不同活性氧胁迫下Bacillus sp. F26以抗氧化物酶合成为特征的应激响应

采用不同的活性氧发生源, 研究了· 、H2O2和OH·胁迫下Bacillus sp. F26以抗氧化物酶合成为特征的应激响应。结果表明, 细胞对氧胁迫的应激响应程度取决于活性氧种类、胁迫程度和形式(瞬时和持续)。Bacillus sp. F26对H2O2胁迫的响应程度最高, 过氧化氢酶的快速合成对细胞抵抗H2O2胁迫至关重要, 当细胞及时分解进入胞内的H2O2, 胁迫对细胞的氧化损伤程度并不高, 相反会刺激细胞的生长和底物消耗, 当胁迫超过过氧化氢酶的分解能力时, H2O2会迅速抑制细胞生长和过氧化氢酶合成; 由于 ·与细胞作用的方式和效果与H2O2不同, 超氧化物歧化酶和过氧化氢酶的快速合成并不能保证细胞及时有效地清除胞内的活性氧, 因此, 细胞对 ·胁迫的响应程度要低于H2O2胁迫; 在所考察的3种活性氧中, OH·胁迫(Fenton反应体系)对细胞的氧化损伤程度最大, 胁迫强烈地抑制了细胞生长和抗氧化物酶的合成。由此表明, 由于不同活性氧的化学性质有所不同, 细胞对不同种类、程度和形式的活性氧胁迫会表现出不同的生物学效应, 为了提高自身对氧胁迫的抵抗能力, 微生物会通过自身的代谢调节适应新的环境, 包括调整抗氧化物酶合成水平、改变生长速度以及底物消耗速率等。     

抗体包被瘤细胞膜引发人血多形核白细胞化学发光

用抗体包被K562细胞膜碎片(Ab-M)刺激人血多形核白细胞(PMN)产生化学发光,对其发光动力学及活性氧代谢特征进行了比较,结果表明Ab-M引发PMN发光动力学与酵母多糖不同.用秋水仙碱干扰PMN膜结构完整性可抑制其发光产额,Ca²⁺可促增PMN发光,提示PMN氧代谢的调控与Fc受体和Ca²⁺动员有关;活性氧系PMN实施细胞毒效应的重要物质.     

不同活性氧胁迫下Bacillus sp. F26以抗氧化物酶合成为特征的应激响应

采用不同的活性氧发生源, 研究了· 、H2O2和OH·胁迫下Bacillus sp. F26以抗氧化物酶合成为特征的应激响应。结果表明, 细胞对氧胁迫的应激响应程度取决于活性氧种类、胁迫程度和形式(瞬时和持续)。Bacillus sp. F26对H2O2胁迫的响应程度最高, 过氧化氢酶的快速合成对细胞抵抗H2O2胁迫至关重要, 当细胞及时分解进入胞内的H2O2, 胁迫对细胞的氧化损伤程度并不高, 相反会刺激细胞的生长和底物消耗, 当胁迫超过过氧化氢酶的分解能力时, H2O2会迅速抑制细胞生长和过氧化氢酶合成; 由于 ·与细胞作用的方式和效果与H2O2不同, 超氧化物歧化酶和过氧化氢酶的快速合成并不能保证细胞及时有效地清除胞内的活性氧, 因此, 细胞对 ·胁迫的响应程度要低于H2O2胁迫; 在所考察的3种活性氧中, OH·胁迫(Fenton反应体系)对细胞的氧化损伤程度最大, 胁迫强烈地抑制了细胞生长和抗氧化物酶的合成。由此表明, 由于不同活性氧的化学性质有所不同, 细胞对不同种类、程度和形式的活性氧胁迫会表现出不同的生物学效应, 为了提高自身对氧胁迫的抵抗能力, 微生物会通过自身的代谢调节适应新的环境, 包括调整抗氧化物酶合成水平、改变生长速度以及底物消耗速率等。     

