L—SOD对DDC诱发大鼠急性胃粘膜损伤的保护作用

本实验通过皮下注射ＤＤＣ（二乙基二硫代氨基甲酸钠）诱发大鼠急性胃粘膜损伤（ＡＧ－ＭＬ）模型，观察脂质体携载ＳＯＤ（Ｌ－ＳＯＤ）对此损伤的保护作用。发现ＤＤＣ能剂量依赖地诱发ＡＧＭＬ。预先静脉注射Ｌ－ＳＯＤ（３００００Ｕ／ｋｇ），可使胃粘膜ＳＯＤ和ＧＳＨ－Ｐｘ活性受到保护，ＭＤＡ含量少（Ｐ＜０．０５），胃粘膜血流量（ＧＭＢＦ）提高１２％，粘膜损伤指数下降６０％。表明ＤＤＣ能稳定诱发ＡＧＭＬ，Ｌ－ＳＯ     

麻风病人血液超氧化物歧化酶的研究

用亚硝酸法测定各型麻风病（ｎ＝７３）及健康人（ｎ＝１５）血浆中ＳＯＤ总量、Ｍｎ－ＳＯＤ和Ｃｕ、Ｚｎ－ＳＯＤ含量；发现各型麻风病人血浆中ＳＯＤ总量和Ｍｎ－ＳＯＤ含量均比正常人高（Ｐ＜０．０１），而Ｃｕ、Ｚｎ－ＳＯＤ含量无显著性差异（Ｐ＞０．５）。提示麻风病人血浆中ＳＯＤ总量升高，受Ｍｎ－ＳＯＤ的影响；后者存在于细菌体内，从而证明麻风病人体内的ＳＯＤ主要来源于麻风分枝杆菌。     

大鼠全脑缺血再灌后,丙二醛及超氧化物歧化酶活性的变化

大鼠全脑缺血30分钟再灌5分钟,脑组织丙二醛(MDA)含量显著高于对照组,再灌15分钟达高峰;同时脑组织超氧化物歧化酶(SOD)的活性在全脑缺血期下降,提示脂质过氧化主要发生于全脑缺血再灌注早期。     

超氧化物歧化酶在某些慢性肾疾患时的变化

超氧化物歧化酶在某些慢性肾疾患时的变化解放军三Ｏ九医院（北京１０００９１）张林，齐子荣，孙玲，石海滨，周伟超氧化物歧化酶（ｓｕｐｅｒｏｘｉｄｅｄｉｓｍｕｔａｓｅ，ＳＯＤ）是人体内一种重要的氧自由基清除剂，它在人体防御机制中具有重要作用。在正常情况下，...     

血吸虫病兔肠系膜上动脉夹闭休克时内脏超氧化物歧化酶的变化

本实验在血吸虫病兔肠系膜上动脉夹闭休克(SMAO)模型上,测定内脏SOD活力(n=10),并与正常兔合并SMAO组(n=7)和假手术组(n=6)对照。旨在探讨自由基反应及肝脏在多器官功能衰竭(MOF)中的作用。病理检查提示,血吸虫病兔合并SMAO组内脏有明显损伤。SOD活力测定:血吸虫病兔与正常兔合并SMAO时内脏SOD明显低于假手术组(P<0.01)。血吸虫病兔合并SMAO组肝、肺、胃SOD明显低于正常兔合并SMAO组,分别为2541/2993、1235/1656、1072/1578,(P<0.01),肾无显著性差异(1500/1558)。本研究表明,自由基反应是休克并发MOF的原因之一,合并有血吸虫肝病时更易发生MOF。     

肺癌组织铜锌超氧化物歧化酶免疫组化的研究

自由基（Ｏ２＾－等）与肺癌的关系一直是近年来人们关注的重要领域，国内外已有学者研究发现肺癌病人血清中的Ｃｕ，Ｚｎ－ＳＯＤ水平有显著变化，推测可能与肺癌组织内产生的ＳＯＤ量有关。本实验运用Ｃｕ，Ｚｎ－ＳＯＤＭｃＡｂ对肺癌组织进行免疫组化定位定量检测，探讨ＳＯＤ与肺癌的关系。结果观察到阳性染色的肺癌细胞浆内可见粗大、团块状强染色颗粒、以鳞癌细胞最为明显，腺癌细胞相对细小、分布均匀，部分颗粒在细胞膜上可     

