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The PsaE protein is located at the reducing side of photosystem I (PSI) and is involved in docking the soluble electron acceptors, particularly ferredoxin. However, deletion of the psaE gene in the cyanobacterium Synechocystis sp. strain PCC 6803 inhibited neither photoautotrophic growth, nor in vivo linear and cyclic electron flows. Using photoacoustic spectroscopy, we detected an oxygen-dependent, PSI-mediated energy storage activity in the DeltapsaE null mutant, which was not present in the wild type (WT). The expression of the genes encoding catalase (katG) and iron superoxide dismutase (sodB) was upregulated in the DeltapsaE mutant, and the increase in katG expression was correlated with an increase in catalase activity of the cells. When catalases were inhibited by sodium azide, the production of reactive oxygen species was enhanced in DeltapsaE relative to WT. Moreover, sodium azide strongly impaired photoautotrophic growth of the DeltapsaE mutant cells while WT was much less sensitive to this inhibitor. The katG gene was deleted in the DeltapsaE mutant, and the resulting double mutant was more photosensitive than the single mutants, showing cell bleaching and lipid peroxidation in high light. Our results show that the presence of the PsaE polypeptide at the reducing side of PSI has a function in avoidance of electron leakage to oxygen in the light (Mehler reaction) and the resulting formation of toxic oxygen species. PsaE-deficient Synechocystis cells can counteract the chronic photoreduction of oxygen by increasing their capacity to detoxify reactive oxygen species.

Plants, like most living organisms, spontaneously emit photons of visible light. This ultraweak endogenous chemiluminescence is linked to the oxidative metabolism, with lipid peroxidation constituting a major source of photons in plants. We imaged this signal using a very sensitive cooled CCD camera and analysed its spectral characteristics using bandpass interference filters. In vitro oxidation of lipids induced luminescence throughout the visible spectrum (450–850 nm). However, luminescence in the red spectral domain (>640 nm) occurred first, then declined in parallel with the appearance of the emission in the blue-green (<600 nm). This temporal separation suggests that the chemical species emitting in the blue-green are secondary products, possibly deriving from the red light-emitting species. This conversion did not seem to occur in planta because spontaneous chemiluminescence from plant tissues (leaves, roots) occurred only in the red/far-red light domain (>640 nm), peaking at 700–750 nm. The spectrum of plant chemiluminescence was independent of chlorophyll. The in vivo signal was modulated by cellular detoxification mechanisms and by changes in the concentration of singlet oxygen in the tissues, although the singlet oxygen luminescence bands did not appear as major bands in the spectra. Our results indicate that the intensity of endogenous chemiluminescence from plant tissues is determined by the balance between the formation of luminescent species through secondary reactions involving lipid peroxide-derived intermediates, including singlet oxygen, and their elimination by metabolizing processes. The kinetic aspects of plant chemiluminescence must be taken into account when using the signal as an oxidative stress marker. [ABSTRACT FROM AUTHOR]

Plastoquinone-9 (PQ-9) is an essential component of photosynthesis that carries electrons in the linear and alternative electron transport chains, and is also a redox sensor that regulates state transitions and gene expression. However, a large fraction of the PQ pool is located outside the thylakoid membranes, in the plastoglobules and the chloroplast envelopes, reflecting a wider range of functions beyond electron transport. This review describes new functions of PQ in photoprotection, as a potent antioxidant, and in chloroplast metabolism as a cofactor in the biosynthesis of chloroplast metabolites. It also focuses on the essential need for tight environmental control of PQ biosynthesis and for active exchange of this compound between the thylakoid membranes and the plastoglobules. Through its multiple functions, PQ connects photosynthesis with metabolism, light acclimation, and stress tolerance. Plastoquinone (PQ)-9 is an electron carrier that plays an essential role in photosynthesis where it is involved in linear and alternative electron flows. However, the functions of PQ go far beyond photosynthesis. PQ-9 is a multilocation compound that is partitioned in the chloroplast between thylakoids, plastoglobules, and envelopes. Its distribution is modulated dynamically by various regulatory enzymes as a function of the environmental conditions. The redox state of the PQ pool plays a crucial role in various functional and metabolic processes, such as light acclimation, biosynthesis of metabolites, and gene expression. PQ is a potent antioxidant that scavenges reactive oxygen species and mitigates lipid peroxidation in planta , supplementing the photoprotection provided by β-carotene in photosystem II and tocopherols in the thylakoid lipid phase. [ABSTRACT FROM AUTHOR]