耐盐和盐敏感型小麦品种对NaCl胁迫的生理响应及耐盐性差异

为探究小麦品种类型对盐胁迫的生理响应及敏感性差异,以耐盐型品种济麦22和盐敏感型品种河农6425为材料,对幼苗期植株施以不同浓度的NaCl胁迫处理,比较分析了两个品种幼苗在胁迫条件下的生长、生理生化和叶绿体荧光特征等方面的差异。结果表明,NaCl胁迫对幼苗地上和地下部分的生长表现浓度依赖性的抑制效应,对耐盐型品种的抑制程度较小。在生理响应方面,幼苗体内的Na⁺含量随NaCl 浓度的增加而上升,K⁺和Ca²⁺含量则表现相反的变化趋势,耐盐型品种幼苗在胁迫处理前、后均具有较高的K⁺/Na⁺比和Ca²⁺/Na⁺比;NaCl胁迫导致幼苗的光系统Ⅱ受损,表现在Fv/Fm、Fv/Fo、qP 和YⅡ 等叶绿体荧光参数数值下降,降幅在耐盐性品种上相对较小。在氧化胁迫和抗氧化系统方面,NaCl胁迫导致幼苗体内活性氧水平的上升和过氧化物酶（POD）、过氧化氢酶（CAT）等抗氧化酶的响应;POD活性在处理后的0-12 d范围内呈先下降后上升的趋势,CAT活性则呈先上升后下降的趋势。耐盐品种的POD活性在胁迫早期受抑制时间较短,随后的响应更迅速且上升幅度更高;耐盐品种的CAT活性上升幅度更高,且在胁迫后期对高浓度NaCl和长时间胁迫导致的酶活性抑制的耐受性更强。耐盐品种抗氧化酶的这一响应特征与其较低的活性氧上升幅度一致,也与其较低水平的代表膜损伤程度的丙二醛（MDA）积累一致。耐盐型品种根部的MDA积累经200 mmol/L NaCl处理1 d后达到峰值,而盐敏感品种根部的MDA积累经150 mmol/L NaCl处理1 d后即达到峰值。以上研究结果表明,耐盐型小麦品种济麦22可分别通过其较强的K⁺/Na⁺、Ca²⁺/Na⁺调节能力和抗氧化酶体系缓解盐胁迫所导致的渗透胁迫和活性氧伤害,从而表现出耐盐的特征。     

皇竹草活性氧代谢对阿特拉津胁迫的响应特征

采用水培实验研究了4个浓度（5、10、20、40 mg·L^-1）除草剂阿特拉津胁迫下,皇竹草（Pennisetum hydridum）叶片内超氧阴离子生成速率、过氧化氢（H₂O₂）含量、超氧化物歧化酶（SOD）活性、过氧化氢酶（CAT）活性、过氧化物酶（POD）活性、丙二醛（MDA）含量、原生质膜透性的变化,探讨皇竹草对阿特拉津的抗性及其生理机制。结果显示:（1）低浓度（5、10 mg·L^-1）的阿特拉津胁迫使皇竹草叶片内超氧阴离子生成速率和CAT活性升高,却使H₂O₂含量及SOD和POD活性降低,但随着培养时间的延长,培养液中阿特拉津浓度的降低导致上述指标又有恢复到正常水平的趋势;而高浓度（40 mg·L^-1）的阿特拉津胁迫则使皇竹草叶片内H₂O₂含量、SOD、POD和CAT活性持续降低。（2）在各胁迫浓度下持续胁迫10 d后,皇竹草叶片内MDA含量开始逐渐升高,并且升高幅度随着胁迫浓度的提高而明显增加,但各胁迫浓度下叶片原生质膜相对透性未见明显的变化。研究表明,皇竹草可能通过活性氧等信号分子调控自身保护酶系统的活性来缓解阿特拉津造成的伤害,从而对低浓度（5、10 mg·L^-1）的阿特拉津胁迫表现出较强抗性。     

