Inhibition Of Electron Flow Research Articles

Is There a Place for New Herbicides Targeting Photosynthetic Electron Transport?

Abstract Due to increased food demand, the need for use of herbicides is both necessary and on the rise. Several herbicide classes target photosynthetic electron transport: HRAC Groups 5, 6 and 22. These herbicides are used in large amounts in many different cropping systems to control several species of broadleaf and grass weeds. This article provides a comprehensive review of what these photosynthesis inhibitors are, how they are used and their mode of action. Presently, commercial herbicides only inhibit electron flow at two different sites photosystem II (PSII) and photosystem I (PSI). Those which inhibit electron flow at PSII block the movement of electrons down the electron transport chain, while those which inhibit at PSI accept electrons. Necrosis developing on the leaves of plants treated with PSII and PSI inhibitors is due to the accumulation of reactive oxygen species. Evolution of resistance, toxicity concerns, and other limitations of these herbicides call for the exploration of new chemistries which can be used to target this pathway.

Suppression of superoxide/hydrogen peroxide production at mitochondrial site IQ decreases fat accumulation, improves glucose tolerance and normalizes fasting insulin concentration in mice fed a high-fat diet.

We developed S1QEL1.719, a novel bioavailable S1QEL (suppressor of site IQ electron leak). S1QEL1.719 prevented superoxide/hydrogen peroxide production at site IQ of mitochondrial complex I in vitro. The free concentration giving half-maximal suppression (IC50) was 52nM. Even at 50-fold higher concentrations S1QEL1.719 did not inhibit superoxide/hydrogen peroxide production from other sites. The IC50 for inhibition of complex I electron flow was 500-fold higher than the IC50 for suppression of superoxide/hydrogen peroxide production from site IQ. S1QEL1.719 was used to test the metabolic effects of suppressing superoxide/hydrogen peroxide production from site IQin vivo. C57BL/6J male mice fed a high-fat chow for one, two or eight weeks had increased body fat, decreased glucose tolerance, and increased fasting insulin concentrations, classic symptoms of metabolic syndrome. Daily prophylactic or therapeutic oral treatment of high-fat-fed animals with S1QEL1.719 decreased fat accumulation, strongly protected against decreased glucose tolerance and prevented or reversed the increase in fasting insulin level. Free exposures in plasma and liver at Cmax were 1-4 fold the IC50 for suppression of superoxide/hydrogen peroxide production at site IQ and substantially below levels that inhibit electron flow through complex I. These results show that the production of superoxide/hydrogen peroxide from mitochondrial site IQin vivo is necessary for the induction and maintenance of glucose intolerance caused by a high-fat diet in mice. They raise the possibility that oral administration of S1QELs may be beneficial in metabolic syndrome.

Paradoxes in judging the inhibition of photosynthetic electron transfer chain using P700 oxidation and dark re-reduction analyses

• P700 redox kinetics analyses to identify functions of photosynthetic inhibitors • DNP-INT is unable to block electron flow between photosystem II and photosystem I • Leakage of electrons from Cytochrome b6f to plastocyanine cause reduction of oxidized P700 • P700 redox kinetics ensures inhibition of electron flow to PSI and alternate electron flow from cytochrome b6f and PQ-pool

The rapid transformation of triclosan in the liver reduces its effectiveness as inhibitor of hepatic energy metabolism