Summary: Singlet oxygen (1O2) is a by‐product of photosynthesis that triggers a signalling pathway leading to stress acclimation or to cell death. By analyzing gene expressions in a 1O2‐overproducing Arabidopsis mutant (ch1) under different light regimes, we show here that the 1O2 signalling pathway involves the endoplasmic reticulum (ER)‐mediated unfolded protein response (UPR). ch1 plants in low light exhibited a moderate activation of UPR genes, in particular bZIP60, and low concentrations of the UPR‐inducer tunicamycin enhanced tolerance to photooxidative stress, together suggesting a role for UPR in plant acclimation to low 1O2 levels. Exposure of ch1 to high light stress ultimately leading to cell death resulted in a marked upregulation of the two UPR branches (bZIP60/IRE1 and bZIP28/bZIP17). Accordingly, mutational suppression of bZIP60 and bZIP28 increased plant phototolerance, and a strong UPR activation by high tunicamycin concentrations promoted high light‐induced cell death. Conversely, light acclimation of ch1 to 1O2 stress put a limitation in the high light‐induced expression of UPR genes, except for the gene encoding the BIP3 chaperone, which was selectively upregulated. BIP3 deletion enhanced Arabidopsis photosensitivity while plants treated with a chemical chaperone exhibited enhanced phototolerance. In conclusion, 1O2 induces the ER‐mediated UPR response that fulfils a dual role in high light stress: a moderate UPR, with selective induction of BIP3, is part of the acclimatory response to 1O2, and a strong activation of the whole UPR is associated with cell death. Significance Statement: Singlet oxygen, produced from photosystem II under conditions of excess light energy, triggers the endoplasmic reticulum‐mediated unfolded protein response (UPR), with different UPR levels inducing different physiological responses to light stress. Moderate activation of UPR participates in the acclimation to singlet oxygen, while strong activation leads to cell death. [ABSTRACT FROM AUTHOR]

Summary: Stressful environmental conditions lead to the production of reactive oxygen species in the chloroplasts, due to limited photosynthesis and enhanced excitation pressure on the photosystems. Among these reactive species, singlet oxygen (1O2), which is generated at the level of the PSII reaction center, is very reactive, readily oxidizing macromolecules in its immediate surroundings, and it has been identified as the principal cause of photooxidative damage in plant leaves. The two β‐carotene molecules present in the PSII reaction center are prime targets of 1O2 oxidation, leading to the formation of various oxidized derivatives. Plants have evolved sensing mechanisms for those PSII‐generated metabolites, which regulate gene expression, putting in place defense mechanisms and alleviating the effects of PSII‐damaging conditions. A new picture is thus emerging which places PSII as a sensor and transducer in plant stress resilience through its capacity to generate signaling metabolites under excess light energy. This review summarizes new advances in the characterization of the apocarotenoids involved in the PSII‐mediated stress response and of the pathways elicited by these molecules, among which is the xenobiotic detoxification. [ABSTRACT FROM AUTHOR]

