Oxygen deficit alleviates phosphate overaccumulation toxicity in OsPHR2 overexpression plants

Overexpression of OsPHR2 increases phosphate (Pi) uptake and causes overaccumulation of Pi in rice plants, which is toxic to rice plants when they are grown in media with a sufficient Pi supply. The toxicity that results from OsPHR2 overexpression can be significantly relieved by growing the plants in a waterlogged paddy field. A comparison of the Pi uptake and growth status of OsPHR2-overexpression plants (PHR2-Oe plants) grown in paddy fields or in a laboratory setting in aerated or stagnant hydroponic conditions indicated that the oxygen limitation that is present in paddy fields and in stagnant rice culture solutions inhibits the Pi overaccumulation toxicity of PHR2-Oe plants by reducing their Pi uptake. Quantitative RT-PCR demonstrated that the expression of Pi-starvation-induced (PSI) genes was induced by oxygen limitation in both wild-type and PHR2-Oe plants. The induction of PSI genes is the consequence of reducing the Pi concentration in stagnant plants. Thus, when evaluating the efficiency of Pi use in rice germplasm or transgenic materials under hydroponic conditions, the impact of the low oxygen condition that exists in waterlogged paddies should be considered.     

Oxygen toxicity in Astasia

1. Exposure of Astasia longa to oxygen+carbon dioxide (95:5) at atmospheric pressure leads to an inhibition of growth rate and of respiration. Growth resumes at the normal rate as soon as the oxygenation is discontinued, but respiration recovers more slowly. 2. Mitochondria prepared from cells exposed to oxygen+carbon dioxide (95:5) during growth have considerably decreased activities of succinate-cytochrome c oxidoreductase, NADH-cytochrome c oxidoreductase, succinate dehydrogenase and succinate oxidase activities as compared with mitochondria obtained from cells exposed to air+carbon dioxide (95:5). Cytochrome oxidase activity is not appreciably inhibited by exposure of the cells to 95% oxygen. 3. The mitochondrial fraction of Astasia contains rhodoquinone. The rhodoquinone concentration increases in cells exposed to 95% oxygen. The content of ergosterol-containing compounds also increases in the mitochondria of cells exposed to 95% oxygen. There is little change in the ubiquinone content of the mitochondrial fraction. The ubiquinone of Astasia appears to be ubiquinone-45.     

Oxygen toxicity is not related to mammalian body size

1. Small mammals have been used to study the effects of O2 toxicity. The aim of the present study was to investigate whether body size should be considered when applying the results of these studies to man. 2. Oxygen toxicity is enhanced as perfusion and metabolism increase: specific animal tissues of high perfusion are more susceptible to O2 toxicity. Exercise, high metabolic rate, and increased brain blood flow enhance O2 toxicity. 3. Increased specific O2 consumption and perfusion as body mass decreases may enhance O2 toxicity in small mammals. 4. Survival time in normobaric hyperoxia (1 atm O2) and the time to first appearance of convulsions in hyperbaric oxygen (4-5 atm) were collected from the literature and showed no relation to body size. 5. Known difference in antioxidant enzyme activity cannot explain the findings. 6. Independence of tissue PO2 on body size, or equal rates of free radical formation and degradation, are suggested as possible mechanisms. 7. Small mammals can serve as a good model for O2 toxicity in man.     

Oxygen toxicity and microbial evolution

It is postulated that the role of oxygen toxicity in the evolution of life strongly depends on the origin of molecular oxygen, due to the strong redox buffering capacity of Precambrian waters containing large amounts of ferrous and manganese cations. The critical selective pressure could be observed only after aerobic photosynthesis had been developed, due to the high local concentration of oxygen in close vicinity of photosynthesizing cells. It is also postulated that early oxygen-evolving organisms excreted a substantial part of this element in the form of hydrogen peroxide. As a consequence of the high reactivity of this compound with ferrous and manganese cations, an important percentage of iron deposits were produced with H2O2 as a major oxidant after the development of aerobic photosynthesis. It is postulated that negatively charged extracellular polymers of simple pro- and eukaryotic organisms function as sacrificial targets of hydroxyl radicals and at the same time as extracellular equivalents of superoxide dismutases, in these two ways protecting cellular membranes against oxidative damage. The role of oxygen toxicity in developing aerobic mechanisms of iron uptake is also discussed.     

