人锰超氧化物歧化酶(hMn-SOD)的研究进展

人锰超氧化物歧化酶（ｈＭｎ－ＳＯＤ）是线粒体基质酶，其基因是诱导表达的。作为细胞内氧自由基的清除剂，具有抗衰老、提高细胞对氧应激反应的耐受性及抑制肿瘤发生等方面的作用。文章从ｈＭｎ－ＳＯＤ的结构、理化性质、分子生物学研究、与衰老、肿瘤的相关性及其临床应用等方面对其进行近期研究成果和未来发展趋势进行了综述。

高氧、维甲酸对胎鼠肺成纤维细胞c-Jun、c-Fos表达的影响

目的 探讨维甲酸对高氧暴露下胎鼠肺成纤维细胞 c- Jun、c- Fos表达的影响。方法 取第 2代胎鼠肺成纤维细胞作体外培养 ,待生长至接近融合状态时 ,随机分为 :空气组 ,空气 +维甲酸组 ,高氧组 ,高氧 +维甲酸组。于培养30 m in和 1、 2、 6、 12、 2 4、 4 8、 72 h时 ,行细胞固定后 ,应用免疫组化方法检测 c- Jun、c- Fos表达强度并结合计算机图像处理系统进行分析。结果 与空气组相比 ,高氧 1h时 c- Jun表达明显增强 (P<0 .0 1) ,6～ 12 h时达高峰 ,以后开始下降 ,但仍高于正常水平 (P<0 .0 1) ;c- Fos的表达在高氧 30 m in即增强 (P<0 .0 1) ,2～ 6 h达高峰 ,以后开始下降 ,2 4 h后恢复到正常水平。维甲酸能明显下调高氧所诱导的 c- Jun、c- Fos高表达 ,但并不能完全阻止 c- Jun、c- Fos的过度表达。结论 c- Jun、c- Fos可能参与了高氧暴露下胎鼠肺成纤维细胞的信号转导过程 ;维甲酸可部分抑制由高氧所诱导的 c- Jun、 c-

氧应激反应与抗氧药物

氧是人正常代谢必需的成分，在人体中，需要用氧产生能量以驱动人体内很多反应以维持生命，但在代谢过程中，会产生一些能损坏细胞的自由基，自由基是带有电荷的分子，是在有氧代谢中产生的氧活性基团，如超氧阴离子（O2^-），羟基基团（OH）及过氧化氢（H2O2）等。这些自由基能攻击细胞，使细胞结构破坏，功能丧失，并最后摧毁细胞，这种情况，总称之为氧应激反应。

腹腔氢气和饱和氢盐水对家兔心肌缺血再灌注损伤及超微结构的影响

目的探讨腹腔氢气和静脉饱和氢盐水对家兔心肌缺血/再灌注损伤及心肌超微结构的影响。方法将40只家兔麻醉开胸随机分为假手术组(A组)、模型对照组(B组)、腹腔氢气组(C组)和饱和氢盐水组(B组)各10只。假手术组冠脉穿线不结扎,余3组冠脉结扎60min后再灌注同时,B组5只腹腔氧气10mL/kg一次性注入,5只静脉生理盐水10mL/kg10min泵入,C组腹腔氢气10mL/kg10min注入;D组静脉饱和氢盐水10mL/kg泵入。B组、C组D组均再灌480min。结果 A组、C组、D组超氧化物歧化酶(SOD)明显高于B组,但A组、C组、D组间两两比较差异无统计学意义(P>0.05);A组、C组、D组抑制羟自由基能力明显大于B组。电镜和Tunnul监测显示:A组、C组、D组细胞凋亡数明显少于B组,心肌结构相对完整,线粒体细胞核损伤较小,仅见少量溶酶体无自噬体,而B组心肌组织破坏严重细胞膜线粒体脊融合断裂较重,形成空泡部分溶酶体空泡形成,可见多个自噬体。结论两种给氢方法均能保护缺血再灌注损伤,这种保护作用与H_2清除自由基抗炎、抗凋亡有关。腹腔氢气较静脉氢盐水应用方便效果更佳。

