Sleep duration,nightshift work,and the timing of meals and urinary levels of 8-isoprostane and 6-sulfatoxymelatonin in Japanese women

It has been hypothesized that disruption of circadian rhythms affects human health. Shift work and sleep deprivation are thought to disrupt the normal light–dark cycle, although the disruption due to shiftwork may be dependent on sleep deprivation. Both conditions have been suggested to be associated with an increased risk of cardiometabolic disorders. Non-photic environmental factors, such as the timing of eating, are also thought to regulate circadian rhythm and thus, may have effects on health, but the evidence from human studies is scarce. Oxidative stress is a risk factor of cardiometabolic disorders. Some laboratory studies suggest an involvement of circadian clock genes in the regulation of the redox system. The present study aimed to examine the association of sleeping habits, nightshift work, and the timing of meals with urinary levels of 8-isoprostane, a marker of oxidative stress, and 6-sulfatoxymelatonin, the principal metabolite of melatonin. Study subjects were 542 women who had previously attended a breast cancer mass screening in a community in Japan. Information on bedtimes and wake-up times, history of nightshift work, and the timing of meals was obtained by a self-administered questionnaire. The 8-isoprostane and 6-sulfatoxymelatonin were measured using the first morning void of urine and expressed per mg of creatinine. The geometric mean of 8-isoprostane levels was 12.1% higher in women with ≤6 hours of sleep than that in those with >8 hours of sleep on weekdays, and longer sleep duration on weekdays was significantly associated with lower urinary levels of 8-isoprostane after controlling for covariates (p for trend = 0.04). Women who were currently working the nightshift had a 33.3% higher geometric mean of 8-isoprostane levels than those who were not working nightshift (p = 0.03). Urinary 6-sulfatoxymelatonin levels were unrelated to sleep habits or nightshift work. Women who ate breakfast at irregular times had a 19.8% higher geometric mean of 8-isoprostane levels than those who ate breakfast at a regular time or who did not eat (p = 0.02). Women who ate nighttime snacks at irregular times had a 16.2% higher geometric mean of 8-isoprostane levels than those who did not eat nighttime snacks or who ate nighttime snacks at a regular time (p = 0.003). Among women who ate dinner at a regular time, earlier times for dinner were associated with higher 8-isoprostane and 6-sulfatoxymelatonin levels (p values for trends were 0.01 and 0.02, respectively). However, the times of dinner and nighttime snack are overlapping, and the time of last meal of the day was not associated with 8-isoprostane and 6-sulfatoxymelatonin levels. The time of breakfast or lunch was not associated with these biomarkers among women who ate the meal at regular times. Disturbing the rhythmicity of daily life may be associated with oxidative stress.     

Synthesis and evaluation of N-substituted indole-3-carboxamide derivatives as inhibitors of lipid peroxidation and superoxide anion formation

The in vitro antioxidant effects of novel N-substituted indole-3-carboxamides (I3CDs) 1-10 on rat liver microsomal NADPH-dependent lipid peroxidation (LP) levels and their free radicals scavenging properties were determined by the inhibition of superoxide anion formation (SOD). Among the synthesized compounds, 4, 5, 8 and 9 significantly inhibited SOD with an inhibition range at 84–100% at 10^{? 3} M concentration. The presence of halo substituents both ortho- and para- positions of these compounds resulted 100% inhibition of SOD. Comparison the activity results of halogenated and non-halogenated derivatives suggested that the halogenated compounds are more active than the non-halogenated compounds. On the other hand, the introduction of a para fluoro benzyl in the 1-position of indole (compounds 7, 8) has more impact on the SOD inhibition when the benzamide ring was mono halogenated. However, none of other compounds had a significant inhibitory effects on the level of lipid peroxidation.     

