Effect of Reducing Nitric Oxide in <Emphasis Type="Italic">Rumex</Emphasis> K-1 Leaves on the Photoprotection of Photosystem II Under High Temperature with Strong Light

The purpose of this study was to explore the effect of reducing nitric oxide (NO) in Rumex K-1 leaves on the photoprotection of photosystem II (PSII) under high temperature with strong light. Reducing the content of NO in Rumex K-1 leaves significantly aggravated the PSII photoinhibition and net degradation of D1 protein under high temperature with strong light, but not under high temperature in the darkness. The reduction of NO remarkably inhibited the electron transport of PSII in the leaves under high temperature and strong light, which resulted in an increase in excitation pressure and an over-accumulation of reactive oxygen species (ROS). The over-accumulation of ROS further damaged PSII. However, when the synthesis of D1 protein was inhibited, the D1 protein content and PSII activity were no longer influenced by reducing NO content in the leaves. The reduction of NO in leaves decreased the activities of ROS scavenger enzymes after treatment with high temperature and strong light for 2 h, which enhanced the over-accumulation of ROS to damage photosynthetic apparatus severely. All of these results suggest that NO was involved in the synthesis of D1 protein. Maintaining physiologically appropriate NO content in leaves will alleviate net degradation of D1 protein under high temperature with strong light to keep photosynthetic electrons flowing smoothly, which mitigates the accumulation of ROS in photosystems to avoid damage to the photosynthetic apparatus. Therefore, NO plays an important role in maintaining higher PSII photosynthetic performance under high temperature with strong light.     

Responses of the photosynthetic machinery of Spirulina maxima to induced reactive oxygen species

The photosynthetic machinery of Spirulina maxima was studied when subjected to induced reactive oxygen species (ROS) to examine the organism's responses to stress. Significant decreases in both photosynthetic efficiency and growth rate were observed. Exposure to 0.01 mmol H(2)O(2)/(g cell), which induced the lowest specific intracellular ROS level (siROS) led to a 15% decrease in specific growth rate; an increase in siROS by 70-fold led to a 25% decrease in specific growth rate. Similarly, siROS induced by 0.01 mmol H(2)O(2)/(g cell) led to 15% inhibition in photosynthetic efficiency, while an increase in siROS by 40- or 70-fold led to about 60% inhibition in photosynthetic efficiency. To further understand the effects of induced ROS on photosynthetic machinery, we performed a detailed pigmentation analysis as well as analyzed Phycobilisomes (PBS), Photosystem II (PSII), and Photosystem I (PSI), the three important components of cyanobacterial photosynthetic apparatus. We found carotenoids (beta-carotene and lutein) to be most sensitive to siROS. Also, specific levels of phycocyanin and allophycocyanin, which are important PBS pigments, decreased significantly in response to H(2)O(2). Further, electron transport assays revealed that ROS cause damage primarily to PSII, whereas they do not significantly affect PSI in comparison; siROS induced by 0.01 mmol H(2)O(2)/(g cell) led to a 15% inhibition of PSII, and increase in siROS by 9-, 40-, and 70-fold led to 22%, 36%, and 46% inhibition, respectively.     

Oxidative stress in cyanobacteria

Reactive oxygen species (ROS) are byproducts of aerobic metabolism and potent agents that cause oxidative damage. In oxygenic photosynthetic organisms such as cyanobacteria, ROS are inevitably generated by photosynthetic electron transport, especially when the intensity of light-driven electron transport outpaces the rate of electron consumption during CO₂ fixation. Because cyanobacteria in their natural habitat are often exposed to changing external conditions, such as drastic fluctuations of light intensities, their ability to perceive ROS and to rapidly initiate antioxidant defences is crucial for their survival. This review summarizes recent findings and outlines important perspectives in this field.     