Abstract: The Arabidopsis vte1 mutant is devoid of tocopherol and plastochromanol (PC‐8). When exposed to excess light energy, vte1 produced more singlet oxygen (1O2) and suffered from extensive oxidative damage compared with the wild type. Here, we show that overexpressing the solanesyl diphosphate synthase 1 (SPS1) gene in vte1 induced a marked accumulation of total plastoquinone (PQ‐9) and rendered the vte1 SPS1oex plants tolerant to photooxidative stress, indicating that PQ‐9 can replace tocopherol and PC‐8 in photoprotection. High total PQ‐9 levels were associated with a noticeable decrease in 1O2 production and higher levels of Hydroxyplastoquinone (PQ‐C), a 1O2‐specific PQ‐9 oxidation product. The extra PQ‐9 molecules in the vte1 SPS1oex plants were stored in the plastoglobules and the chloroplast envelopes, rather than in the thylakoid membranes, whereas PQ‐C was found almost exclusively in the thylakoid membranes. Upon exposure of wild‐type plants to high light, the thylakoid PQ‐9 pool decreased, whereas the extrathylakoid pool remained unchanged. In vte1 and vte1 SPS1oex plants, the PQ‐9 losses in high light were strongly amplified, affecting also the extrathylakoid pool, and PQ‐C was found in high amounts in the thylakoids. We conclude that the thylakoid PQ‐9 pool acts as a 1O2 scavenger and is replenished from the extrathylakoid stock. [ABSTRACT FROM AUTHOR]

Summary: Prenylquinols (tocochromanols and plastoquinols) serve as efficient physical and chemical quenchers of singlet oxygen (1O2) formed during high light stress in higher plants. Although quenching of 1O2 by prenylquinols has been previously studied, direct evidence for chemical quenching of 1O2 by plastoquinols and their oxidation products is limited in vivo. In the present study, the role of plastoquinol‐9 (PQH2‐9) in chemical quenching of 1O2 was studied in Arabidopsis thaliana lines overexpressing the SOLANESYL DIPHOSPHATE SYNTHASE 1 gene (SPS1oex) involved in PQH2‐9 and plastochromanol‐8 biosynthesis. In this work, direct evidence for chemical quenching of 1O2 by plastoquinols and their oxidation products is presented, which is obtained by microscopic techniques in vivo. Chemical quenching of 1O2 was associated with consumption of PQH2‐9 and formation of its various oxidized forms. Oxidation of PQH2‐9 by 1O2 leads to plastoquinone‐9 (PQ‐9), which is subsequently oxidized to hydroxyplastoquinone‐9 [PQ(OH)‐9]. We provide here evidence that oxidation of PQ(OH)‐9 by 1O2 results in the formation of trihydroxyplastoquinone‐9 [PQ(OH)3‐9]. It is concluded here that PQH2‐9 serves as an efficient 1O2 chemical quencher in Arabidopsis, and PQ(OH)3‐9 can be considered as a natural product of 1O2 reaction with PQ(OH)‐9. The understanding of the mechanisms underlying 1O2 chemical quenching provides information on the role of plastoquinols and their oxidation products in the response of plants to photooxidative stress. [ABSTRACT FROM AUTHOR]

Singlet oxygen (1O2) signalling in plants is essential to trigger both acclimatory mechanisms and programmed cell death under high light stress. However, because of its chemical features, 1O2 requires mediators, and the players involved in this pathway are largely unknown. The β-carotene oxidation product, β-cyclocitral, is one such mediator. Produced in the chloroplast, β-cyclocitral induces changes in nuclear gene expression leading to photoacclimation. Recently, the METHYLENE BLUE SENSITIVITY protein MBS has been identified as a key player in 1O2 signalling leading to tolerance to high light. Here, we provide evidence that MBS1 is essential for acclimation to 1O2 and cross-talks with β-cyclocitral to mediate transfer of the 1O2 signal to the nucleus, leading to photoacclimation. The presented results position MBS1 downstream of β-cyclocitral in 1O2 signalling and suggest an additional role for MBS1 in the regulation of plant growth and development under chronic 1O2 production. [ABSTRACT FROM AUTHOR]