Triclosan (5-chloro-2'-[2,4-dichlorophenoxi]-phenol) is a polychlorinated biphenolic antimicrobial, utilized as antiseptic and preservative in hygiene products and medical equipment. Triclosan causes mitochondrial dysfunction (uncoupling, inhibition of electron flow), as demonstrated in isolated rat liver mitochondria. These actions in the mitochondria could compromise energy-dependent metabolic fluxes in the liver. For this reason, the present work aimed at investigating how these effects on isolated mitochondria translate to the whole and intact hepatocyte. For accomplishing this, the isolated perfused rat liver was utilized, a system that preserves both microcirculation and the cell-to-cell interactions. In addition, the single-pass triclosan hepatic transformation was also evaluated by HPLC as well as the direct action of triclosan on gluconeogenic enzymes. The results revealed that triclosan decreased anabolic processes (e.g., gluconeogenesis) and increased catabolic processes (e.g., glycolysis, ammonia output) in the liver, generally with a complex pattern of concentration dependences. Unlike the effects on isolated mitochondria, which occur in the micromolar range, the effects on intact liver required the 10−5 to 10−4 M range. The most probable cause for this behavior is the very high single-pass transformation of triclosan, which was superior to 95% at the portal concentration of 100 μM. The concentration gradient along the sinusoidal bed is, thus, very pronounced and the response of the liver reflects mainly that of the periportal cells. The high rates of hepatic biotransformation may be a probable explanation for the low acute toxicity of triclosan upon oral ingestion.

Proteomic analysis reveals different responses to drought between the Cleome spinosa (C3) and Cleome gynandra (C4)

The global emergence of low water availability causes extensive damage to crops in many regions. Although the responses of plants to drought stress have been extensively investigated, molecular studies on plants with different carboxylation pathways are limited. Therefore, we aimed to identify quantitative differences in proteins functioning in differential drought tolerance of C3 (Cleome spinosa) and C4 (C. gynandra) species. Proteomic analysis functionally characterized 33 differentially accumulated proteins in C. spinosa and 15 proteins in C. gynandra leaves. The identified proteins were involved in multiple aspects of leaf metabolism such as photosynthesis, energy metabolism, protein metabolism, and stress defense. The up-regulated accumulation of RuBisCO proteins may have contributed to carboxylation in stressed C. spinosa, but RuBisCO activase proteins were severely down-regulated. Additionally, down-regulation of ferredoxin-nicotinamide adenine dinucleotide phosphate (NADP) reductase and oxygen-evolving enhancer proteins was only found in C. spinosa, which possibly related to the inhibition of electron flow. The up-regulation of enolase may contribute to the energy requirement in C. gynandra, while down-regulation of glycolytic enzymes, such as fructose-bisphosphate aldolase and triosephosphate isomerase, was found in C. spinosa suggesting the impaired energy metabolism under drought stress. The proteomic analysis suggests different adaptive strategies between C. spinosa and C. gynandra against drought stress.

Inhibition of plastoquinol oxidation at the cytochrome b6f complex by dinitrophenyl ether of iodonitrothymol (DNP-INT) depends on irradiance and H+ uptake by thylakoid membranes

Inhibitory analysis is a useful tool for studying reactions in the photosynthetic apparatus. After introducing by Aachim Trebst in 1978, dinitrophenylether of iodonitrothymol (DNP-INT), a competitive inhibitor of plastoquinol oxidation at the cytochrome (cyt.) b6f complex, has been widely applied to study reactions occurring in the plastoquinone pool and the cyt. b6f complex. Here we examine the inhibitory efficiency of DNP-INT by implementing three approaches to estimate the extent of blockage of electron flow from the plastoquinone pool to photosystem I in isolated thylakoids from spinach (Spinacia oleracea). We confirm that DNP-INT is a potent inhibitor of electron flow to photosystem I and demonstrate that inhibitory action of DNP-INT depends on irradiance and H+ uptake by thylakoid membranes. Based on these findings, we infer that affinity of the quinol-oxidizing site of the cyt. b6f complex to DNP-INT is increased in the light due to hydrogen bonding between DNP-INT molecules and acidic amino acid residue(s), which is (are) protonated in the light.