Photoproduction of hydrogen by photosynthetic bacteria from sewage and waste water

Numerous prokaryotes, belonging to physiologically and taxonomically different groups, are able to produce hydrogen. Some photosynthetic bacteria have the property of light-dependent production of hydrogen from organic substrates. We isolated several photosynthetic purple and green bacteria from enrichment cultures made from the water of a waste-water pond of a cool-drink refilling station. After testing them for their ability to use various organic compounds as carbon source, and sulphide, thiosulphate and organic compounds as electron donor, we selected the fastest-growing isolate, aRhodopseudomonas, for a study of its ability to produce molecular hydrogen in presence of light. Immobilized cells of this isolate produced significant amounts of hydrogen from both sewage and waste water     

氧气在黑暗-水淹诱导植物叶片光合机构损伤中的作用

本研究排除了光照和根部信号的影响,在完全黑暗条件下对离体叶片进行水淹处理,并在处理过程中分别通入空气或者氮气来控制水淹过程中水中的含氧量。通过分析叶片叶绿素含量、活性氧含量以及叶片光化学活性的变化,探讨叶片水淹时水中缺氧因素对叶片光合机构的直接影响及作用机制。结果表明,与放置在湿润空气中的对照叶片相比,黑暗-水淹处理叶片的最大光化学效率（Fv/Fm）、捕获的激子将电子传递到QA以后的其他电子受体的概率（ψo）均发生显著下降。然而,黑暗．水淹处理36h后,叶片的叶绿素含量并未下降,叶片中H2O2含量也未大量增加。另外,黑暗一水淹导致的叶片光化学活性的下降随着水中含氧量下降的加剧而加剧,补充氧气可以缓解甚至消除这一伤害。这表明黑暗．水淹处理过程中叶片光合机构的伤害与叶片衰老或活性氧的积累无关,而是由于水中缺氧因素对光合机构的直接伤害所致。     

Susceptibility of mitochondrial electron-transport complexes to oxidative damage. Focus on cytochrome c oxidase

Abstract

Reactive oxygen species (ROS) are associated with a number of mitochondrial disorders. These include: ischemia/reperfusion injury, Parkinson's disease, Alzheimer's disease, neurodegenerative diseases, and other age-related degenerative changes. ROS can be generated at numerous sites within the cell, but the mitochondrial electron transport chain is recognized as the major source of intracellular ROS. Two mitochondrial electron-transfer complexes are major sources of ROS: complex I and complex III. Oxidative damage to either of these complexes, or to electron transport complexes that are in close proximity to these ROS sources, e.g., cytochrome c oxidase, would be expected to inhibit electron transport. Such inhibition would lead to increased electron leakage and more ROS production, much like the well-known effect of adding electron transport inhibitors. Recent studies reveal that ROS and lipid peroxidation products are effective inhibitors of the electron-transport complexes. In some cases, inactivation of enzymes correlates with chemical modification of only a small number of unusually reactive amino acids. In this article, we review current knowledge of ROS-induced alterations within three complexes: (1) complex IV; (2) complex III; and (3) complex I. Our goal is to identify “hot spots” within each complex that are easily chemically modified and could be responsible for ROS-induced inhibition of the individual complexes. Special attention has been placed on ROS-induced damage to cardiolipin that is tightly bound to each of the inner membrane protein complexes. Peroxidation of the bound cardiolipin is thought to be particularly important since its close proximity and long residence time on the protein make it an especially effective reagent for subsequent ROS-induced damage to these proteins.     

Heat stress: an overview of molecular responses in photosynthesis

The primary targets of thermal damage in plants are the oxygen evolving complex along with the associated cofactors in photosystem II (PSII), carbon fixation by Rubisco and the ATP generating system. Recent investigations on the combined action of moderate light intensity and heat stress suggest that moderately high temperatures do not cause serious PSII damage but inhibit the repair of PSII. The latter largely involves de novo synthesis of proteins, particularly the D1 protein of the photosynthetic machinery that is damaged due to generation of reactive oxygen species (ROS), resulting in the reduction of carbon fixation and oxygen evolution, as well as disruption of the linear electron flow. The attack of ROS during moderate heat stress principally affects the repair system of PSII, but not directly the PSII reaction center (RC). Heat stress additionally induces cleavage and aggregation of RC proteins; the mechanisms of such processes are as yet unclear. On the other hand, membrane linked sensors seem to trigger the accumulation of compatible solutes like glycinebetaine in the neighborhood of PSII membranes. They also induce the expression of stress proteins that alleviate the ROS-mediated inhibition of repair of the stress damaged photosynthetic machinery and are required for the acclimation process. In this review we summarize the recent progress in the studies of molecular mechanisms involved during moderate heat stress on the photosynthetic machinery, especially in PSII.     