Mercury toxicity in plants

Mercury poisoning has become a problem of current interest as a result of environmental pollution on a global scale. Natural emissions of mercury form two-thirds of the input; manmade releases form about one-third. Considerable amounts of mercury may be added to agricultural land with sludge, fertilizers, lime, and manures. The most important sources of contaminating agricultural soil have been the use of organic mercurials as a seed-coat dressing to prevent fungal diseases in seeds. In general, the effect of treatment on germination is favorable when recommended dosages are used. Injury to the seed increases in direct proportion to increasing rates of application. The availability of soil mercury to plants is low, and there is a tendency for mercury to accumulate in roots, indicating that the roots serve as a barrier to mercury uptake. Mercury concentration in aboveground parts of plants appears to depend largely on foliar uptake of Hg⁰ volatilized from the soil. Uptake of mercury has been found to be plant specific in bryophytes, lichens, wetland plants, woody plants, and crop plants. Factors affecting plant uptake include soil or sediment organic content, carbon exchange capacity, oxide and carbonate content, redox potential, formulation used, and total metal content. In general, mercury uptake in plants could be related to pollution level. With lower levels of mercury pollution, the amounts in crops are below the permissible levels. Aquatic plants have shown to be bioaccumulators of mercury. Mercury concentrations in the plants (stems and leaves) are always greater when the metal is introduced in organic form. In freshwater aquatic vascular plants, differences in uptake rate depend on the species of plant, seasonal growthrate changes, and the metal ion being absorbed. Some of the mercury emitted from the source into the atmosphere is absorbed by plant leaves and migrates to humus through fallen leaves. Mercury-vapor uptake by leaves of the C₃ speciesoats, barley, and wheat is five times greater than that by leaves of the C₄ species corn, sorghum, and crabgrass. Such differential uptake by C₃ and C₄ species is largely attributable to internal resistance to mercury-vapor binding. Airborne mercury thus seems to contribute significantly to the mercury content of crops and thereby to its intake by humans as food. Accumulation, toxicity response, and mercury distribution differ between plants exposed through shoots or through roots, even when internal mercury concentrations in the treated plants are similar. Throughfall and litterfall play a significant role in the cycling and deposition of mercury. The possible causal mechanisms of mercury toxicity are changes in the permeability of the cell membrane, reactions of sulphydryl (-SH) groups with cations, affinity for reacting with phosphate groups and active groups of ADP or ATP, and replacement of essential ions, mainly major cations. In general, inorganic forms are thought to be more available to plants than are organic ones. Plants can be exposed to mercurials either by direct administration as antifungal agents, mainly to crop plants through seed treatment or foliar spray, or by accident. The end points screened are seed germination, seedling growth, relative growth of roots and shoots, and, in some case, studies of leaf-area index, internode development, and other anatomical characters. Accidental exposures occur through soil, water, and air pollution. The level of toxicity is usually tested under laboratory conditions using a wide range of concentrations and different periods of exposure. Additional parameters include biochemical assays and genetical studies. The absorption of organic and inorganic mercury from soil by plants is low, and there is a barrier to mercury translocation from plant roots to tops. Thus, large increases in mercury levels in soil produce only modest increases in mercury levels in plants by direct uptake from soil. Injuries to cereal seeds caused by organic mercurials has been characterized by abnormal germination and hypertrophy of the roots and coleoptile. Mercury affects both light and dark reactions of photosynthesis. Substitution of the central atom of chlorophyll, magnesium, by mercury in vivo prevents photosynthetic light harvesting in the affected chlorophyll molecules, resulting in a breakdown of photosynthesis. The reaction varies with light intensity. A concentration and time-dependent protective effect of GSH seems to be mediated by the restricted uptake of the metal involving cytoplasmic protein synthesis. Plant