The circadian clock helps plants measure daylength and adapt to changes in the day-night rhythm. We found that changes in the light-dark regime triggered stress responses, eventually leading to cell death, in leaves of Arabidopsis thaliana plants with reduced cytokinin levels or defective cytokinin signaling. Prolonged light treatment followed by a dark period induced stress and cell death marker genes while reducing photosynthetic efficiency. This response, called circadian stress, is also characterized by altered expression of clock and clock output genes. In particular, this treatment strongly reduced the expression of CIRCADIAN CLOCK ASSOCIATED1 (CCA1) and LATE ELONGATED HYPOCOTYL (LHY). Intriguingly, similar changes in gene expression and cell death were observed in clock mutants lacking proper CCA1 and LHY function. Circadian stress caused strong changes in reactive oxygen species- and jasmonic acid (JA)-related gene expression. The activation of the JA pathway, involving the accumulation of JA metabolites, was crucial for the induction of cell death, since the cell death phenotype was strongly reduced in the jasmonate resistant1 mutant background. We propose that adaptation to circadian stress regimes requires a normal cytokinin status which, acting primarily through the AHK3 receptor, supports circadian clock function to guard against the detrimental effects of circadian stress. [ABSTRACT FROM AUTHOR]

The production of reactive oxygen species (ROS) is an unavoidable consequence of oxygenic photosynthesis. Singlet oxygen (1O2) is a highly reactive species to which has been attributed a major destructive role during the execution of ROS-induced cell death in photosynthetic tissues exposed to excess light. The study of the specific biological activity of 1O2 in plants has been hindered by its high reactivity and short lifetime, the concurrent production of other ROS under photooxidative stress, and limited in vivo detection methods. However, during the last 15 years, the isolation and characterization of two 1O2-overproducing mutants in Arabidopsis thaliana, flu and ch1, has allowed the identification of genetically controlled 1O2 cell death pathways and a 1O2 acclimation pathway that are triggered at sub-cytotoxic concentrations of 1O2. The study of flu has revealed the control of cell death by the plastid proteins EXECUTER (EX)1 and EX2. In ch1, oxidized derivatives of β-carotene, such as β-cyclocitral and dihydroactinidiolide, have been identified as important upstream messengers in the 1O2 signaling pathway that leads to stress acclimation. In both the flu and ch1 mutants, phytohormones act as important promoters or inhibitors of cell death. In particular, jasmonate has emerged as a key player in the decision between acclimation and cell death in response to 1O2. Although the flu and ch1 mutants show many similarities, especially regarding their gene expression profiles, key differences, such as EXECUTER-independent cell death in ch1, have also been observed and will need further investigation to be fully understood. [ABSTRACT FROM AUTHOR]

Carotenoids are known to play important roles in plants as antioxidants, accessory light-harvesting pigments, and attractants for pollinators and seed dispersers. A new function for carotenoids has recently emerged, which relates to the response of plants to environmental stresses. Reactive oxygen species, especially singlet oxygen, produced in the chloroplasts under stress conditions, can oxidize carotenoids leading to a variety of oxidized products, including aldehydes, ketones, endoperoxides and lactones. Some of those carotenoid derivatives, such as volatile β-cyclocitral, derived from the oxidation of β-carotene, are reactive electrophile species that are bioactive and can induce changes in gene expression leading to acclimation to stress conditions. This review summarizes the current knowledge on the non-enzymatic oxidation of carotenoids, the bioactivity of the resulting cleavage compounds and their functions as stress signals in plants. [ABSTRACT FROM AUTHOR]

Singlet oxygen (1O2) is a reactive oxygen species that can function as a stress signal in plant leaves leading to programmed cell death. In microalgae, 1O2 -induced transcriptomic changes result in acclimation to 1O2. Here, using a chlorophyll b –less Arabidopsis thaliana mutant (chlorina1 [ ch1 ]), we show that this phenomenon can also occur in vascular plants. The ch1 mutant is highly photosensitive due to a selective increase in the release of 1O2 by photosystem II. Under photooxidative stress conditions, the gene expression profile of ch1 mutant leaves very much resembled the gene responses to 1O2 reported in the Arabidopsis mutant flu. Preexposure of ch1 plants to moderately elevated light intensities eliminated photooxidative damage without suppressing 1O2 formation, indicating acclimation to 1O2. Substantial differences in gene expression were observed between acclimation and high-light stress: A number of transcription factors were selectively induced by acclimation, and contrasting effects were observed for the jasmonate pathway. Jasmonate biosynthesis was strongly induced in ch1 mutant plants under high-light stress and was noticeably repressed under acclimation conditions, suggesting the involvement of this hormone in 1O2 -induced cell death. This was confirmed by the decreased tolerance to photooxidative damage of jasmonate-treated ch1 plants and by the increased tolerance of the jasmonate-deficient mutant delayed-dehiscence2. [ABSTRACT FROM AUTHOR]