Determination of 3-nitrotyrosine in human urine at the basal state by gas chromatography-tandem mass spectrometry and evaluation of the excretion after oral intake

3-Nitrotyrosine (NO(2)Tyr) is a potential biomarker of reactive-nitrogen species (RNS) including peroxynitrite. 3-Nitrotyrosine occurs in human plasma in its free and protein-associated forms and is excreted in the urine. Measurement of 3-nitrotyrosine in human plasma is invasive and associated with numerous methodological problems. Recently, we have described an accurate method based on gas chromatography (GC)-tandem mass spectrometry (MS) for circulating 3-nitrotyrosine. The present article describes the extension of this method to urinary 3-nitrotyrosine. The method involves separation of urinary 3-nitrotyrosine from nitrite, nitrate and l-tyrosine by HPLC, preparation of the n-propyl-pentafluoropropionyltrimethylsilyl ether derivatives of endogenous 3-nitrotyrosine and the internal standard 3-nitro-l-[(2)H(3)]tyrosine, and GC-tandem MS quantification in the selected-reaction monitoring mode under negative-ion chemical ionization conditions. In urine of ten apparently healthy volunteers (years of age, 36.5+/-7.2) 3-nitrotyrosine levels were determined to be 8.4+/-10.4 nM (range, 1.6-33.2 nM) or 0.46+/-0.49 nmol/mmol creatinine (range, 0.05-1.30 nmol/mmol creatinine). The present GC-tandem MS method provides accurate values of 3-nitrotyrosine in human urine at the basal state. After oral intake of 3-nitro-l-tyrosine by a healthy volunteer (27.6 microg/kg body weight) 3-nitro-l-tyrosine appeared rapidly in the urine and was excreted following a biphasic pharmacokinetic profile. Approximately one third of administered 3-nitro-l-tyrosine was excreted within the first 8 h. The suitability of the non-invasive measurement of urinary 3-nitrotyrosine as a method of assessment of oxidative stress in humans remains to be established.     

Aluminium-induced production of oxygen radicals, lipid peroxidation and DNA damage in seedlings of rice (Oryza sativa)

The effect of aluminium (Al) on seedlings of two rice cultivars, Pusa Basmati and Vikas was investigated after different hours of exposure to 80 mol/L of external Al supply. With increasing time of exposure, the growing seedlings readily absorbed Al and its localization was greater in roots than shoots. Prolonged exposure to Al intensified lipid peroxidation, changed the activities of SOD and peroxidase and caused DNA damage. However, differential responses were observed between the seedlings of two rice cultivars under Al stress. A close inverse relationship existed between decreased root growth and increased Al accumulation, lipid peroxidation, SOD, peroxidase activities and DNA damage. The results demonstrate that roots are the major sites of Al localization and accumulation of Al promoted oxygen free radicals mediated peroxidation of membranes as evidenced by increased MDA levels and the activities of SOD and peroxidase. Our results for the first time showed that Al can cause DNA damage in rice.     

Singlet oxygen and photo-oxidative stress management in plants and algae

Photosynthetic organisms constantly face the threat of photo-oxidative stress from fluctuating light conditions and environmental stress. Plants and algae have developed an array of defences to protect the chloroplast from reactive oxygen species. Genetic and physiological studies have shown that antioxidant responses are important to high-light acclimation, both by directly scavenging or quenching reactive oxygen intermediates and by contributing reducing power for alternative electron transport pathways and excess energy dissipation. At present, the signalling events leading to up-regulation of antioxidant defences in high light remain a mystery. Recent advances toward understanding acclimation to oxidative stress in both photosynthetic and non-photosynthetic model organisms may illuminate how plants and algae respond to high-light stress. Although the role of hydrogen peroxide in high-light acclimation has been investigated, less is known about responses to singlet oxygen, a form of reactive oxygen that poses a significant threat specifically to photosynthetic organisms. This review will discuss some intriguing new findings in that area, focusing on recent findings regarding the nature of singlet-oxygen responses in the chloroplast.     

野牛草叶片活性氧及其清除系统对水分胁迫的响应

逆境条件下活性氧产生及其清除效率是衡量植物抗性的重要指标,而活性氧对植物组织的氧化伤害和抗氧化酶活性常因材料的遗传或生理差异性而发生变化。以同一基因型的野牛草(Buchloe dactyloides(Nutt.)Engelm'texoka')克隆分株叶片为材料,采用Hoagland营养液培养,研究了10%、20%和30%PEG-6000模拟干旱胁迫下,野牛草叶片活性氧的产生、脂质过氧化和抗氧化酶活性变化规律。结果表明:随着PEG-6000浓度的增加及胁迫时间的延长,超氧阴离子(O2-.)的产生速率、过氧化氢(H2O2)和丙二醛(MDA)含量均显著增加;超氧化物歧化酶(SOD EC1.15.1.1)、愈创木酚过氧化物酶(G-POD EC1.11.1.7)和过氧化氢酶(CATEC1.11.1.6)活性呈先上升后下降的变化趋势;SOD、G-POD与CAT活性达到峰值的时间随PEG-6000浓度的增加而提前。认为水分胁迫下,抗氧化酶可有效清除活性氧自由基,但随胁迫时间的延长,抗氧化酶活性受到抑制。     

