicate that CTRP6 likely attenuates cerebral ischemia/reperfusion injury through activation of the sirtuin-1 signaling pathway.

Consilience and unity in ocular anterior segment research

In his beautiful book,Consilience:The Unity of Knowledge,the eminent biologist Edward O Wilson,advocates the need for integration and reconciliation across the sciences.He defines consilience as“literally a‘jumping together’of knowledge with a linking of facts…to create a common groundwork of explanation”.It is the premise of this paper that as much as basic biomedical research is in need of data generation using the latest available techniques–unifying available knowledge is just as critical.This involves the necessity to resolve contradictory findings,reduce silos,and acknowledge complexity.We take the cornea and the lens as case studies of our premise.Specifically,in this perspective,we discuss the conflicting and fragmented information on protein aggregation,oxidative damage,and fibrosis.These are fields of study that are integrally tied to anterior segment research.Our goal is to highlight the vital need for Wilson’s consilience and unity of knowledge which in turn should lead to enhanced rigor and reproducibility,and most importantly,to greater understanding and not simply knowing.

Effects of Imazethapyr-Based Herbicide Formulation in the Zebrafish (Danio rerio) Hepatocyte Cell Line (ZF-L): Cytotoxicity and Oxidative Stress

Seizures of agrochemical formulations have increased in Brazil and Rio Grande do Sul is among the Brazilian states with the highest number of seizures of these products obtained illicitly. The use of illicit formulations can cause significant harm to agricultural production, the environment, and non-target species. This study evaluated the cytotoxicity and oxidative stress of a seized formulation containing the herbicide imazethapyr (IMZT). Characterization of the herbicide included gas chromatography-mass spectrometry (GC-MS) and thermal analyses (thermogravimetric analysis (TGA) and differential scanning calorimetry (DSC)). Hemolytic and cytotoxicity assays in ZF-L hepatic cells showed IC50 values of 12.75 µg/mL, 3.01 µg/mL, 2.67 µg/mL, and 1.61 µg/mL for erythrocytes, [3(4,5-dimethyl)-2 bromide-5 diphenyl tetrazolium] (MTT), neutral red (NR), and lactate dehydrogenase (LDH) assays, respectively. The median IC50 of 2.84 µg/mL was used in oxidative stress assays, revealing increased reactive oxygen species (ROS) production, reduced total sulfhydryl content, and decreased superoxide dismutase (SOD) and catalase (CAT) activity. This study is the first to report in vitro oxidative stress induced by IMZT in the ZF-L cell line, emphasizing the importance of in vitro assays for assessing the toxic effects of seized agrochemicals on human health and the environment.

Abnormal Reactions of Free Radicals and Oxidative Damages in the Bodies of Patients With Chronic Glomerulonephritis

Objective To study the abnormal reactions of a series of free radicals and the oxidative damages induced by free radical abnormal reactions in the bodies of patients with chronic glomerulonephritis. Methods Eighty chronic glomerulonephritis patients (CGNP) and eighty healthy adult volunteers (HAV) were enrolled in a random control study, in which concentrations of nitric oxide (NO) in plasma, lipoperoxides (LPO) in plasma and in erythrocytes, and vitamin C (VC), vitamin E (VE) and beta-carotene (?CAR) in plasma as well as activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined with spectrophotometric assays. Results Compared with the average values of the above biochemical parameters in the HAV group, the average values of NO in plasma, and LPO in plasma and erythrocytes in the CGNP group were significantly increased (P = 0.0001), while those of VC, VE and -CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the CGNP group were significantly decreased (P = 0.0001). Pearson product-moment correlation analysis showed that with increase of the concentration of blood creatinine as well as prolongation of the course of disease in the CGNP, the concentrations of NO in plasma, and LPO in plasma and erythrocytes in the CGNP increased gradually, while the concentrations of VC, VE and ?CAR in plasma as well as the activities of SOD, CAT and GPX in erythrocytes in the CGNP decreased gradually (P = 0.002454 0.000001). The relative risk ratio (RR) of the above biochemical parameters reflecting oxidative damages in the bodies of CGNP ranged from 6.061 to 72.429. The reliability coefficient (alpha) that the above biochemical parameters were used to reflect the oxidative damages of the CGNP was 0.8137, standardized item alpha = 0.9728, Hotelling抯 T-Squared = 1135680.191, F = 53274.6478, P = 0.000001. Conclusions The findings in this study show that in the bodies of CGNP a series of free radical chain reactions result in severe pathological aggravation and induce oxidative damages in their bodies. Therefore, suitable dose of antioxidants should be supplemented to them so as to alleviate oxidative damages in their bodies.