1O2 (singlet oxygen) is a reactive O2 species produced from triplet excited chlorophylls in the chloroplasts, especially when plants are exposed to excess light energy. Similarly to other active O2 species, 1O2 has a dual effect: It is toxic, causing oxidation of biomolecules, and it can act as a signal molecule that leads to cell death or to acclimation. Carotenoids are considered to be the main 1O2 quenchers in chloroplasts, and we show here that light stress induces the oxidation of the carotenoid β-carotene in Arabidopsis plants, leading to the accumulation of different volatile derivatives. One such compound, β-cyclocitral, was found to induce changes in the expression of a large set of genes that have been identified as 1O2 responsive genes. In contrast, β-cyclocitral had little effect on the expression of H2O2 gene markers. β-Cyclocitral-induced reprogramming of gene expression was associated with an increased tolerance to photooxidative stress. The results indicate that β-cyclocitral is a stress signal produced in high light that is able to induce defense mechanisms and represents a likely messenger involved in the 1O2 signaling pathway in plants. [ABSTRACT FROM AUTHOR]

Singlet oxygen (1O2) is a singular reactive oxygen species (ROS) that is produced constitutively in plant leaves in light via chlorophylls that act as photosensitizers. This 1O2 production is spatially resolved within thylakoid membranes and is enhanced under light stress conditions. 1O2 can also be produced by phytotoxins during plant–pathogen interactions. 1O2 is highly reactive, can be toxic to cells and can be involved in the signaling of programmed cell death or acclimation processes. Here, we summarize current knowledge on 1O2 management in plants and on the biological effects of this peculiar ROS. Compared with other ROS, 1O2 has received relatively little attention, but recent developments indicate that it has a crucial role in the responses of plants to light. [Copyright &y& Elsevier]

Living organisms spontaneously emit faint light, and this autoluminescence is stimulated in response to many stresses. This phenomenon is attributable to the endogenous production of excited states during oxidative reactions, particularly during peroxidation of lipids, which generates light-emitting molecules such as triplet carbonyls and singlet oxygen. Using highly sensitive cameras, it is now possible to remotely image spontaneous luminescence with a good spatial resolution, providing a new non-invasive tool for mapping oxidative stress and lipid peroxidation in plants. [Copyright &y& Elsevier]

Abstract: The products of the isiAB operon are a chlorophyll antenna protein (IsiA) and flavodoxin (IsiB), which accumulate in cyanobacteria grown under iron starvation conditions. Here we show that strong light triggers de-repression of isiAB transcription and leads to IsiA and flavodoxin accumulation under iron replete conditions. Genetic deletion of isiAB resulted in a photosensitive phenotype, with accumulation of reactive oxygen species and cell bleaching in high light, while the flavodoxin-deficient isiB null mutant expressing isiA was phototolerant. We conclude that IsiA protects cyanobacteria from photooxidative stress. IsiA is the first example of a chlorophyll antenna protein outside the extended LHC family that is induced transiently by high light and that fulfills a photoprotective role. [Copyright &y& Elsevier]