cells contain aquaporins, proteins that facilitate the transport of water, in the vacuolar membrane (tonoplast) and the plasma membrane. Many aquaporins are mercury sensitive, and in AQP1 a mercury-sensitive cysteine residue (Cys-189) is present adjacent to a conserved Asn-Pro-Ala motif. At low concentrations mercury has a toxic effect on the degrading capabilities of microorganisms. Sensitivity to the metal can be enhanced by a reduction in pH, and tolerance of mercury by microorganisms has been found to be in the order: total population > nitrogen fixers > nitrifiers. Numerous experiments have been carried out to study the genetic effects of mercury compounds in experimental test systems using a variety of genetic endpoints. The most noticeable and consistent effect is the induction of c-mitosis through disturbance of the spindle activity, resulting in the formation of polyploid and aneuploid cells and c-tumors. Organomercurials have been reported to be 200 times more potent than inorganic mercury. Exposure to inorganic mercury reduces mitotic index in the root-tip cells and increases the frequency of chromosomal aberrations in degrees directly proportional to the concentrations used and to the duration of exposure. The period of recovery after removal of mercury is inversely related to the concentration and duration of exposure. Bacterial plasmids encode resistance systems for toxic metal ions, including Hg²⁺, functioning by energy-dependent efflux of toxic ions through ATPases and chemiosmotic cationproton antiporters. The inducible mercury resistance (mer) operon encodes both a mercuric ion uptake and detoxification enzymes. In gram-negative bacteria a periplasmic protein,MerP, an inner-membrane transport protein,MerT, and a cytoplasmic enzyme, mercuric reductase, theMerA protein, are responsible for the transport of mercuric ions into cells and their reduction to elemental mercury, Hg(II). InThiobacillus ferrooxidans, an acidophilic chemoautotrophic bacterium sensitive to mercury ions, a group of mercury-resistant strains, which volatilize mercury, has been isolated. The entire coding sequence of the mercury-ion resistance gene has been located in a 2.3 kb fragment of chromosomal DNA (encoding 56,000 and 16,000 molecular-weight proteins) from strain E-l 5 ofEscherichia coli. Higher plants andSchizosaccharomyces pombe respond to heavy-metal stress of mercury by synthesizing phytochelatins (PCs) that act as chelators. The strength of Hg(II) binding to glutathione and phytochelatins follows the order: γGlu-Cys-Gly(γGlu-Cys)₂Gly(γGlu-Cys)₃Gly(γGlu-Cys)₄Gly. Suspension cultures of haploid tobacco,Nicotiana tabacum, cells were subjected to ethyl methane sulfonate to raise mercury-tolerant plantlets. HgCl₂-tolerant variants were selected from nitrosoguanidine (NTG)-treated suspension cell cultures of cow pea,Vigna unguiculata, initiated from hypocotyl callus and incubated with 18 ⧎g/ml HgCl₂. Experiments have been carried out to develop mercury-tolerant plants ofHordeum vulgare through previous exposure to low doses of mercury and subsequent planting of the next generation in mercury-contaminated soil. Phytoremediation involves the use of plants to extract, detoxify, and/or sequester environmental pollutants from soil and water. Transgenic plants cleave mercury ions from methylmercury complexes, reduce mercury ions to the metallic form, take up metallic mercury through their roots, and evolve less toxic elemental mercury. Genetically engineered plants contain modified forms of bacterial genes that break down methyl mercury and reduce mercury ions. The first gene successfully inserted into plants wasmerA, which codes for a mercuric ion reductase enzyme, reducing ionic mercury to the less toxic elemental form.MerB codes for an organomercurial lyase protein that cleaves mercury ions from highly toxic methyl mercury compounds. Plants with themerB gene have been shown to detoxify methyl mercury in soil and water. Both genes have been successfully expressed inArabidopsis thaliana, Brassica (mustard),Nicotiana tabacum (tobacco), andLiriodendron tulipifera (tulip poplar). Plants currently being transformed include cattails, wild rice, andSpartina, another wetland plant. The problem of mercury contamination can be reduced appreciably by combining the standard methods of phytoremediation—removal of mercury from polluted areas through scavenger plants—with raising such plants both by routine mutagenesis and by genetic engineering. The different transgenics raised utilizing the two genesmerA andmerB are very hopeful prospects.     