Effect of melatonin priming on photosynthetic capacity of tomato leaves under low-temperature stress

Melatonin has different functions in plant growth and development, especially in the protection of plants suffering from various forms of abiotic stress. We explored the effect of melatonin priming on photosynthetic activity of tomato (Lycopersicon esculentum L.) leaves. Our results showed that 100 µM is the optimal concentration used for alleviation of the damage to photosynthetic apparatus. Melatonin priming both in the form of leaf spray and direct root application was found to reduce the damage to photosynthetic apparatus, and increase the electron transfer rate and quantum yield of PSI and PSII photochemistry, to protect the thylakoid membrane from damage caused by low-temperature stress. Our study provides fundamental information for further research on the molecular mechanism of melatonin function in regulating photosynthesis.     

The SnRK2.10 kinase mitigates the adverse effects of salinity by protecting photosynthetic machinery

SNF1-Related protein kinases Type 2 (SnRK2) are plant-specific enzymes widely distributed across the plant kingdom. They are key players controlling abscisic acid (ABA)-dependent and ABA-independent signaling pathways in the plant response to osmotic stress. Here we established that SnRK2.4 and SnRK2.10, ABA-nonactivated kinases, are activated in Arabidopsis thaliana rosettes during the early response to salt stress and contribute to leaf growth retardation under prolonged salinity but act by maintaining different salt-triggered mechanisms. Under salinity, snrk2.10 insertion mutants were impaired in the reconstruction and rearrangement of damaged core and antenna protein complexes in photosystem II (PSII), which led to stronger non-photochemical quenching, lower maximal quantum yield of PSII, and lower adaptation of the photosynthetic apparatus to high light intensity. The observed effects were likely caused by disturbed accumulation and phosphorylation status of the main PSII core and antenna proteins. Finally, we found a higher accumulation of reactive oxygen species (ROS) in the snrk2.10 mutant leaves under a few-day-long exposure to salinity which also could contribute to the stronger damage of the photosynthetic apparatus and cause other deleterious effects affecting plant growth. We found that the snrk2.4 mutant plants did not display substantial changes in photosynthesis. Overall, our results indicate that SnRK2.10 is activated in leaves shortly after plant exposure to salinity and contributes to salt stress tolerance by maintaining efficient photosynthesis and preventing oxidative damage.     

Production of reactive oxygen species by photosystem II

Photosysthetic cleavage of water molecules to molecular oxygen is a crucial process for all aerobic life on the Earth. Light-driven oxidation of water occurs in photosystem II (PSII) — a pigment-protein complex embedded in the thylakoid membrane of plants, algae and cyanobacteria. Electron transport across the thylakoid membrane terminated by NADPH and ATP formation is inadvertently coupled with the formation of reactive oxygen species (ROS). Reactive oxygen species are mainly produced by photosystem I; however, under certain circumstances, PSII contributes to the overall formation of ROS in the thylakoid membrane. Under limitation of electron transport reaction between both photosystems, photoreduction of molecular oxygen by the reducing side of PSII generates a superoxide anion radical, its dismutation to hydrogen peroxide and the subsequent formation of a hydroxyl radical terminates the overall process of ROS formation on the PSII electron acceptor side. On the PSII electron donor side, partial or complete inhibition of enzymatic activity of the water-splitting manganese complex is coupled with incomplete oxidation of water to hydrogen peroxide. The review points out the mechanistic aspects in the production of ROS on both the electron acceptor and electron donor side of PSII.     