多器官功能障碍评分系统:3个评分标准预测多器官功能障碍综合征结局关联性和准确性的比较与评估

目的研究高原急性呼吸窘迫综合征(HARDS)/多器官功能障碍综合征(MODS)各项诊断指标参数的变化特点,比较3个MODS评分标准预测结局的准确性。方法统一按通用的MODS诊断标准将540例ARDS/MODS患者按海拔高度分为平原对照组(CG,<430m,n=113)、中度高原1组(H1G,1517m,n=314)、中度高原2组(H2G,2261～2400m,n=78)和高原组(HG,2808～3400m,n=35)。4组分别用平原地区ARDS/MODS评分诊断标准(庐山会议评分标准和Marshall评分标准)以及兰州修订的HARDS/MODS评分标准(兰州标准),建立3个标准的数据统计模型,分别绘制受试者运行特征性曲线(ROC曲线),计算约登指数(Yoden)和最佳界值,验证3个标准在不同海拔高度预测ARDS/MODS结局的准确性;用向前逐步回归模式对影响MODS结局的多因素进行分析。结果用庐山、Marshall和兰州标准检验平原和高原不同海拔高度MODS总分的ROC曲线下面积,预测结局的敏感度、特异度及其最佳界值,结果显示,随海拔梯度上升,兰州标准明显优于庐山和Marshall标准,多元Logistic回归分析也以兰州标准的影响因素最大。结论1通用的ARDS/MODS诊断标准中某些参数界值可能不适合中度高原以上地区,建立HARDS/MODS标准是必要的,兰州标准随海拔梯度升高有进一步提高预测准确性的趋势。2海拔高度大于1500m以上地区?

Endurance exercise and gut microbiota:A review

Background: The physiological and biochemical demands of intense exercise elicit both muscle-based and systemic responses. The main adaptations to endurance exercise include the correction of electrolyte imbalance, a decrease in glycogen storage and the increase of oxidative stress, intestinal permeability, muscle damage, and systemic inflammatory response. Adaptations to exercise might be influenced by the gut microbiota, which plays an important role in the production, storage, and expenditure of energy obtained from the diet as well as in inflammation,redox reactions, and hydration status.Methods: A systematic and comprehensive search of electronic databases, including MEDLINE, Scopus, Clinical Trials.gov, Science Direct,Springer Link, and EMBASE was done. The search process was completed using the keywords: "endurance", "exercise", "immune response","microbiota", "nutrition", and "probiotics".Results: Reviewed literature supports the hypothesis that intestinal microbiota might be able to provide a measureable, effective marker of an athlete's immune function and that microbial composition analysis might also be sensitive enough to detect exercise-induced stress and metabolic disorders. The review also supports the hypothesis that modifying the microbiota through the use of probiotics could be an important therapeutic tool to improve athletes' overall general health, performance, and energy availability while controlling inflammation and redox levels.Conclusion: The present review provides a comprehensive overview of how gut microbiota may have a key role in controlling the oxidative stress and inflammatory responses as well as improving metabolism and energy expenditure during intense exercise.

Effects of phosphate precursors on morphology and oxygen evolution reaction activity of NiFe(oxy)hydroxide on nickel foams

NiFe(oxy)hydroxides nanosheets were synthesized on nickel foams via co-precipitation and electrochemical activation. It is found that the phosphate precursors(Na_(3)PO_(4), Na_(2)HPO_(4)and NaH_(2)PO_(4)) have diverse effects on the morphology and thus the oxygen evolution reaction activity of the formed final catalysts. The resulting NiFe(oxy)hydroxides nanosheets prepared with Na_(2)HPO_(4)demonstrate a low overpotential of 205 m V to achieve a current density of 50 mA/cm^(2) with a Tafel slope down to 30 mV/dec in 1 mol/L KOH, and remain stable for 20 h during stability test.