Allergens of the urushiol family promote mitochondrial dysfunction by inhibiting the electron transport at the level of cytochromes b and chemically modify cytochrome c1

BackgroundUrushiols are pro-electrophilic haptens that cause severe contact dermatitis mediated by CD8+ effector T-cells and downregulated by CD4+ T-cells. However, the molecular mechanism by which urushiols stimulate innate immunity in the initial stages of this allergic reaction is poorly understood. Here we explore the sub-cellular mechanisms by which urushiols initiate the allergic response.ResultsElectron microscopy observations of mouse ears exposed to litreol (3-n-pentadecyl-10-enyl-catechol]) showed keratinocytes containing swollen mitochondria with round electron-dense inclusion bodies in the matrix. Biochemical analyses of sub-mitochondrial fractions revealed an inhibitory effect of urushiols on electron flow through the mitochondrial respiratory chain, which requires both the aliphatic and catecholic moieties of these allergens. Moreover, urushiols extracted from poison ivy/oak (mixtures of 3-n-pentadecyl-8,11,13 enyl/3-n-heptadecyl-8,11 enyl catechol) exerted a higher inhibitory effect on mitochondrial respiration than did pentadecyl catechol or litreol, indicating that the higher number of unsaturations in the aliphatic chain, stronger the allergenicity of urushiols. Furthermore, the analysis of radioactive proteins isolated from mitochondria incubated with 3H-litreol, indicated that this urushiol was bound to cytochrome c1. According to the proximity of cytochromes c1 and b, functional evidence indicated the site of electron flow inhibition was within complex III, in between cytochromes bL (cyt b566) and bH (cyt b562).ConclusionOur data provide functional and molecular evidence indicating that the interruption of the mitochondrial electron transport chain constitutes an important mechanism by which urushiols initiates the allergic response. Thus, mitochondria may constitute a source of cellular targets for generating neoantigens involved in the T-cell mediated allergy induced by urushiols.

Effects of heat stress on photosystem II activity and antioxidant enzymes in two maize cultivars.

The main reason for the maize genotype "DKC7221" to be heat tolerant is to have higher photosynthetic activity under heat stress conditions. The genotype "P3167" is sensitive to high temperature because of the heat-induced inhibition in photosynthetic electron transport reactions. In the present study, the effect of heat stress (45ºC for 20min) on some physiological changes was investigated through a chlorophyll afluorescence technique, and some endogenous resistance mechanisms (activities of some antioxidant enzymes, free proline, and reduced ascorbate contents) in two maize cultivars (Zea mays L. cvs. P3167 and DKC7221). Chlorophyll fluorescence measurements demonstrated that heat stress led to the reduction in the efficiency of the Hill reaction, accumulation of inactive reaction centers, inhibition of electron flow from reaction centers to the plastoquinone pool, and induction of non-photochemical dissipation of absorbed light energy. Changes in Φo/(1 - Φo), SFIABS and PIABS indicated that electron transport reactions in P3167 were almost completely inhibited by heat stress. In DKC7221, however, photosynthetic electron transport reactions were maintained under heat stress conditions. As a result of impairment in the photosynthetic efficiency in P3167 under heat stress, oxidative stress appeared as shown by lower antioxidant activity, accumulation of H2O2, malondialdehyde, and formazon and photooxidative injuries in chlorophyll pigments in the leaf tissue. DKC7221, on the other hand, had a higher antioxidant efficiency and lower oxidative damage under heat stress. FeSOD activity was found to be responsible for the dismutation of superoxide radicals in both maize genotypes under heat stress. As a result, it may be concluded that the genotype DKC7221 is more tolerant to heat stress than P3167.

The effect of pesticides on the mtDNA integrity and bioenergetic properties of potato mitochondria

Potato (Solanum tuberosum L.) is one of the most common crops in the world, and it is very susceptible to a wide range of pests such as insects and fungi. The use of pesticides often results in the suppression of seed germination and plant growth, in particular, due to their effect on the respiratory chain of mitochondria. There are numerous studies of the effect of pesticides on animal mitochondria, but their interference with the electron transport in plant mitochondria is not well documented. We present the data showing that a number of pesticides inhibit electron flow, and other pesticides uncouple the respiratory chain. Among the studied pesticides engaging the alternative pathways of electron transport, dithianon led to an increase in the rate of H2O2 production but did not cause a strong increase in the amount of mtDNA damage as compared to other pesticides. In general, the main negative effect of the studied pesticides is manifested in a decrease of membrane potential with the maintenance of the rate of oxygen consumption and a low rate of H2O2 production. The mtDNA damage is caused mainly by pesticides belonging to the pyrethroid class and remains minor as compared to its damage in animals. Our data indicate that the respiratory chain of plant mitochondria is more resistant to pesticides as compared to animal mitochondria due to the presence of the alternative pathways of electron transport.

