Influence of 0.5 ppm nitrogen dioxide exposure of mice of macrophage congregation in the lungs

The lungs of 12 mice, half of which were exposed to continuous 0.5 ppm nitrogen dioxide for 3 weeks, were explanted in culture, and the instances of macrophage congregation were quantitated according to numbers of target cells involved, categories of congregation from three to 11 or more, numbers of macrophages participating in each category for the total cultures, and the influence of delaying explantation for 24 and 96 hr. A total of 9042 macrophages and 2140 epithelial and spindle target cells were counted in the outgrowths from 306 explants. The incidence of macrophage congregation (or numbers of target cells) was greater for the cultures from the NO2-exposed animals, both with respect to total incidences between groups (p leads to) and the 0-hr (p less than 0.001) and 24-hr (p less than 0.01) culture subgroups. In addition, the values for T3 to T6 macrophage congregation were individually and consistently greater for the exposed animal group. Postmortem interval stress at 96 hr appeared to result in large colonies, but they were reduced greatly in number. Also the incidence of macrophage congregation fell by 28% as compared to 0-hr and 24-hr subgroups.     

Comparison of effects of in vivo nitrogen dioxide exposure starting from different periods on alveolar macrophage activity, assessed by a chemiluminescence technique in Brown-Norway rats.

Nitrogen dioxide (NO2) has been extensively studied for its immune modulating effects on pulmonary cells. Alveolar macrophages (AMs) play an important role in pulmonary immunity. The Brown-Norway (BN) rat has been studied as a high-risk model of allergic diseases. In this study, BN rats were exposed to NO2 from the embryonic or weanling period (EP or WP, respectively). To evaluate the effects of NO2 exposure on pulmonary immunity, the activity levels of rat AMs were assessed as reactive oxygen species-generating capacity, measured by a chemiluminescence (CL) technique, and as cytokine-producing ability. Except for 0.2 ppm of NO2 exposure, the CL responses of AMs obtained from the WP group at 12 weeks old were suppressed significantly. Changes of the cytokine-producing levels suggest that inflammatory reactions are terminated at 12 weeks in the EP group. Correlations between the CL responses and the cytokine levels reveal that NO2 exposure may modulate the direction of AM activation. The CL technique is thought to be useful to evaluate changes in AM activity. In this study, the results suggest that, using the high-risk model of allergic diseases, NO2 exposure from the weanling period has stronger effects on AM activity.     

More than a 600-fold variation in nitrogen dioxide assimilation among 217 plant taxa

Assimilation of nitrogen dioxide in response to fumigation with ¹⁵N-labelled nitrogen dioxide was studied in 217 plant taxa. The taxa included 50 wild herbaceous plants collected from roadsides (42 genera, 15 families), 60 cultivated herbaceous plants (55 genera, 30 families) and 107 cultivated woody plants (74 genera, 45 families). Two parameters, the 'NO₂-N content', or NO₂-derived reduced nitrogen content in fumigated plant leaves (mg N g^–1 dry weight), and the 'NO₂-utilization index', or percentage of the NO₂-derived reduced nitrogen in the total reduced nitrogen, were determined. The NO₂-N content differed 657-fold between the highest ( Eucalyptus viminalis ; 6·57) and lowest ( Tillandsia ionantha and T. caput-medusae ; 0·01) values in the 217 taxa; 62-fold in a family (Theaceae) and 26-fold in a species ( Solidago altissima ). Nine species had NO₂-utilization indices greater than 10%, of which Magnolia kobus , Eucalyptus viminalis , Populus nigra , Nicotiana tabacum and Erechtites hieracifolia had NO₂-N contents > 4·9. These plants can be considered 'NO₂-philic' because in them NO₂-nitrogen has an important function(s). The Compositae and Myrtaceae had high values for both parameters, whereas the monocots and gymnosperms had low ones. These findings suggest that the metabolic pathway of NO₂-nitrogen differs among plant species. The information presented here will be useful for creating a novel vegetation technology to reduce the atmospheric concentration of nitrogen dioxide.     

Curcumin inhibits nitrogen dioxide induced oxidation of hemoglobin

Curcumin protects hemoglobin from nitrogen dioxide induced oxidation. Curcumin was also found to scavenge nitrogen dioxide in a concentration dependent way. The study also explains the ability of curcumin to protect hemoglobin from nitrite induced oxidation, where nitrogen dioxide is a key intermediate.     