Tissue-specific bioaccumulation and oxidative stress responses in juvenile Japanese flounder (Paralichthys olivaceus) exposed to mercury

To understand mercury （Hg） toxicity in marine fish, we measured Hg accumulation in juvenile Japanese flounder （Paralichthys olivaceus） and assessed the effects on growth and antioxidant responses. After Hg exposure （control, 5, 40, and 160 gg/L Hg） for 28 d, fish growth was significantly reduced. The accumulation of Hg in fish was dose-dependent and tissue-specific, with the maximum accumulation in kidney and liver, followed by gills, hone, and muscle. Different antioxidants responded differently to Hg exposure to cope with the induction of lipid peroxidation （LPO）, which was also tissue-specific and dose- dependent. As Hg concentration increased, superoxide dismutase （SOD） and catalase （CAT） activities increased significantly, whereas glutathione S-transferase （GST） activity and glutathione （GSH） levels decreased significantly in the gills. SOD and glutathione peroxidase （GPx） activities and the GSH level increased significantly in the liver. SOD activity and GSH levels increased significantly, but CAT activity decreased significantly with an increase in Hg concentration in the kidney. LPO was induced significantly by elevated Hg in the gills and kidney but was least affected in the liver. Therefore, oxidative stress biomarkers in gills were more sensitive than those in the liver and kidney to Hg exposure. Thus, the gills have potential as bioindicators for evaluating Hg toxicity in juvenile flounder.

Oxidative stress responses of submerged macrophyte Vallisneria asiatica to different concentrations of cyanobacteria

In a 10-day aquarium experiment, this investigation examines macrophyte restoration in eutrophic Lake Taihu, the physiological effects of different plant biomass levels and of increasing natural cyanobacterial concentrations on a submerged macrophyte, Vallisneria asiatica. Cyanobacterial stress suppressed the superoxide dismutase （SOD） activity of the plant＇s leaves and induced the catalase （CAT） and peroxidase （POD） activities of its roots. The soluble protein content in V. asiatica decreased with an increase in natural cyanobacterial concentrations, whereas the malonaldehyde （MDA） increased significantly at chlorophyll a （Chl a） concentrations of 222 and 262 μg/L in water. V. asiatica adapted to the stress caused by cyanobacterial concentrations by adjusting its antioxidant defense system to remove the excessive reactive oxygen species when the algal Chl a concentration was 〉109 μg/L. Additionally, high biomass of V. asiatica （2 222 g FW/m^2） can inhibit the reproduction of cyanobacteria more significantly than low biomass （1 111 g FW/m^2）. High biomass of V. asiatica increased the oxidative stress in an individual plant when the initial Chl a concentration in the water reached 222 and 262 μg/L, as expressed by the increased MDA in leaves, compared with low biomass of K asiatica. This provides a basis for controlling cyanobacterial concentrations and V. asiatica biomass for the recovery of V. asiatica in eutrophic Lake Taihu.

A tetragonal tungsten bronze-type photocatalyst:Ferro-paraelectric phase transition and photocatalysis

Although ferroelectrics have potential applications in photocatalysis due to their highly efficient charge separation, their mechanism of charge separation is still unknown. A ferroelectric Sr0.7Ba0.3Nb2O6 （SBN‐70） semiconductor with a low ferro‐paraelectric phase transition （65℃） was studied. The photocatalytic activity for H2 production by ferroelectric and paraelectric SBN‐70 was examined. The spontaneous polarization in the ferroelectric phase strongly affected the photocata‐lytic performance and parallel ferroelectric domains significantly promoted photogenerated charge separation to result in better photocatalytic H2 production. This knowledge provides an important basis for the fabrication of ferroelectric photocatalysts with improved charge separation ability.