The cost of photoinhibition

Photoinhibition is an inevitable consequence of oxygenic photosynthesis. However, the concept of a 'photoinhibition-proof' plant in which photosystem II (PSII) is immune to photodamage is useful as a benchmark for considering the performances of plants with varying mixes of mechanisms which limit the extent of photodamage and which repair photodamage. Some photodamage is bound to occur, and the energy costs of repair are the direct costs of repair plus the photosynthesis foregone during repair. One mechanism permitting partial avoidance of photodamage is restriction of the number of photons incident on the photosynthetic apparatus per unit time, achieved by phototactic movement of motile algae to places with lower incident photosynthetically active radiation (PAR), by phototactic movement of plastids within cells to positions that minimize the incident PAR and by photonastic relative movements of parts of photolithotrophs attached to a substrate. The other means of avoiding photodamage is dissipating excitation of photosynthetic pigments including state transitions, non-photochemical quenching by one of the xanthophyll cycles or some other process and photochemical quenching by increased electron flow through PSII involving CO? and other acceptors, including the engagement of additional electron transport pathways. These mechanisms inevitably have the potential to decrease the rate of growth. As well as the decreased photosynthetic rates as a result of photodamage and the restrictions on photosynthesis imposed by the repair, avoidance, quenching and scavenging mechanisms, there are also additional energy, nitrogen and phosphorus costs of producing and operating repair, avoidance, quenching and scavenging mechanisms. A comparison is also made between the costs of photoinhibition and those of other plant functions impeded by the occurrence of oxygenic photosynthesis, i.e. the competitive inhibition of the carboxylase activity of ribulose bisphosphate carboxylase-oxygenase by oxygen via the oxygenase activity, and oxygen damage to nitrogenase in diazotrophic organisms.     

Hydrogen peroxide and the evolution of oxygenic photosynthesis

The early atmosphere of the Earth is considered to have been reducing (H₂ rich) or neutral (CO₂-N₂). The present atmosphere by contrast is highly oxidizing (20% O₂). The source of this oxygen is generally agreed to have been oxygenic photosynthesis, whereby organisms use water as the electron donor in the production of organic matter, liberating oxygen into the atmosphere. A major question in the evolution of life is how oxygenic photosynthesis could have evolved under anoxic conditions — and also when this capability evolved. It seems unlikely that water would be employed as the electron donor in anoxic environments that were rich in reducing agents such as ferrous or sulfide ions which could play that role. The abiotic production of atmospheric oxidants could have provided a mechanism by which locally oxidizing conditions were sustained within spatially confined habitats thus removing the available reductants and forcing photosynthetic organisms to utilize water as the electron donor. We suggest that atmospheric H₂O₂ played the key role in inducing oxygenic photosynthesis because as peroxide increased in a local environment, organisms would not only be faced with a loss of reductant, but they would also be pressed to develop the biochemical apparatus (e.g., catalase) that would ultimately be needed to protect against the products of oxygenic photosynthesis. This scenario allows for the early evolution of oxygenic photosynthesis while global conditions were still anaerobic.     

Characterization of target site of aluminum phytotoxicity in photosynthetic electron transport by fluorescence techniques in tobacco leaves

Aluminum (Al) toxicity limits crop yield in acidic soil through affecting diverse metabolic processes, especially photosynthesis. The aim of this work was to examine the effect of Al on photosynthetic electron transport in vivo as determined by chlorophyll fluorescence and delayed fluorescence of tobacco leaves. Results showed that Al treatment inhibited the photosynthetic rate and electron transfer, and decreased photosystem (PS) II photochemical activity in a time- and concentration-dependent manner, which could not be obviously alleviated by the addition of the reactive oxygen species (ROS) scavenger ascorbic acid (AsA). These results suggested that photosynthetic electron transfer chain components, especially PSII, might be directly damaged by Al instead of in an ROS-dependent manner. Furthermore, the fluorescence imaging and biochemical analysis exhibited that Al, after entering the cells, could accumulate in the chloroplasts, which paralleled the decreased content of Fe in the chloroplast. The changes in the chlorophyll fluorescence decay curve, the delayed fluorescence decay curve and the chlorophyll fluorescence parameters indicated that Al, through interacting with or replacing the non-heme iron between Q(A) and Q(B), caused the inhibition of electron transfer between Q(A) and Q(B), resulting in PSII photochemical damage and inhibition of the photosynthetic rate. In summary, our results characterized the target site of Al phytotoxicity in photosynthetic electron transport, providing new insight into the mechanism of Al phytotoxicity-induced chloroplast dysfunction and photosynthetic damage.     