1,2,4-三氯苯胁迫对萌发大豆种子中活性氧的影响

以盆栽法研究了不同浓度 1,2 ,4 三氯苯 (TCB)胁迫对萌发大豆种子中活性氧代谢的影响 .结果表明 ,10 0～ 30 0 μg·g-1TCB胁迫初期 (1～ 3天 )促使萌发大豆种子呼吸强度升高及其峰值提前出现 ,超氧阴离子自由基 (O2 - )及过氧化氢 (H2 O2 )的积累显著增加 ,同时伴随丙二醛 (MDA)含量升高 ,显示发生膜脂质过氧化作用 .TCB胁迫 1～ 6天使活性氧清除酶功能紊乱 ,其中过氧化物酶 (POD)活性升高 ,超氧化物岐化酶 (SOD)活性开始上升后转为下降 .在萌发大豆种子受TCB胁迫伤害过程中 ,活性氧代谢失衡造成的膜脂质过氧化将起着重要作用 .     

外源SNP对干旱胁迫下不同马铃薯品种叶片抗氧化酶活性的影响

以正常水分状态、轻度干旱胁迫、中度干旱胁迫和重度干旱胁迫下的马铃薯抗旱品种‘底西瑞’和干旱敏感品种‘大西洋’ 植株为材料,于现蕾期采用0（对照）和0.01 mmol·L^-1 SNP分别喷施各处理植株,对不同处理下2个品种的植株形态、叶片超氧阴离子和H₂O₂含量以及抗氧化酶活性进行比较分析,探讨外源SNP对干旱状态下马铃薯的生理应答机制,为马铃薯的抗旱栽培提供新的技术理论支持。结果显示：（1）SNP喷施对重度水分胁迫下马铃薯植株的正常生长具有一定的保护作用。（2）在干旱胁迫条件下,马铃薯叶片POD活性在品种‘底西瑞’中增加而在品种‘大西洋’中降低,超氧阴离子含量和H₂O₂含量以及CAT和APX活性在各品种中均增加,但超氧阴离子含量和H₂O₂含量增加程度与胁迫程度无关。（3）抗旱品种‘底西瑞’在干旱胁迫下的超氧阴离子含量低于干旱敏感品种‘大西洋’,而其POD、CAT和APX活性则高于‘大西洋’; 0.01 mmol·L^-1SNP处理未改变马铃薯叶片中超氧阴离子和H₂O₂含量随土壤水分的变化趋势,但改变了‘大西洋’叶片中SOD、POD、CAT活性以及‘底西瑞’叶片中APX活性的变化趋势。（4）外源喷施0.01 mmol·L^-1SNP降低了‘底西瑞’在中度和重度胁迫下以及‘大西洋’在轻度和中度胁迫下超氧阴离子含量,提高了干旱胁迫下‘底西瑞’和‘大西洋’的POD和APX活性。研究表明,POD、CAT和APX可作为马铃薯水分胁迫下的应答以及品种抗旱性的筛选指标,外源SNP可通过诱导增强干旱胁迫下马铃薯的抗氧化酶活性来提高其抗旱性。     

外源H2O2对盐胁迫下小白菜种子萌发和幼苗生理特性的影响

以小白菜"甜脆青"为试材,研究不同浓度（5、10、25、50和100 mmol/L）过氧化氢（H₂O₂）浸种处理对100 mmol/L NaCl胁迫下小白菜（Brassica chinensis L.）种子萌发、幼苗生长及生理特性的影响。结果表明：100 mmol/L NaCl胁迫明显抑制小白菜种子的萌发状况和幼苗生长,发芽势、发芽指数、活力指数及幼苗根和芽长度和鲜重均明显降低,根和芽中CAT的活性及K⁺含量明显受到抑制,渗透调节物质、活性氧和MDA含量显著增加。不同浓度H₂O₂浸种处理提高了NaCl胁迫下小白菜种子发芽势、发芽指数和活力指数,促进小白菜根和芽的生长,增强了NaCl胁迫下根和芽中SOD、CAT和APX的活性及K⁺含量,降低O₂^-·产生速率及H₂O₂和MDA含量,进一步促进脯氨酸和可溶性糖含量的增加,降低体内Na⁺含量。其中以10 mmol/L H₂O₂处理缓解盐胁迫效果最好,明显缓解NaCl胁迫对小白菜种子萌发和幼苗生长的抑制。     