When exposed to unfavorable environmental conditions, plants can absorb light energy in excess of their photosynthetic capacities, with the surplus energy leading to the production of reactive oxygen species and photooxidative stress. Subsequent lipid peroxidation generates toxic reactive carbonyl species whose accumulation culminates in cell death. β-Cyclocitral, an oxidized by-product of β-carotene generated in the chloroplasts, mediates a protective retrograde response that lowers the levels of toxic peroxides and carbonyls, limiting damage to intracellular components. In this study, we elucidate the molecular mechanism induced by β-cyclocitral in Arabidopsis thaliana and show that the xenobiotic detoxification response is involved in the tolerance to excess light energy. The involvement of the xenobiotic response suggests a possible origin for this pathway. Furthermore, we establish the hierarchical structure of this pathway that is mediated by the β-cyclocitral-inducible GRAS protein SCARECROW LIKE14 (SCL14) and involves ANAC102 as a pivotal component upstream of other ANAC transcription factors and of many enzymes of the xenobiotic detoxification response. Finally, the SCL14-dependent protective mechanism is also involved in the low sensitivity of young leaf tissues to high-light stress. [ABSTRACT FROM AUTHOR]

The article discusses a research study which explores the role of carotenoids in Arabidopsis plants. The dihydroactinidiolide and gene expression in Arabidopsis were examined using quantitative reverse transcriptase polymerase chain reaction (RT-PCR). Findings reveal that carotenoid derivative dhA can function as a gene regulator and can play a significant role in the chloroplast retrograde signaling of singlet oxygen (1O2) responsive genes.

Tocochromanols (tocopherols, tocotrienols and plastochromanol-8), isoprenoid quinone (plastoquinone-9 and plastoquinol-9) and carotenoids (carotenes and xanthophylls), are lipid-soluble antioxidants in the chloroplasts, which play an important defensive role against photooxidative stress in plants. In this study, the interplay between the antioxidant activities of those compounds in excess light stress was analyzed in wild-type (WT) Arabidopsis thaliana and in a tocopherol cyclase mutant (vte1), a homogentisate phytyl transferase mutant (vte2) and a tocopherol cyclase overexpressor (VTE1oex). The results reveal a strategy of cooperation and replacement between α-tocopherol, plastochromanol-8, plastoquinone-9/plastoquinol-9 and zeaxanthin. In the first line of defense (non-radical mechanism), singlet oxygen is either physically or chemically quenched by α-tocopherol; however, when α-tocopherol is consumed, zeaxanthin and plastoquinone-9/plastoquinol-9 can provide alternative protection against singlet oxygen toxicity by functional replacement of α-tocopherol either by zeaxanthin for the physical quenching or by plastoquinone-9/plastoquinol-9 for the chemical quenching. When singlet oxygen escapes this first line of defense, it oxidizes lipids and forms lipid hydroperoxides, which are oxidized to lipid peroxyl radicals by ferric iron. In the second line of defense (radical mechanism), lipid peroxyl radicals are scavenged by α-tocopherol. After its consumption, plastochromanol-8 overtakes this function. We provide a comprehensive description of the reaction pathways underlying the non-radical and radical antioxidant activities of α-tocopherol, carotenoids, plastoquinone-9/plastoquinol-9 and plastochromanol-8. The interplay between the different plastid lipid-soluble antioxidants in the non-radical and the radical mechanism provides step by step insights into protection against photooxidative stress in higher plants. Image 1 • Interplay between tocochromanols, isoprenoid quinones and carotenoids is crucial to prevent photooxidative stress. • In first line of defense, interplay of α-tocopherol, total plastoquinone-9 and carotenoids protects plant from singlet oxygen. • Singlet oxygen fled from first line of defense oxidize lipids to lipid hydroperoxides which decomposes to peroxyl radical. • In second line of defense, plastochromanol-8 substitutes α-tocopherol's function in its absence to scavenge peroxyl radicals. [ABSTRACT FROM AUTHOR]