Unfolding pathway and intermolecular interactions of the cytochrome subunit in the bacterial photosynthetic reaction center

Precise folding of photosynthetic proteins and organization of multicomponent assemblies to form functional entities are fundamental to efficient photosynthetic electron transfer. The bacteriochlorophyll b-producing purple bacterium Blastochloris viridis possesses a simplified photosynthetic apparatus. The light-harvesting (LH) antenna complex surrounds the photosynthetic reaction center (RC) to form the RC-LH1 complex. A non-membranous tetraheme cytochrome (4Hcyt) subunit is anchored at the periplasmic surface of the RC, functioning as the electron donor to transfer electrons from mobile electron carriers to the RC. Here, we use atomic force microscopy (AFM) and single-molecule force spectroscopy (SMFS) to probe the long-range organization of the photosynthetic apparatus from Blc. viridis and the unfolding pathway of the 4Hcyt subunit in its native supramolecular assembly with its functional partners. AFM images reveal that the RC-LH1 complexes are densely organized in the photosynthetic membranes, with restricted lateral protein diffusion. Unfolding of the 4Hcyt subunit represents a multi-step process and the unfolding forces of the 4Hcyt α-helices are approximately 121 picoNewtons. Pulling of 4Hcyt could also result in the unfolding of the RC L subunit that binds with the N-terminus of 4Hcyt, suggesting strong interactions between RC subunits. This study provides new insights into the protein folding and interactions of photosynthetic multicomponent complexes, which are essential for their structural and functional integrity to conduct photosynthetic electron flow.     

Molecular mechanisms of photodamage in the Photosystem II complex

Light induced damage of the photosynthetic apparatus is an important and highly complex phenomenon, which affects primarily the Photosystem II complex. Here the author summarizes the current state of understanding of the molecular mechanisms, which are involved in the light induced inactivation of Photosystem II electron transport together with the relevant mechanisms of photoprotection. Short wavelength ultraviolet radiation impairs primarily the Mn?Ca catalytic site of the water oxidizing complex with additional effects on the quinone electron acceptors and tyrosine donors of PSII. The main mechanism of photodamage by visible light appears to be mediated by acceptor side modifications, which develop under conditions of excess excitation in which the capacity of light-independent photosynthetic processes limits the utilization of electrons produced in the initial photoreactions. This situation of excess excitation facilitates the reduction of intersystem electron carriers and Photosystem II acceptors, and thereby induces the formation of reactive oxygen species, especially singlet oxygen whose production is sensitized by triplet chlorophyll formation in the reaction center of Photosystem II. The highly reactive singlet oxygen and other reactive oxygen species, such as H?O? and O??, which can also be formed in Photosystem II initiate damage of electron transport components and protein structure. In parallel with the excess excitation dependent mechanism of photodamage inactivation of the Mn?Ca cluster by visible light may also occur, which impairs electron transfer through the Photosystem II complex and initiates further functional and structural damage of the reaction center via formation of highly oxidizing radicals, such as P 680(+) and Tyr-Z(+). However, the available data do not support the hypothesis that the Mn-dependent mechanism would be the exclusive or dominating pathway of photodamage in the visible spectral range. This article is part of a Special Issue entitled: Photosystem II.     

Multiple effects of inhibition of mitochondrial alternative oxidase pathway on photosynthetic apparatus in Rumex K-1 leaves

The effects of inhibition of mitochondrial alternative oxidase (AOX) respiratory pathway on photosynthetic apparatus in Rumex K-1 leaves were studied. Under high irradiance, the inhibition of AOX pathway caused over-reduction of photosystem (PS) 2 acceptor side, a decrease in the energy transfer in the PS 2 units, damage of donor side of PS 2 and decrease in pool size of electron acceptors. The inhibition of AOX pathway also decreased photosynthetic performance index (PI_ABS), actual photochemical efficiency (Φ_PS2), photochemical quenching (qP) and photosynthetic O₂ evolution rate. The results demonstrate that mitochondrial AOX pathway plays a vital role in photoprotection of photosynthetic apparatus.     

