Lipid Peroxidation In Chloroplasts Research Articles

Genome-wide association analysis of natural variation in seed tocochromanols of barley.

Tocochromanols (tocols for short), commonly called Vitamin E, are lipid-soluble plant antioxidants vital for regulating lipid peroxidation in chloroplasts and seeds. Barley (Hordeum vulgare L.) seeds contain all eight different isoforms of tocols; however, the extent of natural variation in their composition and their underlying genetic basis is not known. Tocol levels in barley seeds were quantified in diverse H. vulgare panels comprising 297 wild lines from a diversity panel and 160 cultivated spring-type accessions from the mini-core panel representing the genetic diversity of the USDA barley germplasm collection. Significant differences were observed in the concentration of tocols between the two panels. To identify the genes associated with tocols, genome-wide association analysis was conducted with single nucleotide polymorphisms (SNPs) from Illumina arrays for the mini-core panel and genotyping-by-sequencing for the wild barley panel. Forty unique SNPs in the wild barley and 27 SNPs in the mini-core panel were significantly associated with various tocols. Marker-trait associations (MTAs) were identified on chromosomes 1, 6, and 7 for key genes in the tocol biosynthesis pathway, which have also been reported in other studies. Several novel MTAs were identified on chromosomes 2, 3, 4 and 5 and were found to be in proximity to genes involved in the generation of precursor metabolites required for tocol biosynthesis. This study provides a valuable resource for barley breeding programs targeting specific isoforms of seed tocols and for investigating the physiological roles of these metabolites in seed longevity, dormancy, and germination.

Mechanisms on inhibition of photosynthesis in Kandelia obovata due to extreme cold events under climate change

Mangroves that grow at the latitudinal extremes of their distribution are susceptible to extreme cold events. Successive enhancement of low temperature stress (seLTS) is a typical characteristic of extreme cold events. Low temperature stress can inhibit mangrove photosynthesis, which often inhibits the growth and development of mangroves. However, the possible reasons for impairment to photosynthesis of mangroves due to extreme cold events remain unclear. Kandelia obovata seedlings in a growth chamber were exposed to 5°C/−2°C (day/night) for 36 h (−2°C for 16 h) with 12 h light per day at 600 μmol m−2 s−1 photosynthetic photon flux density (PPFD) (a low temperature stress, aLTS), then the plants were transferred to the control condition (15°C/10°C (day/night) and allowed to recover for 5 days (R1). The other seedlings were subjected to low temperature treatment with a day/night temperature of 5°C/−1°C in a growth chamber for 24 h. Then these plants were transferred to 5°C/−2°C (day/night) under the same light and climate conditions for 36 h (two low temperature stresses, tLTS). Following the successive enhancement of low temperature treatment, these plants were returned to 15°C/10°C (day/night) for another 5-day recovery period (R2). Results showed that aLTS treatment significantly reduced leaf net photosynthetic rate (P n) and stomatal conductance (G s), while increased intercellular CO2 concentration (C i). Photosynthetic activity of leaves quickly recovered after the plants were returned to control temperature for 5 days (R1). However, decreases in leaf P n were more obvious under tLTS treatment than those under aLTS treatment. This reduced P n might be attributed to stomatal and non-stomatal limitations. Moreover, non-stomatal limitation played a major role in reducing P n during tLTS treatment, as proven by reduced ribulose 1,5-biphosphate carboxylase (RuBPCase) activity. This limitation also enhanced lipid peroxidation in chloroplasts, decreased sucrose-metabolizing enzymes and ratios of both chlorophyll a/chlorophyll b (Chl a/b) and chlorophyll/carotenoids (Chl/Car), and increased protease senescence. Damages of tLTS treatment to photosynthesis were insufficiently alleviated even after the plants were returned to control temperature for 5 days (R2). Successive enhancement of low temperature depressed successful recovery of leaf photosynthesis of K. obovata seedlings mainly by impairing pigment synthesis, antioxidant metabolism, and sucrose translocation, as well as accelerating senescence of endopeptidase. Furthermore, our results suggest that decreases in sucrose content in leaves might also account for increases in reactive oxygen species (ROS) in chloroplasts.

Redox signaling and stress tolerance in plants: a focus on vitamin E.