Blue LED light exposure develops intracellular reactive oxygen species,lipid peroxidation,and subsequent cellular injuries in cultured bovine retinal pigment epithelial cells

Abstract

The effects of blue light emitter diode (LED) light exposure on retinal pigment epithelial cells (RPE cells) were examined to detect cellular damage or change and to clarify its mechanisms. The RPE cells were cultured and exposed by blue (470 nm) LED at 4.8 mW/cm². The cellular viability was determined by XTT assay and cellular injury was determined by the lactate dehydrogenase activity in medium. Intracellular reactive oxygen species (ROS) generation was determined by confocal laser microscope image analysis using dihydrorhodamine 123 and lipid peroxidation was determined by 4-hydroxy-2-nonenal protein-adducts immunofluorescent staining (HNE). At 24 h after 50 J/cm² exposures, cellular viability was significantly decreased to 74% and cellular injury was significantly increased to 365% of control. Immediately after the light exposure, ROS generation was significantly increased to 154%, 177%, and 395% of control and HNE intensity was increased to 211%, 359%, and 746% of control by 1, 10, and 50 J/cm², respectively. These results suggest, at least in part, that oxidative stress is an early step leading to cellular damage by blue LED exposure and cellular oxidative damage would be caused by the blue light exposure at even lower dose (1, 10 J/cm²).     

Effect of ferrous sulphate and ascorbic acid on motility, viability and lipid peroxidation of crossbred cattle bull spermatozoa

Numerous factors influence male fertility, one of these being the oxidative stress, which has elicited enormous interest recently. In sperm, induction of oxidation decreases motility and viability but increases lipid peroxidation (LPO). The optimum dose of ferrous ascorbate (FeAA: FeSO4 + ascorbic acid) for inducing oxidative stress by affecting motility, viability and LPO has been ascertained in local crossbred cattle bull spermatozoa. The fractions of spermatozoa suspended in 2.9% sodium citrate were subjected to three doses of FeAA (100 : 500, 150 : 750, 200 : 1000; μmol/l FeSO4 : μmol/l ascorbic acid). These fractions were assessed for various parameters. Increase in the incubation period and promoter concentration induced a decrease in motility and viability, but an increase in LPO. Among three doses of FeAA, 150 : 750 μmol/l ascorbic acid is suggested to be the optimum/best dose as it induces the oxidative stress/LPO to a significant extent and also maintains better motility and viability as compared with the other two doses, and such conditions may enhance the fertilising potential of bull spermatozoa.     

Ascorbic Acid Inhibits Lipid Peroxidation but Enhances DNA Damage in Rat Liver Nuclei Incubated with Iron Ions

In this report we studied DNA damage and lipid peroxidation in rat liver nuclei incubated with iron ions for up to 2 hrs in order to examine whether nuclear DNA damage was dependent on membrane lipid peroxidation. Lipid peroxidation was measured as thio-barbituric acid-reactive substances (TBARS) and DNA damage was measured as 8-OH-deoxyguanosine (8-OH-dG). We showed that Fe(II) induced nuclear lipid peroxidation dose-dependently but only the highest concentration (1.0 mM) used induced appreciable 8-OH-dG. Fe(II1) up to 1 mM induced minimal lipid peroxidation and negligible amounts of 8-OH-dG. Ascorbic acid enhanced Fe(II)-induced lipid peroxidation at a ratio to Fe(II) of 1:l but strongly inhibited peroxidation at ratios of 2.5:l and 5:l. By contrast, ascorbate markedly enhanced DNA damage at all ratios tested and in a concentration-dependent manner. The nuclear DNA damage induced by 1 niM FeSO₄/5 mM ascorbic acid was largely inhibited by iron chelators and by dimethylsulphoxide and manni-tol, indicating the involvement of OH. Hydrogen peroxide and superoxide anions were also involved, as DNA damage was partially inhibited by catalase and, to a lesser extent, by superoxide dismutase. The chain-breaking antioxidants butylated hydroxytoluene and diphenylamine (an alkoxyl radical scavenger) did not inhibit DNA damage. Hence, this study demonstrated that ascorbic acid enhanced Fe(II)-induced DNA base modification which was not dependent on lipid peroxidation in rat liver nuclei.     