Light utilization is finely tuned in photosynthetic organisms to prevent cellular damage. The dissipation of excess absorbed light energy, a process termed nonphotochemical quenching (NPQ), plays an important role in photoprotection. Little is known about the sustained or slowly reversible form(s) of NPQ and whether they are photoprotective, in part due to the lack of mutants. The Arabidopsis thaliana suppressor of quenching1 (soq1) mutant exhibits enhanced sustained NPQ, which we term qH. To identify molecular players involved in qH, we screened for suppressors of soq1 and isolated mutants affecting either chlorophyllide a oxygenase or the chloroplastic lipocalin, now renamed plastid lipocalin (LCNP). Analysis of the mutants confirmed that qH is localized to the peripheral antenna (LHCII) of photosystem II and demonstrated that LCNP is required for qH, either directly (by forming NPQ sites) or indirectly (by modifying the LHCII membrane environment). qH operates under stress conditions such as cold and high light and is photoprotective, as it reduces lipid peroxidation levels. We propose that, under stress conditions, LCNP protects the thylakoid membrane by enabling sustained NPQ in LHCII, thereby preventing singlet oxygen stress. [ABSTRACT FROM AUTHOR]

Plant surfaces form the barrier between a plant and its environment. Upon damage, the wound healing process begins immediately and is accompanied by a rapid production of extracellular reactive oxygen species (ROS), essential in deterring pathogens, signalling responses and cell wall restructuring. Although many enzymes produce extracellular ROS, it is unclear if ROS-producing enzymes act synergistically. We characterised the oxidative burst of superoxide (O 2 − ) and hydrogen peroxide (H 2 O 2 ) that follows wounding in pea ( Pisum sativum L.) seedlings. Rates of ROS production were manipulated by exogenous application of enzyme substrates and inhibitors. The results indicate significant roles for di-amine oxidases (DAO) and peroxidases (Prx) rather than NADPH oxidase. The burst of O 2 − was strongly dependent on the presence of H 2 O 2 produced by DAO. Potential substrates released from wounded seedlings included linoleic acid that, upon exogenous application, strongly stimulated catalase-sensitive O 2 − production. Moreover, a 65 kD plasma membrane (PM) guaiacol Prx was found in the secretome of wounded seedlings and showed dependence on linoleic acid for O 2 − production. Lipoxygenases are suggested to modulate O 2 − production by consuming polyunsaturated fatty acids in the apoplast. Overall, a O 2 − -producing mechanism involving H 2 O 2 -derived from DAO, linoleic acid and a PM-associated Prx is proposed. [ABSTRACT FROM AUTHOR]

Abstract: Barley displays a great genetic diversity, constituting a valuable source to delineate the responses of contrasted genotypes to environmental constraints. Here, we investigated the level of oxidative stress and the participation of antioxidant systems in two barley genotypes: Express, a variety known to be sensitive to drought, and Saïda, an Algerian landrace selected for its tolerance to water deficit. Soil-grown 15-day-old plants were subjected to water deficit for 8 days and then rewatered. We observed that upon water stress Express exhibits compared to Saïda accelerated wilting and a higher level of oxidative stress evaluated by HPLC measurements of lipid peroxidation and by imaging techniques. In parallel, Express plants also display lower levels of catalase and superoxide dismutase activity. No great difference was observed regarding peroxiredoxins and methionine sulfoxide reductases, enzymes detoxifying peroxides and repairing oxidized proteins, respectively. In contrast, upon water stress and recovery, much higher contents and oxidation ratios of glutathione and ascorbate were measured in Express compared to Saïda. Express also shows during water deficit greater increases in the pools of lipophilic antioxidants like xantophyll carotenoids and α-tocopherol. Altogether, these data show that the differential behavior of the two genotypes involves distinct responses regarding antioxidant mechanisms. Indeed, the drought sensitivity of Express compared with Saïda is associated with oxidative damage and a lower enzymatic ROS-scavenging capacity, but in parallel with a much stronger enhancement of most mechanisms involving low-molecular weight antioxidant compounds. [Copyright &y& Elsevier]

We establish here that iron deficiency causes oxidative stress in the cyanobacterium Anabaena sp. strain PCC 7120. Iron starvation leads to a significant increase in reactive oxygen species, whose effect can be abolished by treatment with the antioxidant tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl). Oxidative stress induced by iron starvation could be a common feature of photosynthetic bacteria. [ABSTRACT FROM AUTHOR]