Plants are subject to specific redox processes, in which photosynthesis plays a prominent role. Chloroplasts function in light at high oxygen tensions and are enormous generators of reactive oxygen species, mainly singlet oxygen. This side product of photosynthesis inflicts damage to thylakoid membranes at high concentrations, but at the same time it is an essential component of cellular signaling. Detoxification of singlet oxygen is achieved by different means, including quenching and scavenging by tocopherols, responsible for controlling singlet oxygen levels, and the extent of lipid peroxidation in chloroplasts. Here, environmental conditions leading to excess light in chloroplasts will be used to show the importance of singlet oxygen, tocopherols, and lipid peroxidation in cell signaling. Defects in antioxidant protection (e.g., tocopherol deficiency) can lead to increased photo-oxidative damage, but also to the activation of defense pathways, illustrating the phenotypic plasticity evolved by plants to withstand stress. Most importantly, these studies show how redox signaling processes are integrated within the cell and illustrate the great capacity of plants to adapt to their environment.

Linking tocopherols with cellular signaling in plants

Linking tocopherols with cellular signaling in plants

Interplay between ascorbic acid and lipophilic antioxidant defences in chloroplasts of water-stressed Arabidopsis plants

The effects of low ascorbic acid (Asc) on lipophilic antioxidant defences and lipid peroxidation in chloroplasts were evaluated in the vtc-1 mutant of Arabidopsis thaliana, which had an Asc deficiency in chloroplasts of ca. 60%. Although low Asc did not cause oxidative stress in optimal growth conditions, it increased malondialdehyde levels in chloroplasts by ca. 60%, and reduced α-tocopherol and β-carotene by ca. 85% and 40%, respectively, in water-stressed (WS) mutants. These results are indicative of the interplay between Asc and lipophilic antioxidants in chloroplasts of WS plants in vivo, and show that Asc contributes to the protection of thylakoid membrane lipids from oxidation in stressed plants.

Antioxidant and Chelating Properties of Flavonoids

Flavonoids are a group of naturally occurring, low molecular weight polyphenols of plant origin, which formally should be considered as benzo-γ-pyrone derivatives. This chapter discusses several groups of flavonoids: flavones (I), flavonols (Ia), flavanones (ll), and flavanols (IIa). The members of these groups differ by the number and the positions of hydroxyl substituents in rings A and B. In addition, there are flavonoids that cannot be included in these groups but that are important biological and pharmaceutic agents. Among them are catechin (lll), (+)-cianidanol (IV), and others. Flavonoids have been reported to exert multiple biological effects and to exhibit anti-inflammatory, antiallergic, antiviral, and anticancer activities. It has been suggested that flavonoid activities depend on their antioxidant and chelating properties. This chapter considers the mechanisms of free radical scavenging, antioxidant, and chelating activities of flavonoids, their free radical-mediated nonenzymatic and enzymatic processes and free radical production by cells. The effects of flavonoids against cellular and tissue damage, their toxic effects on tumor cells, and their mutagenic and antimutagenic properties have been discussed. Being polyphenols, flavonoids are the good scavengers of free radicals because of high reactivities of their hydroxyl substituents in a hydrogen atom abstraction reaction. The effects of flavonoids on various superoxide-generating systems have been studied. Flavonoids inhibit the in vitro peroxidative processes such as the autoxidation of linoleic acid, the oxidation of low-density lipoproteins, the peroxidation of phospholipid membranes, microsomal and mitochondrial lipid peroxidation, lipid peroxidation in erythrocyte ghosts, the autoxidation of rat brain homogenates and photooxidation and lipid peroxidation in chloroplasts. It is possible that flavonoids (mainly quercetin) inhibit the growth of malignant cells. That flavonoids have to be metabolically activated to acquire mutagenic activity is not always an obligatory condition. The antimutagenic activity of flavonoids is most probably a consequence of their antioxidant and chelatory properties.