Low temperature induced modulation of photosynthetic induction in non-acclimated and cold-acclimated Arabidopsis thaliana: chlorophyll a fluorescence and gas-exchange measurements.

Cold acclimation modifies the photosynthetic machinery and enables plants to survive at sub-zero temperatures, whereas in warm habitats, many species suffer even at non-freezing temperatures. We have measured chlorophyll a fluorescence (ChlF) and CO2 assimilation to investigate the effects of cold acclimation, and of low temperatures, on a cold-sensitive Arabidopsis thaliana accession C24. Upon excitation with low intensity (40µmol photons m- 2 s- 1) ~ 620nm light, slow (minute range) ChlF transients, at ~ 22°C, showed two waves in the SMT phase (S, semisteady-state; M, maximum; T, terminal steady-state), whereas CO2 assimilation showed a linear increase with time. Low-temperature treatment (down to - 1.5°C) strongly modulated the SMT phase and stimulated a peak in the CO2 assimilation induction curve. We show that the SMT phase, at ~ 22°C, was abolished when measured under high actinic irradiance, or when 3-(3, 4-dichlorophenyl)-1, 1- dimethylurea (DCMU, an inhibitor of electron flow) or methyl viologen (MV, a Photosystem I (PSI) electron acceptor) was added to the system. Our data suggest that stimulation of the SMT wave, at low temperatures, has multiple reasons, which may include changes in both photochemical and biochemical reactions leading to modulations in non-photochemical quenching (NPQ) of the excited state of Chl, "state transitions," as well as changes in the rate of cyclic electron flow through PSI. Further, we suggest that cold acclimation, in accession C24, promotes "state transition" and protects photosystems by preventing high excitation pressure during low-temperature exposure.

Salt stress effects on the photosynthetic electron transport chain in two chickpea lines differing in their salt stress tolerance.

The main objective of this study was to evaluate the effects of salt stress on the photosynthetic electron transport chain using two chickpea lines (Cicer arietinum L.) differing in their salt stress tolerance at the germination stage (AKN 87 and AKN 290). Two weeks after sowing, seedlings were exposed to salt stress for 2weeks and irrigated with 200ml of 200mM NaCl every 2days. The polyphasic OJIP fluorescence transient and the 820-nm transmission kinetics (photosystem I) were used to evaluate the effects of salt stress on the functionality of the photosynthetic electron transport chain. It was observed that a signature for salt stress was a combination of a higher J step (VJ), a smaller IP amplitude, and little or no effect on the primary quantum yield of PSII (φPo). We observed for AKN 290 a shorter leaf life cycle, which may represent a mechanism to cope with salt stress. For severely salt-stressed leaves, an inhibition of electron flow between the PQ pool and P700 was found. The data also suggest that the properties of electron flow beyond PSI are affected by salt stress.

Mitochondrial complex II-derived superoxide is the primary source of mercury toxicity in barley root tip

Enhanced superoxide generation and significant inhibition of succinate dehydrogenase (SDH) activity followed by a strong reduction of root growth were detected in barley seedlings exposed to a 5μM Hg concentration for 30min, which increased further in an Hg dose-dependent manner. While at a 25μM Hg concentration no cell death was detectable, a 50μM Hg treatment triggered cell death in the root meristematic zone, which was markedly intensified after the treatment of roots with 100μM Hg and was detectable in the whole root tips. Generation of superoxide and H2O2 was a very rapid response of root tips occurring even after 5min of exposure to Hg. Application of an NADPH oxidase inhibitor or the inhibition of electron flow in mitochondria by the inhibition of complex I did not influence the Hg-induced H2O2 production. Treatment of roots with thenoyltrifluoroacetone, a non-competitive inhibitor of SDH, markedly reduced root growth and induced both superoxide and H2O2 production in a dose dependent manner. Similar to results obtained in intact roots, Hg strongly inhibited SDH activity in the crude mitochondrial fraction and caused a considerable increase of superoxide production, which was markedly reduced by the competitive inhibitors of SDH. These results indicate that the mitochondrial complex II-derived superoxide is the primary source of Hg toxicity in the barley root tip.