Levels of oxidative damage and proinflammatory cytokines are enhanced in patients with active vitiligo

Vitiligo is an autoimmune depigmenting skin disease characterised by loss of melanocytes wherein oxidative stress is proposed to be the initial triggering factor with subsequent immune dysregulation. This study aimed to evaluate the relationship, if any, between the generation of reactive oxygen species (ROS), markers of oxidative damage and circulating cytokines in patients with active vitiligo. The generation of ROS in erythrocytes and neutrophils was significantly higher in patients with active vitiligo than healthy controls. Alongside, markers of oxidative stress-mediated damage namely lipid peroxidation, DNA damage and protein carbonylation were evaluated. Patients with active vitiligo demonstrated increased lipid and DNA damage but minimal protein damage. There was a significant decline in the free radical scavenging capacity of active vitiligo cases. A positive correlation existed between baseline levels of ROS and lipid peroxidation as also DNA damage. Patients with active vitiligo demonstrated an increase in several proinflammatory (IL-6, TNF-α, IL-1β, IFN-γ and IL-8) and some anti-inflammatory/immunoregulatory (IL-5 and IL-10) cytokines. Importantly, the levels of IFN-γ and IL-10 consistently correlated with the generation of ROS, markers of damage and their free radical scavenging capacity. Taken together, patients with active vitiligo demonstrated an enhanced generation of ROS in erythrocytes and neutrophils which mediated lipid peroxidation, DNA damage and coupled with a decline in their antioxidant capacity created a pro-oxidant milieu that favoured tissue damage and potential generation of neoantigens, accounting for disease progression.     

Influence of indole acetic acid on antioxidant levels and enzyme activities of glucose metabolism in rat liver

Indole acetic acid (IAA) is an auxin and can be synthesized in animals. This compound is metabolized in vitro by peroxidase, producing reactive oxygen species. The toxic effect of indole acetic acid in leukocytes is associated with peroxidase activities and these processes have been implicated in activation of glucose and glutamine metabolism. However, studies in vitro have shown that IAA, in absence of peroxidase, is an antioxidant almost as high in potency as those of other indolic compounds. The purpose of this study was to investigate the possible involvement of a toxic effect of indole acetic acid in the liver, as evidenced by oxidative stress and enzyme activities of the glucose pathway. The animals received IAA by subcutaneous or gavage administration in a phosphate buffered saline (the control group received only the phosphate buffered saline). The other groups received IAA at concentrations of 1 mg, 18 mg and 40 mg per kg of body mass per day. Treatments with 18 mg and 40 mg IAA decreased the activity of catalase by both subcutaneous (30% and 26%) or gavage administration (19% and 28%), respectively. A similar effect was observed on the activity of glutathione peroxidase of animals exposed to 18 mg and 40 mg IAA: A decrease of 34% and 29%, respectively, for subcutaneous administration and a decrease of 29% and 25%, respectively, for gavage administration. However, in neither source of administration did the acid alter superoxide dismutase, glutathione reductase and myeloperoxidase activities. Another alteration was observed in respect of reduced glutathione content in this organ. The lipid peroxidation level showed a significant decrease with subcutaneous (30%, 29% and 24%) and gavage administration (25%, 26% and 24%) using 1 mg, 18 mg and 40 mg of IAA, respectively compared with the control. The reduced glutathione content and catalase activity in the plasma were not altered by either of the two methods of administration. In addition to these findings, after subcutaneous or gavage administration of IAA, the activities of hepatic enzymes of glucose metabolism were not affected (glucokinase, lactate dehydrogenase, glucose-6-phosphate dehydrogenase and citrate synthase). Evidence is presented herein that IAA did not have a pro-oxidant effect in the liver as deduced from a reduction of catalase and glutathione peroxidase activities, a decrease of lipid peroxidation content and no alteration of the pool of reduced glutathione. The effects of IAA were independent of the way of administration.     