高血脂大鼠血清SOD,MDA及脂肪酸含量的变化

高血脂大鼠血清ＳＯＤ、ＭＤＡ及脂肪酸含量的变化梁绪国，相玉忠，张才辉（山东烟台华侨医院心血管病研究室烟台２６４００１）目前认为，冠心病发生、发展的某些病理过程和环节与脂质过氧化损伤有关，而体内各种脂肪酸代谢及脂肪酸与自由基、脂质过氧化物间的关系尚报道...     

正常胃粘膜,癌周粘膜和癌组织中Cu Zn SOD免疫…

本文首次报道了利用兔抗人Ｃｕ Ｚｎ ＳＯＤ抗血清对正常胃粘膜和癌周及癌组织中ＣｕＺｎ ＳＯＤ分布，进行免疫组化定位研究。发现正常胃粘膜组织中Ｃｕ Ｚｎ ＳＯＤ染色强度明显高于癌周粘膜（Ｐ＜０．０５）；癌周粘膜组织明显高于癌组织（Ｐ＜０．０５）。表明胃癌组织中Ｃｕ Ｚｎ ＳＯＤ具有明显降低的现象。结果显示了３９例胃癌组织中Ｃｕ Ｚｎ ＳＯＤ染色阳性强度与术中所见腹腔转移有一定的关系，表现为中度阳性组     

卡托普利抗自由基作用及其免疫活性

卡托普利(CPT,40,80mg/kg,ig)可提高小鼠血清超氧化物歧化酶活性,并减弱酵母多糖激发的小鼠腹腔巨噬细胞鲁米诺依赖的化学发光。CPT(160mg/kg,ig)可降低小鼠血清过氧化脂质含量。用MTT颜色反应法还观察到,CPT(25μg/ml)在体外可抑制刀豆素A诱导的小鼠脾淋巴细胞增殖反应。CPT的上述作用可能是其治疗免疫性疾病的重要机理。     

自由基在肾缺血再灌流损伤中作用的实验研究

本实验选用大鼠右肾切除、左侧肾蒂夹闭60min肾缺血模型,观察缺血、再灌流、再灌流加别嘌呤醇(AP)和再灌流加超氧化物歧化酶(SOD)对动物血清肌酐(Scr)、肾系数和肾形态学变化的影响。结果发现60min肾缺血后再灌流24hr,动物的Scr水平明显高于单纯缺血组动物的水平(P<0.01)和假手术组动物的水平(P<0.01);光镜下肾组织损伤较单纯缺血组动物明显加重,表明再灌流可以加重缺血肾损伤,动物发生缺血性急性肾衰(IARF)。给AP和SOD处理后,肾衰动物的Scr水平、肾系数分别较单纯再灌流组动物明显降低(P<0.01)。整个肾组织病变尤其是线粒体病变、刷状缘损伤大为减轻。说明AP和SOD可以减轻IARF,自由基可能参于肾缺血再灌流损伤,膜和线粒体损伤可能是IARF发病的重要因素。     

Lipoic acid effects on lipid peroxidation level,superoxide dismutase activity and monoamines concentration in rat hippocampus

The purposes of the present work were to verify lipid peroxidation level, superoxide dismutase (SOD) activity and monoamines (dopamine (DA), norepinephrine (NE), serotonin (5-HT)), and their metabolites (3,4-hydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA)) contents in rat hippocampus after lipoic acid (LA) administration. Wistar rats were treated with 0.9% saline (i.p., control group) and LA (10, 20 or 30 mg/kg, i.p., LA10, LA20 and LA30 groups, respectively). After the treatments all groups were observed for 24 h. In LA20 group only there was a significant decrease in lipid peroxidation level. However, no alteration was observed in SOD activity in groups treated with LA. The NE and DA levels were increased only in 20 mg/kg dose of LA in rat hippocampus. Serotonin content and their metabolite 5-HIAA levels was decreased in same dose of LA. On the other hand, DOPAC and HVA levels did not show any significant change. The reduction in lipid peroxidation level and alterations in hippocampal monoamines can be suggested as a possible brain mechanism from this antioxidant. The outcome of the study may have therapeutic implications in the neurodegenerative diseases.     