The immediate wound‐induced oxidative burst of Saccharina latissima depends on light via photosynthetic electron transport

Reactive oxygen species (ROS) produced by an oxidative burst are an important component of the wound response in algae, vascular plants, and animals. In all taxa, ROS production is usually attributed solely to a defense‐related enzyme like NADPH‐oxidase (Nox). However, here we show that the initial, wound‐induced oxidative burst of the kelp Saccharina latissima depends on light and photosynthetic electron transport. We measured oxygen evolution and ROS production at different light levels and in the presence of a photosynthetic inhibitor, and we used spin trapping and electron paramagnetic resonance as an orthogonal method. Using an in vivo chemical probe, we provide data suggesting that wound‐induced ROS production in two distantly related and geographically isolated species of Antarctic macroalgae may be light dependent as well. We propose that electron transport chains are an important and as yet unaddressed component of the wound response, not just for photosynthetic organisms, but for animals via mitochondria as well. This component may have been obscured by the historic use of diphenylene iodonium, which inhibits not only Noxes but also photosynthetic and respiratory electron transport as well. Finally, we anticipate physiological and/or ecological consequences of the light dependence of macroalgal wound‐induced ROS since pathogens and grazers do not disappear in the dark.     

Oxidative damage to thylakoid proteins in water-stressed leaves of wheat (Triticum aestivum)

The production of reactive oxygen species in the chloroplast may increase under water deficit. To determine if this causes oxidative damage to the photosynthetic apparatus, we analyzed the accumulation of oxidatively damaged proteins in thylakoids of water-stressed wheat ( Triticum aestivum L.) leaves. Water stress was imposed on 4-week-old plants by withholding watering for 10 days to reach a soil water potential of about −2.0 MPa. In thylakoids of water-stressed leaves there was an increase in oxidative damage, particularly in polypeptides of 68, 54, 41 and 24 kDa. High molecular mass oxidized (probably cross-linked) proteins accumulated in chloroplasts of droughted leaves. Oxidative damage was associated with a substantial decrease in photosynthetic electron transport activity and photosystem II (PSII) efficiency (F_v/F_m). Treatment of stressed leaves with l -galactono-1,4-lactone (GL) increased their ascorbic acid content and enhanced photochemical and non-photochemical quenching of chlorophyll fluorescence. GL reduced oxidative damage to photosynthetic proteins of droughted plants, but it reverted the decrease in electron transport activity and PSII efficiency only partially, suggesting that other factors also contributed to loss of photosystem activity in droughted plants. Increasing the ascorbic acid content of leaves might be an effective strategy to protect thylakoid membranes from oxidative damage in water-stressed leaves.     

Oxygen and light effects on the expression of the photosynthetic apparatus in Bradyrhizobium sp. C7T1 strain

Photosynthetic bradyrhizobia are nitrogen-fixing symbionts colonizing the stem and roots of some leguminous plants like Aeschynomene. The effect of oxygen and light on the formation of the photosynthetic apparatus of Bradyrhizobium sp. C7T1 strain is described here. Oxygen is required for growth, but at high concentration inhibits the synthesis of bacteriochlorophyll (BChl) and of the photosynthetic apparatus. However, we show that in vitro, aerobic photosynthetic electron transport occurred leading to ADP photophosphorylation. The expression of the photosynthetic apparatus was regulated by oxygen in a manner which did not agree with earlier results in other photosynthetic bradyrhizobia since BChl accumulation was the highest under microaerobic conditions. This strain produces photosynthetic pigments when grown under cyclic illumination or darkness. However, under continuous white light illumination, a Northern blot analysis of the puf operon showed that, the expression of the photosynthetic genes of the antenna was considerable. Under latter conditions BChl accumulation in the cells was dependent on the oxygen concentration. It was not detectable at high oxygen tensions but became accumulated under low oxygen (microaerobiosis). It is known that in photosynthetic bradyrhizobia bacteriophytochrome photoreceptor (BphP) partially controls the synthesis of the photosystem in response to light. In C7T1 strain far-red light illumination did not stimulate the synthesis of the photosynthetic apparatus suggesting the presence of a non-functional BphP-mediated light regulatory mechanism.