Analysis of 8-hydroxydeoxyguanosine among workers exposed to diesel particulate exhaust: comparison with urinary metabolites and PAH air monitoring

Oxidative DNA damage and repair, as measured by 8-hydroxy-2'-deoxyguanosine (8-OHdG) in urine and DNA samples were studied in association with work-related diesel exhaust exposure among garage and waste collection workers. Seasonal variations of the urinary 8-OHdG levels in pre- and two post-workshift urine samples of 29 exposed workers and 36 control persons were evaluated. The mean±SE levels of post-workshift 8-OHdG (μmol/mol crea) were 1.52±0.44 in winter and 1.61±0.33 in summer for the exposed workers, and 1.56±0.61 in winter and 1.43±0.49 in summer for the controls, respectively. No significant difference in the urinary 8-OHdG levels between exposed workers and control subjects in winter (p=0.923) and summer (p=0.350) was observed. A linear mixed model, adjusted for years of employment, age, ex/non-smoking and BMI, indicated no significant dose exposure-relationships between the urinary 8-OHdG and 15 PAH air concentrations nor between the 8-OHdG and 7 PAH monohydroxy-metabolites analyzed in the same workers. 8-OHdG was also analyzed in the mononuclear cell DNA of 19 exposed and 18 control subjects. The mean value of 8-OHdG/non-modified 2'-deoxyguanosine (8-OHdG/105 dG±SE) were 4.89±0.17 for the exposed and 4.11±0.16 for the control persons, which showed no correlation with the urinary 8-OHdG levels (r=0.01, n=28, P=0.96). The PAH exposure at workplaces was mainly composed of volatile compounds, particularly naphthalene, suggesting low exposure through the respiratory tract and a low effect of PAH in ROS induction.     

Menadione perturbs oxidative stress biomarkers and testicular function indices of rats

In this study, we evaluated the influence of menadione on the androgenic, oxidative stress biomarkers, and testicular function indices in rats. Rats (20) were randomized into four groups (A‐D) of five rats each. Rats in groups A, B, C, and D received the vehicle of administration (olive oil), 25, 50, or 100 mg/kg body weight menadione intraperitoneally, respectively, for 7 days. Menadione lowered serum cholesterol, follicle‐stimulating hormone, luteinizing hormone, and testosterone and luteinizing hormone reduced significantly in rats when compared with the control rats. Furthermore, menadione lowered the testicular function indices in the testes of rats. The activities of superoxide dismutase and catalase in the testes of menadione‐treated rats decreased significantly. Also, glutathione was depleted with concomitant malondialdehyde increase. The findings of this study show that menadione induces testicular toxicity by depleting the antioxidant defense system leading to perturbation in the testicular function indices.     

辣椒细胞质雄性不育与活性氧代谢的关系

通过测定辣椒保护酶活性和膜脂过氧化产物,研究了辣椒胞质雄性不育三系与膜脂过氧化的关系.结果表明,从花粉母细胞减数分裂前至花粉成熟期,三系之间SOD活性无明显差异,不育系花药中的CAT和POD活性均显著或极显著低于保持系和恢复系,而O2-·产生效率、MDA含量则显著或极显著高于保持系和恢复系.同时,在花药发育过程中,由于质、核差异,保持系的CAT活性明显高于恢复系,SOD和POD活性保持系和恢复系之间无明显差异.     

Antioxidant metabolism in pearl millet genotypes during compatible and incompatible interaction with downy mildew pathogen

In this study, the ascorbic acid content, lipid peroxidation product, reactive oxygen generation and scavenging enzyme activities were determined in pearl millet [Pennisetum glaucum (L.) R.Br.] leaves. These parameters were analysed at two stages: (i) pre-infection [45 days after sowing (DAS)] and (ii) post-infection [7 days after infection (DAI), i.e. 57 DAS]. Lipid peroxidation product (malondialdehyde content) was recorded higher in compatible interaction at pre-infection stage while it was increased in incompatible interaction at post-infection stage. Resistant genotypes had higher ascorbic acid content at both the stages of analysis. Superoxide dismutase (SOD) activity was higher in susceptible genotypes at pre-infection but after infection it was found to be higher in resistant genotypes. Ascorbate peroxidase, catalase (CAT) and lipoxygenase activities were higher in resistant genotypes at both the stages of analysis. Native PAGE isozyme banding pattern of SOD, CAT, APX and esterase showed some inducible band(s) due to disease infection.     

