Orchids are distributed around the world, however, the factors shaping their specific distribution and habitat preferences are largely unknown. Moreover, many orchids are at risk of becoming threatened as landscapes change, sometimes declining without apparent reason. One important factor affecting plant distribution is nutrient levels in the environment. Nitrates can inhibit not only orchid growth and persistence, but also seed germination. We used in vitro axenic cultures to exactly determine the germination sensitivity of seven orchid species to nitrates and correlated this with soil properties of the natural sites and with the species' habitat preferences. We found high variation in response to nitrate between species. Orchids from oligotrophic habitats were highly sensitive, while orchids from more eutrophic habitats were almost insensitive. Sensitivity to nitrate was also associated with soil parameters that indicated a higher nitrification rate. Our results indicate that nitrate can affect orchid distribution via direct inhibition of seed germination. Nitrate levels in soils are increasing rapidly due to intensification of agricultural processes and concurrent soil pollution, and we propose this increase could cause a decline in some orchid species.

• Keywords
• Orchidaceae, in vitro, Distribution, germination, habitat, nitrate, nitrogen,
• MeSH
• Nitrates * analysis   toxicity   MeSH
• Ecosystem * MeSH
• Orchidaceae * drug effects   physiology   MeSH
• Soil * chemistry   MeSH
• Seeds * drug effects   MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Nitrates * MeSH
• Soil * MeSH

A new method of determination of nitrate was developed, utilizing the nitrate reductase activity of Paracoccus denitrificans in which a further reduction of nitrate is blocked either by a mutation affecting formation of cytochromes c or by inhibition of the electron flow to nitrite reductase by mucidin. After deproteinization of the sample with zinc acetate the nitrite produced is determined colorimetrically.

• MeSH
• Nitrates analysis   metabolism   MeSH
• Nitrites metabolism   MeSH
• Mutagenesis MeSH
• Nitrate Reductase MeSH
• Nitrate Reductases metabolism   MeSH
• Nitrite Reductases genetics   metabolism   MeSH
• Paracoccus denitrificans genetics   metabolism   MeSH
• Enzyme Stability MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Nitrates MeSH
• Nitrites MeSH
• Nitrate Reductase MeSH
• Nitrate Reductases MeSH
• Nitrite Reductases MeSH

Nitrate pollution in water is a worldwide health and environmental concern. Biological nitrate removal of wastewater is widely used countering eutrophication of water bodies; however it could be troublesome and expensive when influent carbon source is insufficient. Here we present a novel process, the microbial fuel cell (MFC)-resistance-type electrical stimulation denitrification process (RtESD) using microbial weak electricity originated from the wastewater, to enhance nitrate removal. Results show that the optimal nitrate dependent denitrification rate (0.027 mg N/L·h) and nitrate removal efficiency (98.1%) can be achieved; partial autotrophic denitrification was enhanced in RtESD under stimulation of 0.2 V of microbial weak electricity (MWE). Aromatic proteins also increased in the presence of 0.2 V MWE stimulation according to three-dimensional excitation-emission matrix (3D-EEM) fluorescence spectroscopy profiles, indicating that electron transfer could be improved in the case of MWE stimulation. Furthermore, the microbial community structure and diversity analysis results demonstrated that MWE stimulation inhibited the heterotrophic denitrifying bacteria and activated the autotrophic denitrifying bacteria in RtESD. Two hypotheses, enhancement of electron transfer and improvement of microorganism activity, were proposed regarding to the MWE stimulated pathways. This study provided a promising method utilizing MWE derived from wastewater to improve the denitrification rate and removal efficiency of nitrate-containing wastewater treatment processes.