An iron-containing superoxide dismutase in Tritrichomonas foetus

Dialysed extracts of Tritrichomonas foetus were found to have superoxide dismutase at substantially higher levels than those found in trypanosomatids and mouse red blood cells. The activity was sensitive to inhibition by H₂O₂ but not by cyanide, suggesting that this organism has iron-containing superoxide dismutase(s). Three isozymes were seen by isoelectric focusing which appeared to be sensitive to inhibition by H₂O₂.     

The effect of superoxide dismutase deficiency on zinc toxicity in Schizosaccharomyces pombe.

Zinc is a metal which is a cofactor in many enzymes and a structural element in zinc finger motifs those are important in relation between DNA and regulator proteins. Little is known about uptake, distribution, toxicity and detoxification of zinc ions in cells. In this study, zinc toxicity and detoxification levels have been compared in wild type and Cu/Zn superoxide dismutase mutant (sod1Delta) cells of the fission yeast Schizosaccharomyces pombe. We evaluated the toxic levels of zinc, total zinc content, lipid peroxidation levels and catalase activities for both strains which were grown in medium containing different concentrations of zinc. sod1Delta mutant showed important growth retardation and has higher lipid peroxidation and catalase activities than wild type. Cu/Zn superoxide dismutase (SOD1) activity of wild type cells was markedly increased when they were treated with elevated levels of zinc. SOD1 mRNA level also significantly increased when the cells treated with higher concentrations of zinc. These results indicate that the mutant cells were more sensitive to zinc stress and seemed to have more oxidative intracellular environment than wild type cells. Our results support the idea that superoxide dismutase is an important factor for zinc detoxification in eukaryotes.     

Characterisation of the manganese superoxide dismutase of Enterococcus faecium

The manganese superoxide dismutase (SodA) of E. faecium strain AUS0004 has been characterised. It is most closely related to Enterococcus hirae, Enterococcus durans, Enterococcus villorium, and Enterococcus mundtii with 100%, 91,55%, 90,85%, and 90,58% homology, respectively, but more distant from SodA of E. faecalis (81.68%). A sodA deletion mutant has been constructed. Compared to the parental strain, the ΔsodA mutant was affected in aerobic growth and more sensitive to hydrogen peroxide (H₂O₂), cumene hydroperoxide (CuOOH), and the superoxide anion (O₂^•-) generator menadione. The E. faecium strain AUS0004 is part of those bacteria accumulating H₂O₂ to high concentrations (around 5 mM) starting from late exponential growth phase. Accumulation of the peroxide was around 25% less in the mutant suggesting that this part of H₂O₂ is due to the dismutation of O₂^•- by SodA. The sodA gene of E. faecium AUS0004 was induced by oxygen, peroxides and menadione but the corresponding regulator remains hitherto unknown. Finally, we showed that SodA activity is important for virulence in the Galleria mellonella model.     

家兔心脏短期缺血后再灌流时心功能的变化及SOD的影响

本实验利用家兔急性心肌缺血后早期再灌流动物模型,观察早期再灌流对心功能的影响,并利用自由基清除剂(超氧化物歧化酶,s0D)探索自由基在其中的可能作用。实验过程中测取心功能指标;观察结束后,分别从缺血区与非缺血区心内膜下取心肌电镜标本。实验发现,单纯再灌流组的心功能指标明显低于持续结扎组,SOD再灌流组的心功能比单纯再灌流组恢复得早、恢复程度高;缺血区心肌超微结构的损伤程度,依次为持续结扎组>单纯再灌流组>SOD再灌流组,非缺血区心肌超微结构只是单纯再灌流组变化较明显。结果表明,自由基对短期缺血后再灌流过程中心功能损伤起着一定的作用,其损伤范围随着再灌流的发生扩散到非缺血区。     