Studies on the mode of action of the herbicidal effect of 2,4,5-trichlorophenoxyacetic acid on germinating Norway spruce

A dramatic effect of 2,4,5-trichlorophenoxyacetic acid on the growth of germinating plants was observed. This effect was expressed as abnormal growth. A pronounced increase in ethylene formation (10-fold) was observed in dark-grown plants treated with 200 μM 2,4,5-trichlorophenoxyacetic acid. In a crude peroxisomal fraction prepared from cotyledons of seedlings treated with 200 μM trichlorophenoxyacetic acid, large increases in fatty acyl-CoA oxidase (6.9-fold) and catalase (2.7-fold) activities were observed. A reduced activity of photosystem 11 was observed in chloroplasts from cotyledons of seedlings treated with 2,4,5-trichlorophenoxyacetic acid. In the dark-grown seedlings, this activity decreased to 35% of control. An inhibitory effect of 2,4,5-trichlorophenoxyacetic acid on photosystem II was also found in in vitro experiments with chloroplasts isolated from cotyledons of untreated plants. An increase in lipid peroxidation in chloroplasts treated with 200 μM 2,4,5-trichlorophenoxyacetic acid was also observed. Electron microscope studies on germinating Norway spruce seedlings revealed a pronounced degenerative effect of 2,4,5-trichlorophenoxyacetic acid on chloroplasts, expressed as swollen chloroplats and disorganized orientation of thylakoid membranes. Vesicles were often present in the stroma and the thylakoid. In some chloroplasts, a complete disintegration of compartments was observed. The present study suggests that the principal mode of action of 2,4,5-trichlorophenoxyacetic acid on Norway spruce seedlings is via damage of the thylakoid membrane and inhibition of photosystem II. Additionally, our results support a possible role of increased oxidative stress as an additional mode of action of 2,45-trichlorophenoxyacetic acid.

Generation of free radicals in germinating Norway spruce. Differences in the effect of two different phenolic compounds

SynopsisWe have studied the defences of Norway spruce seeds against pollutants during germination, using two different phenolic compounds, 5-OH-1,4-naphthoquinone (5-OH-NQ)3and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T).Only small effects of 5-OH-NQ on germination of seeds were observed at concentrations up to 200 μM, which could be explained by the formation of a less reactive metabolite of 5-OH-NQ. These results suggest that Norway spruce seeds have a very effective defence system against quinone and quinonederived reactive oxygen species.The effect of 2,4,5-T on seed germination was, however, more pronounced, resulting in an abnormal growth of the seedlings. This behaviour was probably due to a strong increase in ethylene production (10-fold) in these seedlings. Also fatty acyl-CoA oxidase activity, a peroxisomal enzyme of β-oxidation that catalyses the formation of H2O2, was found to increase 6.9-fold in seedlings germinated in presence of 2,4,5-T. A strong decrease in the activity of photosystem II and an increase in lipid peroxidation in chloroplasts was also observed.

Sulfite-Induced Lipid Peroxidation in Chloroplasts as Determined by Ethane Production

Ethane formation, as a measure of lipid peroxidation, was studied in spinach (Spinacia oleracea L.) chloroplasts exposed to sulfite. Ethane formation required sulfite and light, and occurred with concomitant oxidation of sulfite to sulfate. In the dark, both ethane formation and sulfite oxidation were inhibited. Ethane formation was stimulated by ferric or ferrous ions and inhibited by ethylenediamine tetraacetate. The photosynthetic electron transport modulators, 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU) and phenazine methosulfate, inhibited both sulfite oxidation and ethane formation. Methyl viologen greatly stimulated ethane formation, but had little effect on sulfite oxidation. Methyl viologen, in the absence of sulfite, caused only a small amount of ethane formation in comparison to that produced with sulfite alone. Sulfite oxidation and ethane formation were effectively inhibited by the radical scavengers, 1,2-dihydroxybenzene-3,5-disulfonic acid and ascorbate. Ethanol, a hydroxyl radical scavenger, inhibited ethane formation only to a small degree; formate, which converts hydroxyl radical to superoxide radical, caused a small stimulation in both sulfite oxidation and ethane formation. Superoxide dismutase inhibited ethane formation by 50% when added at a concentration equivalent to that of the endogenous activity. Singlet oxygen did not appear to play a role in ethane formation, inasmuch as the singlet oxygen scavengers, sodium azide and 1,4-diazobicyclo-[2,2,2]-octane, were not inhibitory. These data are consistent with the view that O(2) is reduced by the photosynthetic electron transport system to superoxide anion, which in turn initiates the free radical oxidation of sulfite, and the free radicals produced during sulfite oxidation were responsible for the peroxidation of membrane lipids, resulting in the formation of ethane.

Effect of light on lipid peroxidation in chloroplasts

Effect of light on lipid peroxidation in chloroplasts