Alterations of gene expression profiles induced by sulfur dioxide in rat lungs

Sulfur dioxide (SO₂) is a ubiquitous air pollutant, presents in low concentrations in urban air and in higher concentrations in working environment. Few data are available on the effects of being exposed to this pollutant on the molecular mechanism, although some biochemical changes in lipid metabolism, intermediary metabolism and oxidative stress have been detected. The present investigation aimed at analyzing the gene expression profiles of the lungs of Wistar rats short-term (20 ppm, 6 h/day, for seven days) and long-term (5 ppm, 1 h/day, for 30 days) exposed to SO₂ by Affymetrix GeneChip (RAE230A) analysis. It was found that 31 genes, containing 18 known genes and 13 novel genes, were up-regulated, and 31 genes, containing 20 known genes and 11 novel genes, were down-regulated in rats short-term exposed to SO₂ compared with control rats. While there were 176 genes, containing 82 known genes and 94 novel genes, were up-regulated, and 85 genes, containing 46 known genes and 39 novel genes, were down-regulated in rats long-term exposed to SO₂ compared with control rats. It is suggested that: (1) SO₂ exerts its effects by different mechanisms in vivo at high-dose short-term inhalation and at low-dose long-term inhalation; (2) a notable feature of the gene expression profile was the decreased expression of genes related to oxidative phosphorylation in lungs of rats short-term exposed to SO₂, which shows high-dose short-term exposed to SO₂ may cause the deterioration of mitochondrial functions; (3) discriminating genes in lungs of rats long-term exposed to SO₂ included those involved in fatty acid metabolism, immune, inflammatory, oxidative stress, oncogene, tumor suppresser and extracellular matrix. The mechanism of low-dose long-term exposed to SO₂ is more complex. __________ Translated from Journal of Shanxi University (Nat Sci Ed), 2006, 29(3): 225–236 [译自: 山西大学学报(自然科学版)]     

Alterations of gene expression profiles induced by sulfur dioxide in rat lungs

Sulfur dioxide (SO2) is a ubiquitous air pollutant presents in low concentrations in urban air and in higher concentrations in working environment.Few data are avail-able on the effects of being exposed to this pollutant on the molecular mechanism,although some biochemical changes in lipid metabolism,intermediary metabolism and oxidative stress have been detected.The present investigation aimed at analyzing the gene expression profiles of the lungs of Wistar rats short-term (20 ppm,6 h/day,for seven days) and long.term (5 ppm,1 h/day,for 30 days) exposed to SO2 by Affymetrix GeneChip (RAE230A) analysis.It was found that 31 genes,containing 18 known genes and 13 novel genes were up-regulated,and 31 genes,containing 20 known genes and 11 novel genes,were down-regulated in rats short-term exposed to SO2 compared with control rats.While there were 176 genes,containing 82 known genes and 94 novel genes were up-regulated,and 85 genes,containing 46 known genes and 39 novel genes,were down-regulated in rats long-term exposed to SO2 compared with control rats.It is suggested that:(1) SO2 exerts its effects by different mechanisms in vivo at high-dose short-term inhalation and at low-dose long-term inhalation;(2) a notable feature of the gene expression profile was the decreased expression of genes related to oxidative phosphorylation in lungs of rats short-term exposed to SO2,which shows high-dose short-term exposed to SO2 may cause the deterioration of mitochondrial functions;(3)discriminating genes in lungs of rats long-term exposed to SO2 included those involved in fatty acid metabolism,immune,inflammatory,oxidative stress,oncogene,tumor suppresser and extracellular matrix.The mechanism of low-dose long-term exposed to SO2 is more complex.     

Atmospheric nitrogen dioxide gas is a plant vitalization signal to increase plant size and the contents of cell constituents

We report the unexpected novel finding that exogenously supplied atmospheric NO2 at an ambient concentration is a plant vitalization signal to double shoot size and the contents of cell constituents. When seedlings of Nicotiana plumbaginifolia were grown for 10 wk under natural light and irrigation with 10 mm KNO3 in air containing (+NO2 plants) or not containing (-NO2 plants) 15NO2 (150 +/- 50 ppb), shoot biomass, total leaf area, and contents per shoot of carbon (C), nitrogen (N), sulphur (S), phosphorus (P), potassium (K), calcium (Ca), magnesium (Mg), free amino acids and crude proteins were all approximately 2 times greater in +NO2 plants than in -NO2 plants. In mass spectrometric analysis of the 15N/14N ratio, it was found that NO2-derived N (NO2-N) comprised < 3% of total plant N, indicating that the contribution of NO2-N to total N was very minor. It thus seems very likely that the primary role of NO2 is as a multifunctional signal to stimulate plant growth, nutrient uptake and metabolism.     