超氧化物歧化酶在心肌再灌注性损伤中的作用

本实验在大鼠离体心脏灌注模型上,模拟心肌缺血再灌注过程(旷置30分钟,再灌注45分钟),结果发现:再灌注后,心脏频发室颤,组织水肿明显,脂质过氧化终产物丙二醛较正常时显著增加,冠脉流出液中乳酸脱氢酶呈一持续高水平释放,心肌组织ATP酶活性明显下降。再灌注开始后给予超氧化物歧化酶(SOD)。能够减轻以上心肌再灌注性损伤现象。这一结果提示:1)活性氧参与了心肌再灌注损伤现象的发生。2)再灌注开始后给予SOD仍有明显疗效,这为临床上在再灌注开始后应用SOD提供了一定的实验依据。     

山茛菪碱与川芎嗪预防肺水肿时大鼠血气及红细胞超氧化物歧化酶的变化

肾上腺素所致肺水肿类似中枢性肺水肿,具有动力性及非动力性双重机制。此时,动脉血中PaO_2、O_2Sat明显下降、PaCO_2明显上升,pH下降,红细胞超氧化物歧化酶含量下降,654-2与川芎嚓能防止上述异常变化,并使之趋于正常。实验显示了654-2及川芎嗪对肺水肿防止作用的部分机理。     

In silico analysis of nickel containing superoxide dismutase evolution and regulation

Superoxide dismutases are essential enzymes involved in detoxification of reactive oxygen by dismutation of the superoxide radical anion. A class of nickel containing superoxide dismutases has been described for streptomycetes and cyanobacteria. In silico analysis was used to study the distribution of genes coding for NiSOD in other taxa and to elucidate signals linked to nickel incorporation and maturation of NiSOD. Data mining revealed homologous proteins from actinobacteria, proteobacteria, chlamydiae, and eukarya (green algae) thus allowing a comparison of protein structural elements. Nickel ligands and maturation signals for N‐terminal proteolysis were highly conserved. Genomic sequences surrounding genes encoding NiSOD homologs were compared in order to detect putative accessory enzymes involved in maturation. An endopeptidase gene linked to sodN coding for NiSOD was found in actinobacteria and cyanobacteria, but not in other taxa. The distribution of NiSOD encoding sequences showed four clusters which are not consistent with the phylogeny of the species. In addition, the different genomic context argues for heterologous gene transfer, most likely from actinobacteria to other taxa. In order to address regulation by nickel availability and incorporation into the mature protein, we present first evidence for putative regulatory nucleotide sequences which will be useful in future studies on nickel uptake and incorporation. (© 2009 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)     

Therapeutic potential of superoxide dismutase (SOD) for resolution of inflammation

Neutrophils play essential roles in several inflammatory reactions. Oxidant/antioxidant imbalance is thought to be partially involved in the pathogenesis of the disorders. Under the conditions of oxidative stress, superoxide dismutase (SOD) acts as an endogenous cellular defense system to degrade superoxide (O₂⁻) into oxygen and hydrogen peroxide. Therefore, SOD is potentially useful as a therapeutic agent for treatment of inflammatory disorders. A further mechanism that may contribute to the efficacy of SOD is the regulation of neutrophil apoptosis. For the resolution of infl ammation, the activated neutrophils must be safely removed by apoptosis. Neutrophil apoptosis has been suggested as a possible target for the control of neutrophil-mediated tissue injury. Exogenously added SOD induces neutrophil apoptosis, and hydrogen peroxide has been suggested to be a possible major mediator of ROS-induced neutrophil apoptosis in a caspase-dependent manner. If the drug can be delivered efficiently to the inflammatory site, SOD may be useful as an inhibitory mediator of neutrophil-mediated inflammation. Received 6 December 2005; returned for revision 15 February 2006; returned for final revision 23 March 2006; accepted by M. Katori 15 April 2006