Antioxidant responses of chickpea plants subjected to boron toxicity

This study investigated oxidative stress and the antioxidant response to boron (B) of chickpea cultivars differing in their tolerance to drought. Three‐week‐old chickpea seedlings were subjected to 0.05 (control), 1.6 or 6.4 mm B in the form of boric acid (H₃BO₃) for 7 days. At the end of the treatment period, shoot length, dry weight, chlorophyll fluorescence, B concentration, malondialdehyte content and the antioxidant enzymes superoxide dismutase (SOD), peroxidase (POX), catalase (CAT), ascorbate peroxidase (APX) and glutathione reductase (GR) were measured. The 1.6 mm B treatment did not cause significant changes in shoot length of cultivars, although shoot length increased in the drought‐tolerant Gökce and decreased in the drought‐sensitive Küsmen after 6.4 mm B treatment. Dry weights of both cultivars decreased with 6.4 mm B treatment. Chlorophyll fluorescence (Fv/Fm) did not change in Gökce at either B level. Nor did it change in Küsmen with 1.6 mm B but Fv/Fm decreased with 6.4 mm B. Boron concentration in the shoots of both cultivars increased significantly with increasing levels of applied B. Significant increases in total SOD activity were observed in shoots of both cultivars given 1.6 and 6.4 mm B. Shoot extracts exhibited five activity bands, two of which were identified as MnSOD and Cu/ZnSOD. In comparison to the control group, all enzyme activities (except APX and SOD) decreased with 1.6 mm B stress. GR activity decreased, while activities of CAT, POX and APX did not change with 6.4 mm B in Küsmen. On the other hand, activities of CAT, APX and SOD increased in Gökce at both B levels. In addition, lipid peroxidation was higher in Küsmen than in Gökce, indicating more damage by B to membrane lipids in the former cultivar. These results suggest that (i) Gökce is tolerant and Küsmen is sensitive to B, and (ii) B tolerance of Gökce might be closely related to increased capacity of the antioxidative system (total SOD, CAT and APX) to scavenge reactive oxygen species and thus suppress lipid peroxidation under B stress. To the best of our knowledge, this is the first report on the antioxidant response of chickpea seedlings to B toxicity.     

Oxygen toxicity in a fission yeast

Continuous exposure of synchronous cultures of Schizosaccharomyces pombe to 2.0 atmospheres oxygen beginning at any point in the first two-thirds of the cell cycle prevented subsequent cell division. Similar exposure during the last one-third of the cell cycle did not prevent cell division. The inhibition of division was totally reversible. Exposure to 2.0 atmospheres oxygen for 2.5 hours did not affect oxygen consumption. Oxygen at 1.0 atmospheres reduced growth rate and protein synthesis by 44%. Similar exposure to 1.0 atmospheres reduced transport of glycine-¹⁴C, L-leucine-¹⁴C, and uracil-¹⁴C by 95%, 73%, and 89% respectively. Analysis of the kinetics of uptake of these materials showed noncompetitive inhibition of transport by oxygen. The primary effect in rapidly appearing oxygen toxicity apparently involved interference with the transport capabilities of the cell membrane.     