Mitochondrial nitric oxide production supported by reverse electron transfer

Heart phosphorylating electron transfer particles (ETPH) produced NO at 1.2 ± 0.1 nmol NO. min−1 mg protein−1 by the mtNOS catalyzed reaction. These particles showed a NAD+ reductase activity of 64 ± 3 nmol min−1 mg protein−1 sustained by reverse electron transfer (RET) at expenses of ATP and succinate. The same particles, without NADPH and in conditions of RET produced 0.97 ± 0.07 nmol NO. min−1 mg protein−1. Rotenone inhibited NO production supported by RET measured in ETPH and in coupled mitochondria, but did not reduce the activity of recombinant nNOS, indicating that the inhibitory effect of rotenone on NO production is due to an electron flow inhibition and not to a direct action on mtNOS structure. NO production sustained by RET corresponds to 20% of the total amount of NO released from heart coupled mitochondria. A mitochondrial fraction enriched in complex I produced 1.7 ± 0.2 nmol NO. min−1 mg protein−1 and reacted with anti-75 kDa complex I subunit and anti-nNOS antibodies, suggesting that complex I and mtNOS are located contiguously. These data show that mitochondrial NO production can be supported by RET, and suggest that mtNOS is next to complex I, reaffirming the idea of a functional association between these proteins.

Nondestructive evaluation of photosynthesis by delayed luminescence in Arabidopsis in Petri dishes.

Nondestructive evaluation of photosynthesis is a valuable tool in the field and laboratory. Delayed luminescence (DL) can reflect charge recombination through the backflow of electrons. However, DL detection has not yet been adapted for whole plants in Petri dishes. To compensate for differences in DL decay between sibling Arabidopsis plants grown under the same conditions, we developed a time-sequential double measurement method. Using this method, we examined the influence of photosynthetic electron flow inhibitors, and differences in the DL decay curves were categorized by considering the initial and late phases of the decay curves, as well as their intermediate slopes. The appearance of concavity and convexity in DL curves in Arabidopsis was different from unicellular algae, suggesting complexity in the photosynthetic machinery of higher plants. This detection method should be invaluable for evaluating photosynthetic defects in higher plants under sterile conditions without interrupting plant culture.

Selective Targeting of Heme Protein in Cytochrome P450 and Nitric Oxide Synthase by Diphenyleneiodonium.

Cytochrome P450 (CYP) enzymes mediate mixed-function oxidation reactions important in drug metabolism. The aromatic heterocyclic cation, diphenyleneiodonium (DPI), binds flavin in cytochrome P450 reductase and inhibits CYP-mediated activity. DPI also inhibits CYP by directly interacting with heme. Herein, we report that DPI effectively inhibits a number of CYP-related monooxygenase reactions including NADPH oxidase, a microsomal enzyme activity that generates hydrogen peroxide in the absence of metabolizing substrates. Inhibition of monooxygenase by DPI was time and concentration dependent with IC50's ranging from 0.06 to 1.9 μM. Higher (4.6-23.9 μM), but not lower (0.06-1.9 μM), concentrations of DPI inhibited electron flow via cytochrome P450 reductase, as measured by its ability to reduce cytochrome c and mediate quinone redox cycling. Similar results were observed with inducible nitric oxide synthase (iNOS), an enzyme containing a C-terminal reductase domain homologous to cytochrome P450 reductase that mediates reduction of cytochrome c, and an N-terminal heme-thiolate oxygenase domain mediating nitric oxide production. Significantly greater concentrations of DPI were required to inhibit cytochrome c reduction by iNOS (IC50 = 3.5 µM) than nitric oxide production (IC50 = 0.16 µM). Difference spectra of liver microsomes, recombinant CYPs, and iNOS demonstrated that DPI altered heme-carbon monoxide interactions. In the presence of NADPH, DPI treatment of microsomes and iNOS yielded a type II spectral shift. These data indicate that DPI interacts with both flavin and heme in CYPs and iNOS. Increased sensitivity for inhibition of CYP-mediated metabolism and nitric oxide production by iNOS indicates that DPI targets heme moieties within the enzymes.