Silver Nanoparticles Synthesized by Laser Ablation in Acetone： Influence of Ablation Time and Their Reactivity with Oxygen in the Air

In this work, a method is proposed to control silver nanoparticle dimensions produced by laser ablation varying the ablation time and introducing a sonication phase between ablation and the successive deposition on the substrate. The absorption spectra during laser ablation show a main band, which identifies the dimensions of main particles. The appearance of secondary bands indicates the beginning of an aggregation process with the formation of a small concentration of particles which are spheroid in shape. SEM （secondary electron microscope） images of particle produced with different ablation times confirm the results of absorption measurements. X-ray photoelectron spectroscopy and cathodo-luminescence spectroscopy indicate a high reactivity of the nanoparticles deposited on a substrate. They react with oxygen in the air forming an oxide layer which reveals a luminescence in the blue region.

慢性低压低氧对大鼠心肌组织COX-1蛋白及ROS、SOD和CAT水平的影响

目的:本文主要探讨高原低氧对心肌损伤是否通过氧化应激反应机制。方法:将85只大鼠分为高原组和平原组,高原组在海拔4 300m的地区喂养30天,然后取标本。用ELISA方法测量血清或血浆中HIF(低氧诱导因子)、ROS(活性氧)、SOD(超氧化物歧化酶)和CAT(过氧氢酶)的水平,并用West blot方法测定COX-1蛋白表达水平。结果:相比平原组、高原组大鼠血清中HIF-1明显升高,ROS水平显著下降,P<0.000 1,SOD和CAT水平不变或略低,但没有显著性差异;心肌组织中COX-1蛋白表达明显下降,P<0.05。电镜表明心肌细胞线粒体数量减少,水肿,甚至出现结构的破坏。结论:慢性低氧并非通过氧化应激反应引起组织损伤,而是直接性损伤线粒体。

低压缺氧对大鼠脑皮质基因表达谱及其TAC1和MT1A变化的影响

暴露于急性缺氧环境会发生缺氧应激反应，过强的缺氧应激反应可导致机体各种功能出现衰竭，机体的神经系统、呼吸系统、循环系统等会受到不同程度的损伤，从而引起机体一系列功能、代谢和结构的病理生理学改变，最终导致心、脑等重要脏器由于能量供应不足而死亡。

Effects of 60-day NO_2 fumigation on growth,oxidative stress and antioxidative response in Cinnamomum camphora seedlings

Objective： To study the oxidative stress and antioxidative response of Cinnamomum camphora seedlings exposed to nitrogen dioxide （NO2） fumigation. Methods： Measurements were made up of the growth, chlorophyll content, chlorophyll fluorescence, antioxidant system and lipid peroxidation of one-year-old C. camphora seedlings exposed to NO2 （0.1, 0.5, and 4 μl/L） fumigation in open top chambers over a period of 60 d. Results： After the first 30 d, 0.5 and 4.0 μl/L NO2 showed insignificant effects on the growth of C. camphora seedlings. However, exposure to 0.5 and 4.0 pilL NO2 for 15 d significantly reduced their chlorophyll content （P〈0.05）, enhanced their malondialdehyde （MDA） content and superoxide dismutase （SOD） activity （P〈0.05）, and also significantly reduced the maximal quantum yield of PSII in the dark [the ratio of variable fluorescence to maximal fluorescence （Fv/Fm）] （P〈0.05）. In the latter 30 d, 0.5μl/L NO2 showed a positive effect on the vitality of the seedlings, which was reflected by a recovery in the ratio of Fv/Fm and chlorophyll content, and obviously enhanced growth, SOD activity, ascorbate （AsA） content and glutathione reductase （GR） activity （P〈0.05）; 4.0 pilL NO2 then showed a negative effect, indicated by significant reductions in chlorophyll content and the ratio of Fv/Fm, and inhibited growth （P〈0.05）. Conclusion： The results suggest adaptation of C. camphora seedlings to 60-d exposure to 0.1 and 0.5 μl/L NO2, but not to 60-d exposure to 4.0 pilL NO2 C. camphora seedlings may protect themselves from injury by strengthening their antioxidant system in response to NO2-induced oxidative stress.