Increased oxidative stress and oxidative damage associated with chronic bacterial prostatitis

Aim： To investigate whether chronic bacterial prostatitis might increase oxidative stress and oxidative damage in chronic bacterial prostatitis patients （CBPP）, and to explore its possible mechanism. Methods： Enrolled in a casecontrol study were 70 randomly sampled CBPP and 70 randomly sampled healthy adult volunteers （HAV）, on whom plasma nitric oxide （NO）, vitamin C （VC）, vitamin E （VE） and β-carotene （β-CAR） level, erythrocyte malondialdehyde （MDA） level, as well as erythrocyte superoxide dismutase （SOD）, catalase （CAT） and glutathione peroxidase （GPX） activities were determined by spectrophotometry. Results： Compared with the HAV group, values of plasma NO and erythrocyte MDA in the CBPP group were significantly increased （P 〈 0.001）; those of plasma VC, VE and β-CAR as well as erythrocyte SOD, CAT and GPX activities in the CBPP group were significantly decreased （P 〈 0.001）. Findings from partial correlation for the 70 CBPP showed that with prolonged course of disease, values of NO and MDA were gradually increased （P 〈 0.001）, and those of VC, VE, β-CAR, SOD, CAT and GPX were gradually decreased （P 〈 0.05- 0.001）. The findings from stepwise regression for the 70 CBPP suggested that the model was Y= -13.2077 ＋ 0.1894MDA ＋ 0.0415NO - 0.1999GPX, F = 18.2047, P 〈 0.001, r = 0.6729, P 〈 0.001. Conclusion： The findings suggest that there exist increased oxidative stress and oxidative damage induced by chronic bacterial prostatitis in the patients, and such phenomenon was closely related to the course of disease.

Dietary resveratrol attenuation of intestinal inflammation and oxidative damage is linked to the alteration of gut microbiota and butyrate in piglets challenged with deoxynivalenol

Background:Deoxynivalenol(DON)is a widespread mycotoxin that induces intestinal inflammation and oxidative stress in humans and animals.Resveratrol(RES)effectively exerts anti-inflammatory and antioxidant effects.However,the protective effects of RES on alleviating DON toxicity in piglets and the underlying mechanism remain unclear.Therefore,this study aimed to investigate the effect of RES on growth performance,gut health and the gut microbiota in DON-challenged piglets.A total of 64 weaned piglets[Duroc×(Landrace×Yorkshire),21-d-old,6.97±0.10 kg body weight(BW)]were randomly allocated to 4 treatment groups(8 replicate pens per treatment,each pen containing 2 males;n=16 per treatment)for 28 d.The piglets were fed a control diet(CON)or the CON diet supplemented with 300 mg RES/kg diet(RES group),3.8 mg DON/kg diet(DON)or both(DON+RES)in a 2×2 factorial design.Results:DON-challenged piglets fed the RES-supplemented diet had significantly decreased D-lactate concentrations and tumor necrosis factor alpha(TNF-α)and interleukin 1 beta(IL-1β)mRNA and protein expression,and increased zonula occludens-1(ZO-1)mRNA and protein expression compared with those of DON-challenged piglets fed the unsupplemented diet(P<0.05).Compared with unsupplemented DON-challenged piglets,infected piglets fed a diet with RES showed significantly decreased malondialdehyde(MDA)levelsand increased mRNA expression of antioxidant enzymes and antioxidant genes(i.e.,GCLC,GCLM,HO-1,SOD1 and NQO-1)and glutamatecysteine-ligase modulatory subunit(GCLM)protein expression(P<0.05).Moreover,RES supplementation significantly abrogated the increase in the proportion of TUNEL-positive cells and the protein expression of caspase3 in DON-challenged piglets(P<0.05).Finally,RES supplementation significantly increased the abundance of Roseburia and butyrate concentrations,while decreasing the abundances of Bacteroides and unidentified-Enterobacteriaceae in DON-challenged piglets compared with DON-challenged piglets alone(P<0.05).Conclusions:RES supplementation improved gut health in DON-challenged piglets by strengthening intestinal barrier function,alleviating intestinal inflammation and oxidative damage,and positively modulating the gut microbiota.The protective effects of RES on gut health may be linked to increased Roseburia and butyrate concentrations,and decreased levels of Bacteroides and unidentified-Enterobacteriaceae.