• Keywords
• Microbial fuel cell (MFC), Microbial weak electricity (MWE), Nitrate (NO(3)(−)-N) containing wastewater, Resistance-type electrical stimulation denitrification (RtESD),
• MeSH
• Bioreactors MeSH
• Denitrification MeSH
• Nitrates * MeSH
• Nitrogen MeSH
• Electricity MeSH
• Wastewater * MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Nitrates * MeSH
• Nitrogen MeSH
• Waste Water * MeSH

Many orchid species are threatened, while some disappear from their natural habitats without obvious reasons. Eutrophication has been suggested as a possible factor and nitrate, which is able to suppress non-symbiotic orchid seed germination even at very low concentrations, and could pose a serious threat for natural orchid populations. Early ontogenesis of all orchids entirely depends on orchid mycorrhizal symbiosis, and at this initial mycoheterotrophic stage, many terrestrial green orchids associate with polyphyletic fungal symbionts (i.e., mycobionts), collectively called "rhizoctonias." We asked whether these fungi might also have some non-nutritional roles, i.e., whether they might confer resistance to eutrophication. To test this hypothesis, we co-cultivated seeds of the terrestrial orchid Dactylorhiza majalis with five rhizoctonias (two Tulasnella, two Ceratobasidium and one Serendipita isolate) at various ecologically meaningful nitrate concentrations (0 to 100 mg/L). With the exception of one Tulasnella isolate, all mycobionts supported the growth of protocorms and formed orchid mycorrhiza, i.e., intracellular hyphal pelotons, in the protocorms. Nitrate suppressed asymbiotic, as well as symbiotic, seed germination in all but one fungal treatment; the seeds co-cultivated with one of the Ceratobasidium isolates were indeed insensitive to nitrate. We conclude that nitrates also negatively affect symbiotic orchid germination, depending on the available compatible mycobionts. Thus, eutrophication with nitrate may decrease the number of orchid mycobionts capable of supporting seed germination.

• Keywords
• Nitrate, Orchid mycorrhiza, Orchid seed germination, Protocorm development, Symbiotic fungi, Terrestrial green orchids,
• MeSH
• Nitrates MeSH
• Germination MeSH
• Mycorrhizae * MeSH
• Orchidaceae * MeSH
• Seeds MeSH
• Symbiosis MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Nitrates MeSH

Mineral nutrition is one of the key environmental factors determining plant development and growth. Nitrate is the major form of macronutrient nitrogen that plants take up from the soil. Fluctuating availability or deficiency of this element severely limits plant growth and negatively affects crop production in the agricultural system. To cope with the heterogeneity of nitrate distribution in soil, plants evolved a complex regulatory mechanism that allows rapid adjustment of physiological and developmental processes to the status of this nutrient. The root, as a major exploitation organ that controls the uptake of nitrate to the plant body, acts as a regulatory hub that, according to nitrate availability, coordinates the growth and development of other plant organs. Here, we identified a regulatory framework, where cytokinin response factors (CRFs) play a central role as a molecular readout of the nitrate status in roots to guide shoot adaptive developmental response. We show that nitrate-driven activation of NLP7, a master regulator of nitrate response in plants, fine tunes biosynthesis of cytokinin in roots and its translocation to shoots where it enhances expression of CRFs. CRFs, through direct transcriptional regulation of PIN auxin transporters, promote the flow of auxin and thereby stimulate the development of shoot organs.

• Keywords
• macronutrient, nitrate, plant development,
• MeSH
• Cytokinins metabolism   MeSH
• Nitrates * metabolism   MeSH
• Plant Roots metabolism   MeSH
• Indoleacetic Acids * metabolism   MeSH
• Soil MeSH
• Gene Expression Regulation, Plant MeSH
• Signal Transduction MeSH
• Plant Shoots MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Cytokinins MeSH
• Nitrates * MeSH
• Indoleacetic Acids * MeSH
• Soil MeSH

This study deals with the effects of the agents that dissipate the individual components of the proton motive force (short-chain fatty acids, nigericin, and valinomycin) upon the methyl viologen-coupled nitrate reductase activity in intact cells. Substitution of butyrate or acetate for chloride in Tris-buffered assay media resulted in a marked inhibition at pH 7. In a Tris--chloride buffer of neutral pH, the reaction was almost fully inhibitable by nigericin. Alkalinisation increased the IC(50) value for nigericin and decreased the maximal inhibition attained. Both types of inhibitions could be reversed by the permeabilisation of cells or by the addition of nitrite, and that caused by nigericin disappeared at high extracellular concentrations of potassium. These data indicate that nitrate transport step relies heavily on the pH gradient at neutral pH. Since the affinity of cells for nitrate was strongly diminished by imposing an inside-positive potassium (or lithium) diffusion potential at alkaline external pH, a potential dependent step may be of significance in the transporter cycle under these conditions. Experiments with sodium-depleted media provided no hints for Na(+) as a possible H(+) substitute.