植物-病原物互作过程中的活性氧

活性氧与水分胁迫、环境污染、衰老及低温等方面的关系已有大量的报道。在植物－病原物互作过程中,病原物作为一种特殊的胁迫因子而起作用。近年来对植物一病原物互作过程中活性氧的研究已成为植物病理生理学研究的一个热点,本文对此作一综述。１植物─-病原物巨作过程的活性氧的产生在正常情况下,植物体内活性氧（ａｃｔｉｖｅｏｘｙｇｅｎｓｐｅｃｉｅｓ,ＡＯＳ,包括超氧阴离子Ｏ－２;过氧化氢Ｈ２Ｏ２;氢氧自由基ＯＨ;单线态氧１Ｏ２）处于低水平状态,在植物过敏性反应（ＨＲ）早期阶段常出现ＡＯＳ迅速释放,这种ＡＯＳ迅速释…     

干旱及活性氧引起小麦膜脂过氧化与脱酯化

水分胁迫下随小麦叶片含水量下降,膜透性增大,两者高度负相关;同时叶片H₂O₂含量和叶片微粒体膜脂过氧化水平都上升,无论在干旱时或在外源O₂^-和·OH作用时,微粒体膜流动性均下降,外源O₂^-和·OH处理微粒体膜后,膜脂过氧化水平明显增高,脂肪酸不饱和度明显下降;同时磷脂减少,游离脂肪酸增加。结果表明干旱可能使植物体内活性氧增多,从而导致膜损伤,这种由活性氧引起的膜损伤是膜脂过氧化和脱酯化共同作用的结果     

Total antioxidant capacity – a novel early bio-chemical marker of oxidative stress in HIV infected individuals

Background  

Oxidative stress induced by the production of reactive oxygen species may play a critical role in the stimulation of HIV replication and the development of immunodeficiency. This study was conducted as there are limited and inconclusive studies on the significance of a novel early marker of oxidative stress which can reflect the total antioxidant capacity in HIV patients,     

The HIV-1 transactivator factor (Tat) induces enterocyte apoptosis through a redox-mediated mechanism

The intestinal mucosa is an important target of human immunodeficiency virus (HIV) infection. HIV virus induces CD4+ T cell loss and epithelial damage which results in increased intestinal permeability. The mechanisms involved in nutrient malabsorption and alterations of intestinal mucosal architecture are unknown. We previously demonstrated that HIV-1 transactivator factor (Tat) induces an enterotoxic effect on intestinal epithelial cells that could be responsible for HIV-associated diarrhea. Since oxidative stress is implicated in the pathogenesis and morbidity of HIV infection, we evaluated whether Tat induces apoptosis of human enterocytes through oxidative stress, and whether the antioxidant N-acetylcysteine (NAC) could prevent it. Caco-2 and HT29 cells or human intestinal mucosa specimens were exposed to Tat alone or combined with NAC. In an in-vitro cell model, Tat increased the generation of reactive oxygen species and decreased antioxidant defenses as judged by a reduction in catalase activity and a reduced (GSH)/oxidized (GSSG) glutathione ratio. Tat also induced cytochrome c release from mitochondria to cytosol, and caspase-3 activation. Rectal dialysis samples from HIV-infected patients were positive for the oxidative stress marker 8-hydroxy-2'-deoxyguanosine. GSH/GSSG imbalance and apoptosis occurred in jejunal specimens from HIV-positive patients at baseline and from HIV-negative specimens exposed to Tat. Experiments with neutralizing anti-Tat antibodies showed that these effects were direct and specific. Pre-treatment with NAC prevented Tat-induced apoptosis and restored the glutathione balance in both the in-vitro and the ex-vivo model. These findings indicate that oxidative stress is one of the mechanism involved in HIV-intestinal disease.     