Ozone Emitted During Copying Process-A Potential Cause of Pathological Oxidative Stress and Potential Oxidative Damage in the Bodies of Operators

To estimate the impact of copying on the indoor air quality, and to investigate whether ozone emitted during such a process induces pathological oxidative stress and potential oxidative damage in the bodies of operators. Methods 67 copying operators (CO) and 67 healthy volunteers (HV) were enrolled in a random control study, in which levels of lipoperoxide (LPO) in plasma and erythrocytes, and levels of vitamin C (VC), vitamin E (VE) and b-carotene (b-CAR) in plasma as well as activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) in erythrocytes were determined by spectrophotometric methods. Results Compared with the HV group, the average values of LPO in plasma and erythrocytes in the CO group were significantly increased (P<0.0001), while those of VC, VE and b-CAR in plasma as well as those of SOD, CAT and GPX in erythrocytes in the CO group were significantly decreased (P<0.0001). Pearson product-moment correlation analysis showed that with increase of ozone level in copying sites and duration of exposure to ozone, the values of LPO in plasma and erythrocytes in the bodies of operators were gradually increased,while those of VC, VE, b-CAR, SOD, CAT and GPX were decreased in the same manner. Odds ratio (OR) of risk of biochemical parameters reflecting potential oxidative damage of the copying operators ranged from 4.440 to 13.516, and 95 % CI of OR was from 2.113 to 34.061. Reliability coefficient () of the biochemical parameters used to reflect the potential oxidative damage of the operators was 0.8156, standardized item =0.9929, P<0.0001. Conclusion Findings in the present study suggest that there exist a series of free radical chain reactions and pathological oxidative stress induced by high dose ozone in the operators, thereby causing potential oxidative and lipoperoxidative damages in their bodies.

An Investigation of Oxidative DNA Damage in Pharmacy Technicians Exposed to Antineoplastic Drugs in Two Chinese Hospitals Using The Urinary 8-OHdG Assay

Objective To investigate oxidative DNA damage in pharmacy technicians preparing antineoplastic drugs at the PIVAS （Pharmacy Intravenous Admixture Service） in two Chinese hospitals. Methods Urinary 8-OHdG served as a biomarker. 5-Fluorouracil （5-FU） concentrations in air, masks and gloves were determined. The spill exposure of each PIVAS technician to antineoplastic drugs was investigated. Eighty subjects were divided into exposed group t, II, and control group I, II. Results 5-FU concentration ratios for gloves and masks in exposed group I were significantly higher than those in exposed group II （P〈0.05 or P〈0.01）. The average urinary 8-OHdG concentrations in exposed group I, control group I, exposed group II, and control group II were 24.69＋0.93, 20.68＋1.07, 20.57＋0.55, and 12.96_＋0.73 ng/mg Cr, respectively. Urinary 8-OHdG concentration in exposed group I was significantly higher than that in control group I or that in exposed group 11 （P〈0.02）. There was a significant correlation between urinary 8-OHdG concentrations and spill frequencies per technician （P〈0.01）. Conclusion There was detectable oxidative DNA damage in PIVAS technicians exposed to antineoplastic drugs. This oxidative DNA damage may be associated with their spill exposure experience and contamination of their personal protective equipment.