• MeSH
• Biological Transport drug effects   MeSH
• Potassium metabolism   MeSH
• Nitrates metabolism   MeSH
• Ionophores pharmacology   MeSH
• Hydrogen-Ion Concentration MeSH
• Nigericin pharmacology   MeSH
• Nitrate Reductase MeSH
• Nitrate Reductases antagonists & inhibitors   MeSH
• Paracoccus denitrificans drug effects   metabolism   MeSH
• Paraquat chemistry   MeSH
• Proton-Motive Force drug effects   physiology   MeSH
• Sodium metabolism   MeSH
• Valinomycin pharmacology   MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Potassium MeSH
• Nitrates MeSH
• Ionophores MeSH
• Nigericin MeSH
• Nitrate Reductase MeSH
• Nitrate Reductases MeSH
• Paraquat MeSH
• Sodium MeSH
• Valinomycin MeSH

Impacts of red beet consumption both on human and animal health are subject of intense research. In particular, products that are not heat-processed contain plethora of bioactive compounds that hold promise against numerous degenerative and aging-associated diseases. However, high level of nitrates (typically more than 2 g NO3- kg-1) whose health effects are perceived with reasoned objections counterbalance these benefits. Following the above, from a certain level, the increased consumption of red beet has contrary impacts, creating a limiting factor not only from the economic point of view but also in terms of beneficial compounds intake. Reduction of NO3- levels (- 35%) has been achieved by soil amendment via increased doses of biochar. The data obtained indicates that the mechanism can be explained as follows. The soil improvement reduces soil density, increases soil temperature, improves water retention, and other prerequisites for increased activity of soil microorganisms. Accelerated metabolism of soil biota turned more nitrogen from fertilizers into organic forms. Hence, less mineral nitrogen is left for red beet intake.

• Keywords
• Biochar, Nitrate levels, Nitrates, Production management, Red beet,
• MeSH
• Beta vulgaris chemistry   growth & development   MeSH
• Charcoal chemistry   MeSH
• Nitrates analysis   MeSH
• Soil Pollutants analysis   MeSH
• Fertilizers * analysis   MeSH
• Soil chemistry   MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• biochar MeSH Browser
• Charcoal MeSH
• Nitrates MeSH
• Soil Pollutants MeSH
• Fertilizers * MeSH
• Soil MeSH

A comparative examination of reduced methyl [MV·](+) and benzyl [BV·](+) viologens (as artificial electron donors for quantitative estimation of the respiratory periplasmic (Nap) and membrane-embedded (Nar) nitrate reductases) using a newly constructed nap mutant strain of Paracocccus denitrificans was done. The activity with [MV·](+) was high in whole-cell assays, confirming that this compound donates electrons to Nar. Initial rates of the more lipophilic [BV·](+) were considerably lower, which was interpreted to be caused by an inhibition of the active transport of nitrate into the cells. Anionophoric activity of [BV·](+) was detectable but too low to effectively circumvent the inhibition of nitrate transporter.

• MeSH
• Single-Cell Analysis MeSH
• Bacterial Proteins chemistry   genetics   metabolism   MeSH
• Benzyl Viologen metabolism   MeSH
• Nitrates metabolism   MeSH
• Kinetics MeSH
• Nitrate Reductase chemistry   genetics   metabolism   MeSH
• Oxidation-Reduction MeSH
• Rhodobacteraceae chemistry   enzymology   genetics   MeSH
• Electron Transport MeSH
• Publication type
• Journal Article MeSH
• Evaluation Study MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Bacterial Proteins MeSH
• Benzyl Viologen MeSH
• Nitrates MeSH
• Nitrate Reductase MeSH