Redox Regulation of Programmed Cell Death in Lymphocytes

A redox imbalance caused by an over-production of prooxidants or a decrease in antioxidants seems to play a role in the programmed cell death that occurs in various developmental programs. Such a physiological function for oxidative stress is particularly applicable to the immune system, wherein individual lymphocytes undergo continuous scrutiny to determine if they should be preserved or programmed to die. Following activation, lymphocytes produced increased levels of reactive oxygen species (ROS) which may serve as intracellular signaling molecules. The ultimate outcome of this increased ROS formation, i.e., lymphocyte proliferation versus programmed cell death, may be dictated by macrophage-derived costimulatory molecules that bolster or diminish lymphocyte antioxidant defenses. HIV-1-infected individuals display multiple symptoms of redox imbalance consistent with their being in oxidative stress, and lymphocytes from such individuals are more prone to undergo apoptosis in vitro. It is suggested that oxidative stress is a physiological mediator of programmed cell death in lymphoid cells, and that HIV disease represents an extreme case of what can happen when regulatory safeguards are compromised.     

Effect of Mild-to-Moderate Smoking on Viral Load,Cytokines, Oxidative Stress,and Cytochrome P450 Enzymes in HIV-Infected Individuals

Mild-to-moderate tobacco smoking is highly prevalent in HIV-infected individuals, and is known to exacerbate HIV pathogenesis. The objective of this study was to determine the specific effects of mild-to-moderate smoking on viral load, cytokine production, and oxidative stress and cytochrome P450 (CYP) pathways in HIV-infected individuals who have not yet received antiretroviral therapy (ART). Thirty-two human subjects were recruited and assigned to four different cohorts as follows: a) HIV negative non-smokers, b) HIV positive non-smokers, c) HIV negative mild-to-moderate smokers, and d) HIV positive mild-to-moderate smokers. Patients were recruited in Cameroon, Africa using strict selection criteria to exclude patients not yet eligible for ART and not receiving conventional or traditional medications. Those with active tuberculosis, hepatitis B or with a history of substance abuse were also excluded. Our results showed an increase in the viral load in the plasma of HIV positive patients who were mild-to-moderate smokers compared to individuals who did not smoke. Furthermore, although we did not observe significant changes in the levels of most pro-inflammatory cytokines, the cytokine IL-8 and MCP-1 showed a significant decrease in the plasma of HIV-infected patients and smokers compared with HIV negative non-smokers. Importantly, HIV-infected individuals and smokers showed a significant increase in oxidative stress compared with HIV negative non-smoker subjects in both plasma and monocytes. To examine the possible pathways involved in increased oxidative stress and viral load, we determined the mRNA levels of several antioxidant and cytochrome P450 enzymes in monocytes. The results showed that the levels of most antioxidants are unaltered, suggesting their inability to counter oxidative stress. While CYP2A6 was induced in smokers, CYP3A4 was induced in HIV and HIV positive smokers compared with HIV negative non-smokers. Overall, the findings suggest a possible association of oxidative stress and perhaps CYP pathway with smoking-mediated increased viral load in HIV positive individuals.     

Supplementation with antioxidant vitamins prevents oxidative modification of DNA in lymphocytes of HIV-infected patients

There is evidence suggesting that patients infected with human immunodeficiency virus (HIV) are under chronic oxidative stress. In the present study, the level of oxidatively modified bases in lymphocyte DNA and some other parameters of oxidative stress were measured in HIV-infected patients (n = 30), as well as in control groups (10 healthy volunteers and 15 HIV-seronegative injected drug users). Additional experiments were conducted using lymphocyte DNA samples from asymptomatic seropositive, HIV-infected patients who were supplemented with antioxidant vitamins A, C, and E or received placebo. Significant increases in the amount of the modified DNA bases were observed in HIV-infected patients when compared with the control group. The concentration of thiobarbituric acid reactive substances (TBARS) was higher and activities of antioxidant enzymes (superoxide dismutase and catalase) were lower in the group of HIV-infected patients in comparison to the control group. Vitamin supplementation resulted in the significant decrease in the levels of all modified DNA bases when compared to the patients who received placebo. The reduction of TBARS and the restoration of the activity of the enzymes were also observed. Our data suggest that people infected with HIV can benefit from treatment with antioxidant vitamins.     