<b>The effect of inhibitors on photosynthetic electron transport chain in canola leaf discs

The mechanisms of photosynthetic electron transport can be elucidated by inhibition of electron flow through the use of specific substances that, when combined with the chlorophyll chlorophyll a fluorescence emission was measured to investigate the effect of several inhibitors of the photosynthetic electron transport chain in canola leaf discs. Leaf discs were incubated in the dark for 2 hours in different solutions: (a) water – control; (b) DCMU at 500 µM; (c) phenanthroline at 10 mM; and (d) hydroxylamine at 10, 50, 100 and 200 mM. Similar effects were observed between DCMU and phenanthroline, the initial fluorescence value was altered, but not the maximum fluorescence, with the disappearance of the IP phase. Hydroxylamine interacted and inhibited the oxygen evolving complex and caused an imbalance between the rate of Q A reduction by photosystem II and the rate of Q A oxidation by photosystem I.

Application on gold nanoparticles-dotted 4-nitrophenylazo graphene in a label-free impedimetric deoxynivalenol immunosensor.

In this paper, we report a new concept to construct a label-free electrochemical inhibition-based immunosensor for the detection of the mycotoxin deoxynivalenol (DON) in cereal samples. The electrochemical impedance spectroscopy of tris(bipyridine) ruthenium (II) chloride was used as a marker enhanced with gold nanoparticles-dotted 4-nitrophenylazo functionalized graphene (AuNp/G/PhNO2) nanocatalyst mediated in Nafion on a glassy carbon electrode. Under the optimized conditions, the formation of immunocomplexes inhibited electron flow and increased the charge transfer resistance of the sensing interface linearly. The change in impedance was proportional to DON concentrations in the range of 6–30 ng/mL with a sensitivity and detection limit of 32.14 ΩL/ng and 0.3 μg/mL, respectively, which compares favorably with the ELISA result. The proposed sensor had a stability of 80.3%, good precision and selectivity in DON standard solution containing different interfering agents, indicating promising application prospect for this strategy in designing impedimetric, electrochemiluminescent, voltammetric or amperometric sensors.

Similarities and Differences in Global Gene Expression Profiles between Herbicide and Pathogen-Induced PSII Inhibition

Plant pathogens, and photosynthesis inhibiting herbicides, can both damage photosystem II (PSII), causing it to be highly sensitive to damage by light energy, and to release high levels of reactive oxygen species (ROS). This photoinhibition of PSII could possibly be the source of the strong oxidative burst associated with the pathogeninduced, hypersensitive defense response (HR). To examine a possible mechanism of how the HR-associated ROS burst could originate from PSII inhibition, we compared the transcriptome responses in soybean undergoing photoinhibition induced by HR, to soybean undergoing photoinhibition induced by the herbicide bentazon, which specially stops PSII electron flow by preventing QB from binding to D1. Most genes shared similar expression patterns between HR and bentazon treatments; however, interesting differences were also observed. The most striking differences were seen with genes related to photosynthesis, where these genes were uniformly down regulated in HR, but were mostly up in response to bentazon. Another interesting difference was seen in genes of the phenylpropanoid pathway. These defense-related genes were mostly down or non-responsive to bentazon, but were generally induced in response to pathogen-induced HR, showing that soybeans activate the phenylpropanoidbased phytoalexins independent of PSII inhibition. We conclude that the PSII inhibition occurring during the HR is not being triggered simply by the inhibition of electron flow through the photosystem centers. Instead, it is more likely that the initial triggers of the HR halt the repair of damaged PSII which leads to enhancing photoinhibition and contributing the rapid production of ROS, sealing the fate of cells undergoing HR; and the triggers independently induce specific aspects of defenses such as the phenylpropanoid pathway.