Development of an electrostatic model predicting copper toxicity to plants

The focus of the present study was to investigate the mechanisms for the alleviation of Cu toxicity in plants by coexistent cations (e.g. Al(3+), Mn(2+), Ca(2+), Mg(2+), H(+), Na(+), and K(+)) and the development of an electrostatic model to predict 50% effect activities (EA50s) accurately. The alleviation of Cu(2+) toxicity was evaluated in several plants in terms of (i) the electrical potential at the outer surface of the plasma membrane (PM) (Ψ(0)(°)) and (ii) competition between cations for sites at the PM involved in the uptake or toxicity of Cu(2+), the latter of which is invoked by the Biotic Ligand Model (BLM) as the sole explanation for the alleviation of toxicity. The addition of coexistent cations into the bulk-phase medium reduces the negativity of Ψ(0)(°) and hence decreases the activity of Cu(2+) at the PM surface. Our analyses suggest that the alleviation of toxicity results primarily from electrostatic effects (i.e. changes in both the Cu(2+) activity at the PM surface and the electrical driving force across the PM), and that BLM-type competitive effects may be of lesser importance in plants. Although this does not exclude the possibility of competition, the data highlight the importance of electrostatic effects. An electrostatic model was developed to predict Cu(2+) toxicity thresholds (EA50s), and the quality of its predictive capacity suggests its potential utility in risk assessment of copper in natural waters and soils.     

Alleviation of nickel toxicity by ammonium supply to sunflower plants

Phytotoxicity of nickel (Ni) varies within plant species and cultivars as well as with the concentration of Ni in the rooting medium. Moreover, it is known that several nutrients can modify the plant response to excess Ni. Nitrogen can be absorbed by plants as different N forms and because N metabolism and Ni are closely related, a hydroponic experiment was conducted to study the effect of Ni toxicity on the growth, nutrient status of the different plant parts and leaf chlorophyll concentrations in sunflower plants (Helianthus annuus L.) cv Quipu grown with different forms of N supply. The plants were grown under controlled conditions for 35 days. Depending on the N source supplied, there were significant differences in the sensitivity of sunflower plants to excess Ni. Tolerance was lowest when grown with NO₃ ⁻ alone. A high Ni and NO₃ ⁻ as the only N source resulted in reduced dry weight and significant decreases in nutrient concentration. Plants supplied with a mixture of NO₃ ⁻ and NH₄ ⁺ absorbed in the presence of Ni in solution about three times less Ni than those supplied with NO₃ ⁻ alone. Consequently, there were great differences in Ni concentrations between treatments. With a N nutrition of 100% NO₃ ⁻-N, Ni supply led to severe growth inhibition. Just contrary, simultaneous supply of NO₃ ⁻ and NH₄ ⁺ not only reduced Ni toxicity, but growth was even stimulated by Ni if supplied to plants fed with NO₃ ⁻ and NH₄ ⁺. This indicates the significant role of the N form supplied in the behaviour of Ni toxicity in sunflower plants. This revised version was published online in June 2006 with corrections to the Cover Date.     

Response of nitrogen metabolism to boron toxicity in tomato plants

Boron (B) toxicity has become important in areas close to the Mediterranean Sea where intensive agriculture has been developed. The objective of this research was to study the effects of B toxicity (0.5 m m and 2.0 m m B) on nitrogen (N) assimilation of two tomato cultivars that are often used in these areas. Leaf biomass, relative leaf growth rate (RGR_L), concentration of B, nitrate (NO₃⁻), ammonium (NH₄⁺), organic N, amino acids and soluble proteins, as well as nitrate reductase (NR), nitrite reductase (NiR), glutamine synthase (GS), glutamate synthetase (GOGAT) and glutamate dehydrogenase (GDH) activities were analysed in leaves. Boron toxicity significantly decreased leaf biomass, RGR_L, organic N, soluble proteins, and NR and NiR activities. The lowest NO₃⁻ and NH₄⁺ concentration in leaves was recorded when plants were supplied with 2.0 m m B in the root medium. Total B, amino acids, activities of GS, GOGAT and GDH increased under B toxicity. Data from the present study prove that B toxicity causes inhibition of NO₃⁻ reduction and increases NH₄⁺ assimilation in tomato plants.