Oxidative and nitrosative signaling in plants: Two branches in the same tree?

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) constitute key features underpinning the dynamic nature of cell signaling systems in plants. Despite their importance in many aspects of cell biology, our understanding of oxidative and especially of nitrosative signaling and their regulation remains poorly understood. Early reports have established that ROS and RNS coordinately regulate plant defense responses to biotic stress. In addition, evidence has accumulated demonstrating that there is a strong cross-talk between oxidative and nitrosative signaling upon abiotic stress conditions. The goal of this mini-review is to provide latest findings showing how both ROS and RNS comprise a coordinated oxidative and nitrosative signaling network that modulates cellular responses in response to environmental stimuli.Key words: abiotic stress, nitrosative stress, oxidative stress, reactive nitrogen species, reactive oxygen species, signaling     

Reactive sulfur species: an emerging concept in oxidative stress

The ingredients of oxidative stress include a variety of reactive species such as reactive oxygen and reactive nitrogen species (ROS, RNS). While sulfur is usually considered as part of cellular antioxidant systems there is mounting evidence that reactive sulfur species (RSS) with stressor properties similar to the ones found in ROS are formed under conditions of oxidative stress. Thiols as well as disulfides are easily oxidised to sulfur species with sulfur in higher oxidation states. Such agents include thiyl radicals, disulfides, sulfenic acids and disulfide-S-oxides. They rapidly oxidise and subsequently inhibit thiol-proteins and enzymes and can be considered as a separate class of oxidative stressors providing new antioxidant drug targets.     

Iron metabolism and HIV infection: reciprocal interactions with potentially harmful consequences?

Humans with advanced human immunodeficiency virus (HIV) infection present some evidence suggestive of iron accumulation. Ferritin concentrations increase with HIV disease progression, and iron accumulates in several tissues. Iron excess may exert negative effects in individuals with HIV. Indeed, iron accumulation seems to be associated with shorter survival, and a number of investigations point to an iron-mediated oxidative stress in subjects with HIV infection. The observations on humans infected with HIV are in part supported by in-vitro findings. Indeed, in-vitro HIV infection is associated with changes in iron metabolism, and an iron-mediated oxidative stress is likely to contribute to viral cytopathogenicity. Furthermore, it is interesting to point out that the interaction between iron and HIV may be reciprocal, since viruses with a life-cycle involving a DNA phase require chelatable iron for optimum replication. This combined evidence suggests that iron metabolism is an important area for virus/host interaction. These observations may be relevant to both laboratory monitoring and clinical treatment of individuals with HIV.     

Oxidative stress induced expression of monodehydroascorbate reductase gene in Eleusine coracana

Abiotic stresses constitute a serious threats to the world food security as they cause significant economic losses in terms of reduction in crop productivity and also greatly limit the geographical locations where crops can be grown. Exposure to abiotic stress causes over-production of reactive oxygen species, leading to oxidative stress in plants. Induction of oxidative stress is primarily responsible for a variety of detrimental changes in the cellular physiology. However, plants have evolved intricate anti-oxidative defence machinery, for their survival under stress. Plant defence strategies for stress tolerance rely on the expression of anti-oxidative genes required for scavenging the toxic reactive oxygen species. Monodehydroascorbate reductase is one of the key anti-oxidant enzyme responsible for scavenging reactive oxygen species. In the present study, efforts have been made to understand the role of monodehydroascorbate reductase in finger millet under different abiotic stresses (drought, salt and UV radiation). The study establishes a differential link between mdar gene expression and enzyme activity under oxidative stress that is validated under different types of imposed stresses. Alteration in correlation between gene expression and enzyme activities under varying magnitude of oxidative stress is elucidated.