Scavenging activity and mechanism study of ferulic acid against reactive carbonyl species acrolein

Acrolein,known as one of the most common reactive carbonyl species,is a toxic small molecule affecting human health in daily life.This study is focused on the scavenging abilities and mechanism of ferulic acid and some other phenolic acids against acrolein.Among the 13 phenolic compounds investigated,ferulic acid was found to have the highest efficiency in scavenging acrolein under physiological 8nditions.Ferulic acid remained at(3.04±1.89)%and acrolein remained at(29.51±4.44)%after being incubated with each other for 24 h.The molecular mechanism of the detoxifying process was also studied.Detoxifying products,namely 2-methoxy-4-vinyIphenol(product 21)and 5-(4-hydroxy-3-methoxyphenyl)pent-4-enal(product 22),were identified though nuclear magnetic resonanee(NMR)and gas chromatography-mass spectrometry(GC-MS),after the scavenging process.Ferulic acid showed significant activity in scavenging acrolein under physiological conditions.This study indicates a new method for inhibiting damage from acrolein.

Effects of Polysaccharides Extracted from Zhu Zi Shen(Rhizoma Panacis Majoris) on Oxidative Stress and Hemodynamics in Rats with Adriamycin-induced Chronic Heart Failure

Objective:To probe into the intervening action of polysaccharides of Zhu Zi Shen(Rhizoma Panacis Majoris)(PZZS) on oxidative stress and hemodynamics in rats with adriamycin-induced chronic congestive heart failure(CHF).Methods:After SD rats were successfully modeled with adriamycin,they were randomly divided into a normal control group,a model group,a PZZS group,and a captopril group,and were administrated respectively.At the end of experiment,the hemodynamic function,whole heart weight index,and the blood CK,SOD,MDA,NO,NOS were detected;and the myocardial morphological examinations were carried out.Results:Compared with the normal control group,the arterial systolic pressure(SBP),diastolic pressure(DBP),mean arterial pressure(MAP),heart rate(HR),left ventricular systolic peak(LVSP),and left ventricular pressure change rate(dp/dtmax) significantly decreased,and left ventricular end diastolic pressure(LVEDP),whole heart weight index,the blood CK,MDA,NO,NOS significantly increased in the model group.PZZS significantly improved the hemodynamic function,lowered the MDA and NO levels,and decreased the CK and NOS activities in the CHF rats.Conclusion:PZZS can improve the hemodynamic function,and alleviate the oxidative stress reaction in the CHF rat.

Activation of STAT3 stimulates AHSP expression in K562 cells

Studies on the chaperone protein α-hemoglobin stabilizing protein （AHSP） reveal that abundant AHSP in erythroid cells en-hance the cells＇ tolerance to oxidative stress imposed by excess a-hemoglobin in pathological conditions. However, the poten-tial intracellular modulation of AHSP expression itself in response to oxidative stress is still unknown. The present study ex-amined the effect and molecular mechanism of STAT3, an oxidative regulator, on the expression of AHSP. AHSP expression increased in K562 cells upon cytokine IL-6-induced STAT3 activation and decreased in STAT3 knock-down K562 cells. Reg-ulation of AHSP in oxidative circumstance was then examined in α-globin-overloaded K562 cells, and real-time PCR showed strengthened expression of both AHSP and STAT3. ChIP analysis showed binding of STAT3 to AHSP promoter and binding was significantly augmented with IL6 stimulation and upon α-globin overexpression. Dual luciferase reporter assays of the wildtype and mutated SB3 element, an IL-6RE site, in the AHSP promoter in K562 cells highlighted the direct regulatory ef-fect of STAT3 on AHSP gene. Finally, direct binding of STAT3 to SB3 site of AHSP promoter was confirmed with EMSA as-says. Our work reveals an adaptive AHSP regulation mediated by the redox-sensitive STAT3 signaling pathway, and provides clues to the therapeutic strategy for AHSP enhancement.