Comparison of the protective effects of resveratrol and pterostilbene against intestinal damage and redox imbalance in weanling piglets

Background: Evidence indicates that early weaning predisposes piglets to intestinal oxidative stress and increases the risk of intestinal dysfunction;however, there are minimal satisfactory treatment strategies for these conditions.This study investigated the potential of resveratrol and its analog, pterostilbene, as antioxidant protectants for regulating intestinal morphology, barrier function, and redox status among weanling piglets.Methods: A total of 144 piglets were selected at 21 days of age and randomly allocated into one of four treatment groups, each of which included six replicates. Piglets in a sow-reared control group were suckling normally between ages 21 and 28 days, while those in weaned groups were fed a basal diet, supplemented with either 300 mg/kg of resveratrol or with 300 mg/kg of pterostilbene. Parameters associated with intestinal injury and redox status were analyzed at the end of the feeding trial.Results: Early weaning disrupted the intestinal function of young piglets, with evidence of increased diamine oxidase activity and D-lactate content in the plasma, shorter villi, an imbalance between cell proliferation and apoptosis, an impaired antioxidant defense system, and severe oxidative damage in the jejunum relative to suckling piglets. Feeding piglets with a resveratrol-supplemented diet partially increased villus height(P = 0.056) and tended to diminish apoptotic cell numbers(P = 0.084) in the jejunum compared with those fed a basal diet. Similarly, these beneficial effects were observed in the pterostilbene-fed piglets. Pterostilbene improved the feed efficiency of weanling piglets between the ages of 21 and 28 days;it also resulted in diminished plasma diamine oxidase activity and D-lactate content relative to untreated weaned piglets(P < 0.05). Notably, pterostilbene restored jejunal antioxidant capacity, an effect that was nearly absent in the resveratrol-fed piglets. Pterostilbene reduced the malondialdehyde and 8-hydroxy-2′-deoxyguanosine contents of jejunal mucosa possibly through its regulatory role in facilitating the nuclear translocation of nuclear factor erythroid-2-related factor 2 and the expression levels of NAD(P)H quinone dehydrogenase 1 and superoxide dismutase 2(P < 0.05).Conclusions: The results indicate that pterostilbene may be more effective than its parent compound in alleviating early weaning-induced intestinal damage and redox imbalance among young piglets.

Effect of methylmercury on some neurotransmitters and oxidative damage of rats

In order to study the molecular mechanism of injury in rat organs induced by methylmercury, and the relationship between neurotransmitter and oxidative damage in the toxicity process of rat injury by methylmercury was studied. The control group was physiological saline of 0.9%, the concentration of exposure groups were 5 mg/(kg5d) and 10 mg/(kg5d) respectively. The content of AChE, ACh, NOS, NO, MDA, SOD, GSH-Px and GSH in different organs of rats were determined with conventional methods. The results showed that after exposure to methylmercury for 7 d, the mercury content in brain of exposure groups increased clearly and had significant difference compared with the control group(P<0.01). In rat's brain, serum, liver and kidney, the content of ACh and AChE were all decreased; the content of NOS and NO were all increased; the content of MDA was increased compared with the control group, the exposure groups had significant difference (P<0.01); the content of SOD, GSH and GSH-Px was decreased compared with the control group, the exposure groups had significant difference(P<0.01). It could be concluded that methylmercury did effect the change of neurotransmitter and free radical. They participated in the toxicity process of injury by methylmercury. The damage of neurotransmitter maybe cause the chaos of free radical and the chaos of free radical may also do more damage to neurotransmitter vice versa.

Putrescine Plays a Positive Role in Salt-Tolerance Mechanisms by Reducing Oxidative Damage in Roots of Vegetable Soybean

Polyamines play important roles in plant tolerance to environmental stress. With the aim of investigating the possible involvement of putrescine （Put） in salt-tolerance mechanisms in vegetable soybean roots, exogenous Put （10 mmol L＂） and its biosynthetic inhibitor D-arginine （D-Arg） （0.5 mmol L-1） were added to nutrient solution when vegetable soybean （Glycine max L. cv. Huning 95-1） seedlings were exposed to 100 mmol L^-11 sodium chloride （NaCl）. The results showed that Put ameliorated but D-Arg aggravated the detrimental effects of NaCl on plant growth and biomass production. Under NaCl stress, levels of free, soluble conjugated and insoluble bound types of Put in roots of vegetable soybean were reduced, whereas those of free, soluble conjugated, and insoluble bound types of spermidine （Spd） and spermine （Spm） were increased. Exogenous Put eliminated the decrease in Put but promoted the increase of Spd and Spm. However, these changes could be reversed by D-Arg. Under NaCl stress, activities of arginine decarboxylase （ADC）, S-adenosylmethionine decarboxylase （SAMDC）, diamine oxidase （DAO）, and polyamine oxidase （PAO） were induced, with exogenous Put promoting and D-Arg reversing these changes. Furthermore, NaCl stress decreased activities of antioxidant enzymes. Exogenous Put alleviated but D-Arg exaggerated these effects of NaCl stress, resulting in the same changes in membrane damage and reactive oxygen species （ROS） production. These results indicated that Put plays a positive role in vegetable soybean roots by activating antioxidant enzymes and thereby attenuating oxidative damage.