Interaction of ascorbate with photosystem I

Ascorbate is one of the key participants of the antioxidant defense in plants. In this work, we have investigated the interaction of ascorbate with the chloroplast electron transport chain and isolated photosystem I (PSI), using the EPR method for monitoring the oxidized centers [Formula: see text] and ascorbate free radicals. Inhibitor analysis of the light-induced redox transients of P700 in spinach thylakoids has demonstrated that ascorbate efficiently donates electrons to [Formula: see text] via plastocyanin. Inhibitors (DCMU and stigmatellin), which block electron transport between photosystem II and Pc, did not disturb the ascorbate capacity for electron donation to [Formula: see text]. Otherwise, inactivation of Pc with CN(-) ions inhibited electron flow from ascorbate to [Formula: see text]. This proves that the main route of electron flow from ascorbate to [Formula: see text] runs through Pc, bypassing the plastoquinone (PQ) pool and the cytochrome b 6 f complex. In contrast to Pc-mediated pathway, direct donation of electrons from ascorbate to [Formula: see text] is a rather slow process. Oxidized ascorbate species act as alternative oxidants for PSI, which intercept electrons directly from the terminal electron acceptors of PSI, thereby stimulating photooxidation of P700. We investigated the interaction of ascorbate with PSI complexes isolated from the wild type cells and the MenB deletion strain of cyanobacterium Synechocystis sp. PCC 6803. In the MenB mutant, PSI contains PQ in the quinone-binding A1-site, which can be substituted by high-potential electron carrier 2,3-dichloro-1,4-naphthoquinone (Cl2NQ). In PSI from the MenB mutant with Cl2NQ in the A1-site, the outflow of electrons from PSI is impeded due to the uphill electron transfer from A1 to the iron-sulfur cluster FX and further to the terminal clusters FA/FB, which manifests itself as a decrease in a steady-state level of [Formula: see text]. The addition of ascorbate promoted photooxidation of P700 due to stimulation of electron outflow from PSI to oxidized ascorbate species. Thus, accepting electrons from PSI and donating them to [Formula: see text], ascorbate can mediate cyclic electron transport around PSI. The physiological significance of ascorbate-mediated electron transport is discussed.

Reactions of Egyptian landraces of Hordeum vulgare and Sorghum bicolor to drought stress, evaluated by the OJIP fluorescence transient analysis

Landraces of barley and of Sorghum bicolor from Egypt were evaluated for their tolerance to drought stress (DS) using the OJIP test of the chl fluorescence fast induction curve. Water was withheld from 4-week-old, pot-grown plants for 8–10 days, until the volumetric soil water content decreased from 30 to below 5 vol% and the leaves reached relative water contents of <60 %. The plants were rewatered and recovery measurements were taken 24 h later. Comparative studies of the most sensitive and the most tolerant lines of both cereals, as evaluated by their Performance Indices (PIabs), revealed a similar behavior in the sensitive lines, i.e., inhibiting effects of DS on PS II connectivity (occurrence of an L band), oxygen evolving complex (occurrence of a K band) and on the J step of the induction curves, associated with an inhibition of electron transport from Q A to Q B . These effects persisted or were even enhanced in the rewatered plants, which resulted in similar deviations of spider plots of the OJIP parameters in the sensitive lines of both species. In the most tolerant barley accession, drought effects on “early” events (i.e., L, K bands) were much smaller or negligible, and there was no pronounced effect on the J step. However, distinct increases of the I step occurred, pointing to inhibited electron flow to the intersystem electron carriers and beyond PS I. The most tolerant Sorghum line, in contrast, revealed nearly no effects of the DS and recovery treatment on the fluorescence induction curves and OJIP parameters.