Knockdown of OLA1,a regulator of oxidative stress response,inhibits motility and invasion of breast cancer cells

To explore the role of a novel Obg-like ATPase 1 （OLA1） in cancer metastasis, small interference RNA （siRNA） was used to knockdown the protein, and the cells were subjected to in vitro cell migration and invasion assays. Knockdown of OLA 1 significantly inhibited cell migration and invasion in breast cancer cell line MDA-MB-231. The knockdown caused no changes in cell growth but affected ROS production. In wound-healing assays, decreased ROS in OLA1-knockdown cells were in situ asso- ciated with the cells＇ decreased motile morphology. Further, treatment ofN-acetylcysteine, a general ROS scavenger, blunted the motility and invasiveness of MDA-MB-231 cells, similar to the effect of OLAl-knockdown. These results suggest that knock- down of OLA1 inhibits breast cancer cell migration and invasion through a mechanism that involves the modulation of intracellular ROS levels.

Telomeres,cardiovascular aging,and potential intervention for cellular senescence

A consistent association has been observed between leukocyte telomere length(LTL)and atherosclerosis,but the mechanisms underlying these associations are still not well understood.Premature biology aging was evident in atherosclerotic plaques,characterized by reduced cell proliferation,irreversible growth arrest and apoptosis,and telomere attrition.As atherosclerosis is a state of chronic low-grade inflammation and increased oxidative stress,shortened LTL in patients with atherosclerosis might stem from the two sources,one is an accelerated rate in hematopoietic stem cells(HSCs)replication to replace leukocytes consumed in the inflammatory process,and another is the increase in the loss of telomere repeats per replication.Thus,diminished HSC reserves at birth and age-dependent telomere attrition afterward are mirrored in shortened LTL during the adulthood.In addition,the inter-individual variation of LTL in the general population can be partly explained by genetic factors regulating telomere maintenance and the rate of HSCs replication.Atherosclerosis is an aging-related disease,and practically all humans develop atherosclerosis if they live long enough.Here we overview the potential roles of LTL dynamics in the imbalance between injurious oxidative stress/inflammation and endothelial repair during the pathogenesis of age-related atherosclerosis,and discuss the possibility that preventing accelerated cellular senescence is a potential target in prevention of atherosclerosis.

Mineralocorticoid receptor: a critical player in vascular remodeling

Vascular remodeling is a pathological condition with structural changes of blood vessels.Both inside-out and outside-in hypothesis have been put forward to describe mechanisms of vascular remodeling.An integrated model of these two hypotheses emphasizes the importance of immune cells such as monocytes/macrophages,T cells,and dendritic cells.These immune cells are at the center stage to orchestrate cellular proliferation,migration,and interactions of themselves and other vascular cells including endothelial cells(ECs),vascular smooth muscle cells(VSMCs),and fibroblasts.These changes on vascular wall lead to inflammation and oxidative stress that are largely responsible for vascular remodeling.Mineralocorticoid receptor(MR)is a classic nuclear receptor.MR agonist promotes inflammation and oxidative stress and therefore exacerbates vascular remodeling.Conversely,MR antagonists have the opposite effects.MR has direct roles on vascular cells through non-genomic or genomic actions to modulate inflammation and oxidative stress.Recent studies using genetic mouse models have revealed that MR in myeloid cells,VSMCs and ECs all contribute to vascular remodeling.In conclusion,data in the past years have demonstrated that MR is a critical control point in modulating vascular remodeling.Studies will continue to provide evidence with more detailed mechanisms to support this notion.