Increased Oxidative Stress and Damage in Patients With Chronic Bacterial Prostatitis

Objective To investigate whether chronic bacterial prostatitis （CBP） increases oxidative stress and damage in patients with CBP, and to explore its possible mechanism. Methods Eighty patients with CBP and 80 healthy adults as controls were enrolled in a case-control study, in which levels of nitric oxide （NO）, vitamin C （VC）, and vitamin E （VE） in plasma, as well as malondialdehyde （MDA）, activities of superoxide dismutase （SOD）, and eatalase （CAT） in erythrocytes were determined by spectrophotometry. Results Compared with the average values of NO, VC, VE, MDA, SOD, and CAT in the healthy control group, those of plasma N O and erythrocyte MDA in the CBP group were significantly increased （P〈0.00 1）, and those of plasma VC and VE as well as erythrocyte SOD and CAT in the CBP group were significantly decreased （P〈0.001）. Findings from partial correlation analysis for course of the disease and NO, VC, VE, MDA, SOD, and CAT in 80 patients with CBP, adjusted for age, suggested that with prolonged course of the disease, values of NO and MDA were gradually increased （P〈0.001）, and those of VC, VE, SOD, and CAT were gradually decreased （P〈0.05-0.001）. The findings from stepwise regression analysis for course of the disease and NO, VC, VE, MDA, SOD, and CAT in CBP group suggested that the model of stepwise regression was Y = -19.1160 ＋0.3112MDA ＋ 0.0337NO, F = 22.1734, P〈0.001, r = 0.6045, P〈0.001. The findings from the reliability analysis for VC, VE, SOD, CAT, NO, and MDA in the CBP group showed that the reliability coefficients＇ alpha （6 items） was 0.7195, P〈0.0001, and the standardized item alpha was 0.9307, P〈0.0001. Conclusion There exist increased oxidative stress and damage induced by chronic bacterial prostatitis in patients, and such a phenomenon is closely related to the course of disease.

Oxidative Damage to Lung Tissue and Peripheral Blood in Endotracheal PM_(2.5)-treated Rats

Objective To investigate the oxidative damage to lung tissue and peripherial blood in PM2.5-treated rats. Methods PM2.5 samples were collected using an auto-sampling instrument in summer and winter. Treated samples were endotracheally instilled into rats. Activity of reduced glutathione peroxidase （GSH-Px） and concentration of malondialdehyde （MDA） were used as oxidative damage biomarkers of lung tissue and peripheral blood detected with the biochemical method. DNA migration length （μm） and rate of tail were used as DNA damage biomarkers of lung tissue and peripheral blood detected with the biochemical method. Results The activity of GSH-Px and the concentration of MDA in lung tissue significantly decreased after exposure to PM2.5 for 7-14 days. In peripheral blood, the concentration of MDA decreased, but the activity of GSH-Px increased 7 and 14 days after experiments. The two indicators had a dose-effect relation and similar changing tendency in lung tissue and peripheral blood. The DNA migration length （μm） and rate of tail in lung tissue and peripheral blood significantly increased 7 and 14 days after exposure to PM2.5. The two indicators had a dose-effect relation and similar changing tendency in lung tissue and peripheral blood. Conclusion PM2.5 has a definite oxidative effect on lung tissue and peripheral blood. The activity of GSH-Px and the concentration of MDA are valuable biomarkers of oxidative lung tissue damage induced by PM2.5. The DNA migration length （μm） and rate of tail are simple and valuable biomarkers of PM2 5-induced DNA damage in lung tissues and peripheral blood. The degree of DNA damage in peripheral blood can predict the degree of DNA damage in lung tissue.