Comparative study of the formation of oxidative damage marker 8-hydroxy-2'-deoxyguanosine (8-OHdG) adduct from the nucleoside 2'-deoxyguanosine by transition metals and suspensions of particulate matter in relation to metal content and redox reactivity

An association between exposure to ambient particulate matter (PM) and increased incidence of mortality and morbidity due to lung cancer and cardiovascular diseases has been demonstrated by recent epidemiological studies. Reactive oxygen species (ROS), especially hydroxyl radicals, generated by PM, have been suggested by many studies as an important factor in the oxidative damage of DNA by PM. The purpose of this study was to characterize quantitatively hydroxyl radical generation by various transition metals in the presence of H₂O₂ in aqueous buffer solution (pH 7.4) and hydroxylation of 2'-deoxyguanosine (dG) to 8-hydroxy-2'-deoxyguanosine (8-OHdG) under similar conditions. The order of metals' redox reactivity and hydroxyl radical production was Fe(II), V(IV), Cu(I), Cr(III), Ni(II), Co(II), Pb(II), Cd(II). Then, we investigated the generation of hydroxyl radicals in the presence of H₂O₂ by various airborne PM samples, such as total suspended particulate (TSP), PM₁₀, PM_2.5 (PM with aerodynamic diameter 10 and 2.5 μm), diesel exhaust particles (DEP), gasoline exhaust particles (GEP) and woodsmoke soot under the same conditions. When suspensions of PMs were incubated with H₂O₂ and dG at pH 7.4, all particles induced hydroxylation of dG and formation of 8-OHdG in a dose-dependent increase. Our findings demonstrated that PM's hydroxyl radical (HO√) generating ability and subsequent dG hydroxylation is associated with the concentration of water-soluble metals, especially Fe and V and other redox or ionizable transition metals and not their total metal content, or insoluble metal oxides, via a Fenton-driven reaction of H₂O₂ with metals. Additionally, we observed, by Electron paramagnetic resonance (EPR), that PM suspensions in the presence of H₂O₂ generated radical species with dG, which were spin-trapped by 2-methyl-2-nitroso-propane (MNP).     

Azadirachta indica acts as a pro‐oxidant and modulates cell cycle associated proteins during DMBA/TPA induced skin carcinogenesis in mice

The present study was designed to determine the modulatory effect of aqueous Azadirachta indica leaf extract (AAILE) on cell cycle–associated proteins during two‐stage skin carcinogenesis in mice. Considering the dual role of reactive oxygen species in cancer and its chemoprevention, the levels of lipid peroxidation (index of peroxidative damage) were also determined. Skin tumours were induced by topical application of 7,12‐dimethylbenz(a)anthracene (DMBA) as a carcinogen followed by the repetitive application of 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) as a promoter. Skin tumours obtained in the DMBA/TPA group exhibited enhanced expression of proliferating cell nuclear antigen (PCNA, index of proliferation), p21 and cyclin D1, with no alterations in p53 expression in comparison to the control group. Tumours in AAILE + DMBA/TPA group exhibited low PCNA and cyclin D1 expression and enhanced expression of p53 and p21 in comparison to the DMBA/TPA group. The skin tumours obtained in the AAILE + DMBA/TPA group exhibited high lipid peroxidation levels in comparison to the tumours obtained in the DMBA/TPA group. The observations of the present study suggest that AAILE behaves as a pro‐oxidant in the tumours, thereby rendering them susceptible to damage, which eventually culminates into its anti‐neoplastic action. Also, cell cycle regulatory proteins may be modulated by AAILE and could affect the progression of cells through the cell cycle. Copyright © 2012 John Wiley & Sons, Ltd.     