When grown anaerobically on a succinate+nitrate (SN) medium, Paracoccus denitrificans forms the membrane-bound, cytoplasmically oriented, chlorate-reducing nitrate reductase Nar, while the periplasmic enzyme Nap is expressed during aerobic growth on butyrate+oxygen (BO) medium. Preincubation of SN cells with chlorate produced a concentration-dependent decrease in nitrate utilization, which could be ascribed to Nar inactivation. Toluenization rendered Nar less sensitive to chlorate, but more sensitive to chlorite, suggesting that the latter compound may be the true inactivator. The Nap enzyme of BO cells was inactivated by both chlorate and chlorite at concentrations that were at least two orders of magnitude lower than those shown to affect Nar. Partial purification of Nap resulted in insensitivity to chlorate and diminished sensitivity to chlorite. Azide was specific for SN cells in protecting nitrate reductase against chlorate attack, the protective effect of nitrate being more pronounced in BO cells. The results are discussed in terms of different metabolic activation of chlorine oxoanions in both types of cells, and limited permeation of chlorite across the cell membrane.

• MeSH
• Chlorates metabolism   pharmacology   MeSH
• Chlorides metabolism   pharmacology   MeSH
• Nitrates metabolism   MeSH
• Enzyme Inhibitors metabolism   pharmacology   MeSH
• Succinic Acid metabolism   MeSH
• Nitrate Reductase antagonists & inhibitors   metabolism   MeSH
• Oxidation-Reduction MeSH
• Paracoccus denitrificans enzymology   metabolism   MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Chlorates MeSH
• Chlorides MeSH
• chlorite MeSH Browser
• Nitrates MeSH
• Enzyme Inhibitors MeSH
• Succinic Acid MeSH
• Nitrate Reductase MeSH

Potassium nitrate (E252) is widely used as a food preservative and has applications in the treatment of high blood pressure however high doses are carcinogenic. Larvae of Galleria mellonella were administered potassium nitrate to establish whether the acute effects in larvae correlated with those evident in mammals. Intra-haemocoel injection of potassium nitrate resulted in a significant increase in the density of circulating haemocytes and a small change in the relative proportions of haemocytes but haemocytes showed a reduced fungicidal ability. Potassium nitrate administration resulted in increased superoxide dismutase activity and in the abundance of a range of proteins associated with mitochondrial function (e.g. mitochondrial aldehyde dehydrogenase, putative mitochondrial Mn superoxide dismutase), metabolism (e.g. triosephosphate isomerase, glyceraldehyde 3 phosphate dehydrogenase) and nitrate metabolism (e.g. aliphatic nitrilase, glutathione S-transferase). A strong correlation exists between the toxicity of a range of food preservatives when tested in G. mellonella larvae and rats. In this work a correlation between the effect of potassium nitrate in larvae and mammals is shown and opens the way to the utilization of insects for studying the in vivo acute and chronic toxicity of xenobiotics.

• Keywords
• Galleria mellonella, In vivo, Potassium nitrate, Toxicity,
• MeSH
• Aldehyde Dehydrogenase metabolism   MeSH
• Aminohydrolases metabolism   MeSH
• Nitrates metabolism   pharmacology   toxicity   MeSH
• Glutathione Transferase metabolism   MeSH
• Glyceraldehyde 3-Phosphate Dehydrogenase (NADP+) metabolism   MeSH
• Hemocytes drug effects   metabolism   MeSH
• Insect Proteins metabolism   MeSH
• Catalase metabolism   MeSH
• Larva drug effects   metabolism   MeSH
• Mitochondrial Proteins metabolism   MeSH
• Moths metabolism   MeSH
• Oxidation-Reduction drug effects   MeSH
• Proteome metabolism   MeSH
• Proteomics MeSH
• Potassium Compounds pharmacology   toxicity   MeSH
• Superoxide Dismutase metabolism   MeSH
• Toxicity Tests, Acute methods   MeSH
• Triose-Phosphate Isomerase metabolism   MeSH
• Animals MeSH
• Check Tag
• Animals MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Aldehyde Dehydrogenase MeSH
• aliphatic nitrilase MeSH Browser
• Aminohydrolases MeSH
• Nitrates MeSH
• Glutathione Transferase MeSH
• Glyceraldehyde 3-Phosphate Dehydrogenase (NADP+) MeSH
• Insect Proteins MeSH
• Catalase MeSH
• Mitochondrial Proteins MeSH
• potassium nitrate MeSH Browser
• Proteome MeSH
• Potassium Compounds MeSH
• Superoxide Dismutase MeSH
• Triose-Phosphate Isomerase MeSH