Antioxidants, Oxidative Damage and Oxygen Deprivation Stress: a Review

Oxidative stress is induced by a wide range of environmentalfactors including UV stress, pathogen invasion (hypersensitivereaction), herbicide action and oxygen shortage. Oxygen deprivationstress in plant cells is distinguished by three physiologicallydifferent states: transient hypoxia, anoxia and reoxygenation.Generation of reactive oxygen species (ROS) is characteristicfor hypoxia and especially for reoxygenation. Of the ROS, hydrogenperoxide (H₂O₂) and superoxide (O₂^·–) are bothproduced in a number of cellular reactions, including the iron-catalysedFenton reaction, and by various enzymes such as lipoxygenases,peroxidases, NADPH oxidase and xanthine oxidase. The main cellularcomponents susceptible to damage by free radicals are lipids(peroxidation of unsaturated fatty acids in membranes), proteins(denaturation), carbohydrates and nucleic acids. Consequencesof hypoxia-induced oxidative stress depend on tissue and/orspecies (i.e. their tolerance to anoxia), on membrane properties,on endogenous antioxidant content and on the ability to inducethe response in the antioxidant system. Effective utilizationof energy resources (starch, sugars) and the switch to anaerobicmetabolism and the preservation of the redox status of the cellare vital for survival. The formation of ROS is prevented byan antioxidant system: low molecular mass antioxidants (ascorbicacid, glutathione, tocopherols), enzymes regenerating the reducedforms of antioxidants, and ROS-interacting enzymes such as SOD,peroxidases and catalases. In plant tissues many phenolic compounds(in addition to tocopherols) are potential antioxidants: flavonoids,tannins and lignin precursors may work as ROS-scavenging compounds.Antioxidants act as a cooperative network, employing a seriesof redox reactions. Interactions between ascorbic acid and glutathione,and ascorbic acid and phenolic compounds are well known. Underoxygen deprivation stress some contradictory results on theantioxidant status have been obtained. Experiments on overexpressionof antioxidant production do not always result in the enhancementof the antioxidative defence, and hence increased antioxidativecapacity does not always correlate positively with the degreeof protection. Here we present a consideration of factors whichpossibly affect the effectiveness of antioxidant protectionunder oxygen deprivation as well as under other environmentalstresses. Such aspects as compartmentalization of ROS formationand antioxidant localization, synthesis and transport of antioxidants,the ability to induce the antioxidant defense and cooperation(and/or compensation) between different antioxidant systemsare the determinants of the competence of the antioxidant system.     

Growth,photosynthetic electron transport,and antioxidant responses of young soybean seedlings to simultaneous exposure of nickel and UV-B stress

The effects of enhanced ultraviolet-B (UV-B, 0.4 W m⁻²) irradiance and nickel (Ni, 0.01, 0.10 and 1.00 mM; Ni_0.01, Ni_0.10, Ni_1.00, respectively) treatment, singly and in combination, on growth, photosynthetic electron transport activity, the contents of reactive oxygen species (ROS), antioxidants, lipid peroxidation, and membrane leakage in soybean seedlings were evaluated. Ni_0.10 and Ni_1.00 and UV-B declined the growth and chlorophyll content, which were further reduced following combined exposure. Contrary to this, Ni_0.01 stimulated growth, however, the effect together with UV-B was inhibitory. Carotenoids showed varied response to both the stresses. Simultaneous exposure of UV-B and Ni as well as UV-B alone reduced the activities of photosystems 1 and 2 (PS1 and PS2) and whole chain activity significantly, while Ni individually, besides strongly inhibiting PS2 and whole chain activity, stimulated the PS1 activity. Both the stresses, alone and together, enhanced the contents of superoxide radical (O ₂ ^⋅− ), hydrogen peroxide (H₂O₂), malondialdehyde (MDA), electrolyte leakage, and proline content, while ascorbate content declined over control. Individual treatments increased the activities of catalase (CAT), peroxidase, and superoxide dismutase (SOD), but Ni_1.00 declined SOD activity significantly. Combined exposure exhibited similar response, however, CAT activity declined even more than in control. Compared to individual effects of UV-B and Ni, the simultaneous exposure resulted in strong inhibition of photosynthetic electron transport and excessive accumulation of ROS, thereby causing severe damage to soybean seedlings.This work was supported by the CSIR, New Delhi, India in the form of JRF to Rajiv Dwivedi.     

低温胁迫下钼对冬小麦抗氧化防御系统及膜脂过氧化的影响

研究了低温（0～5℃）胁迫下钼对冬小麦抗氧化系统和膜脂过氧化的影响。结果表明,低温胁迫下施钼植株电解质渗漏率和丙二醛含量显著降低。施用钼肥提高了冬小麦叶片中抗氧化酶类如超氧化物歧化酶（SOD,EC1．15．1．1）、过氧化物酶（POX,EC1．11．1．7）和过氧化氢酶（CAT,ECl．11．1．6）的活性。低温胁迫下施钼对抗氧化酶（SOD、POX和CAT）活性提高幅度比常温下高。不论常温还是低温下,施铝均提高了冬小麦叶片中抗坏血酸和脯氨酸含量,低温胁迫下提高幅度更大。常温下缺钼和施钼处理后,叶片中类胡萝卜素含量差异不显著;低温下施钼后,冬小麦叶片类胡萝卜素含量显著增加。因此,低温胁迫下施钼植株活性氧清除能力增强、细胞膜伤害减轻可能是冬小麦抗寒力提高的原因之一。