Molecular mechanisms of nitrogen dioxide induced epithelial injury in the lung

The lung can be exposed to a variety of reactive nitrogen intermediates through the inhalation of environmental oxidants and those produced during inflammation. Reactive nitrogen species (RNS) include, nitrogen dioxide (·NO₂) and peroxynitrite (ONOO^–). Classically known as a major component of both indoor and outdoor air pollution, ·NO₂ is a toxic free radical gas. ·NO₂ can also be formed during inflammation by the decomposition of ONOO^– or through peroxidase-catalyzed reactions. Due to their reactive nature, RNS may play an important role in disease pathology. Depending on the dose and the duration of administration, ·NO₂ has been documented to cause pulmonary injury in both animal and human studies. Injury to the lung epithelial cells following exposure to ·NO₂ is characterized by airway denudation followed by compensatory proliferation. The persistent injury and repair process may contribute to airway remodeling, including the development of fibrosis. To better understand the signaling pathways involved in epithelial cell death by ·NO₂ or other RNS, we routinely expose cells in culture to continuous gas-phase ·NO₂. Studies using the ·NO₂ exposure system revealed that lung epithelial cell death occurs in a density dependent manner. In wound healing experiments, ·NO₂ induced cell death is limited to cells localized in the leading edge of the wound. Importantly, ·NO₂-induced death does not appear to be dependent on oxidative stress per se. Potential cell signaling mechanisms will be discussed, which include the mitogen activated protein kinase, c-Jun N-terminal Kinase and the Fas/Fas ligand pathways. During periods of epithelial loss and regeneration that occur in diseases such as asthma or during lung development, epithelial cells in the lung may be uniquely susceptible to death. Understanding the molecular mechanisms of epithelial cell death associated with the exposure to ·NO₂ will be important in designing therapeutics aimed at protecting the lung from persistent injury and repair.     

Photosynthetic photon flux effects on bean response to nitrogen dioxide

Phaseolus vulgaris L. cv. Kinghorn Wax seedlings, supplied with nutrient solution containing either 0 or 5 mM nitrate as sole N source, were exposed to 0.25 μl/l NO₂ for 6 hr each day for 10 days at continuous photosynthetic photon flux (PPF) of 100, 300, 500 or 700 μmol m⁻² sec⁻¹. There was a significant interaction of PPF and nitrate. Shoot and root dry weights increased with increasing PPFs only when nitrate was supplied. The main effects of NO₂ on plant growth were significant; none of the interactions involving NO₂ were significant. Exposure to NO₂ decreased shoot and root dry weight in both the presence and absence of nutrient N and at all PPF levels. All interactions were significant for in vitro leaf nitrate reductase activity (NRA), which increased markedly at PPFs above 100 μmol m⁻² sec⁻¹ when nitrate was supplied. Treatment with NO₂ strongly inhibited enzyme activity in the presence of nitrate, particularly at the 300 μmol m⁻² sec⁻¹ PPF level. These experiments demonstrated that PPF level does not modify the effect of NO₂ on growth but does have a major effect on NRA and on NO₂ effects on NRA in the presence of nutrient nitrate.     

Enhanced ozone exposure of European beech (Fagus sylvatica) stimulates nitrogen mobilization from leaf litter and nitrogen accumulation in the soil

Abstract

In a lysimeter study with young beech trees, the effects of elevated ozone concentration on the decomposition and fate of nitrogen in ¹⁵N‐labeled leaf litter were analyzed after one growing season. Nitrogen in the litter was dominated by a relatively inert, residual fraction, but easily decomposable nitrogen was present in substantial amounts. Nitrogen loss was significantly higher at twice‐ambient ozone which was largely attributed to an enhanced mobilization of residual nitrogen. Enhanced mobilization of nitrogen from litter at twice‐ambient ozone exposure resulted in additional ¹⁵N incorporation into the soil down to 30 cm depth. Only 0.41–0.62% of the nitrogen in the litter was incorporated into plant material at both ozone concentrations. Twice‐ambient ozone exposure changed the distribution of the nitrogen taken up from litter inside the beech trees in favor of the shoot, where it may have been used in biosynthetic processes required for defense reactions.     

Effects of carbon dioxide exposure on early brain development in rats

The developing brain is vulnerable to environmental factors. We investigated the effects of air that contained 0.05, 0.1 and 0.3% CO₂ on the hippocampus, prefrontal cortex (PFC) and amygdala. We focused on the circuitry involved in the neurobiology of anxiety, spatial learning, memory, and on insulin-like growth factor-1 (IGF-1), which is known to play a role in early brain development in rats. Spatial learning and memory were impaired by exposure to 0.3% CO₂ air, while exposure to 0.1 and 0.3% CO₂ air elevated blood corticosterone levels, intensified anxiety behavior, increased superoxide dismutase (SOD) enzyme activity and MDA levels in hippocampus and PFC; glutathione peroxidase (GPx) enzyme activity decreased in the PFC with no associated change in the hippocampus. IGF-1 levels were decreased in the blood, PFC and hippocampus by exposure to both 0.1 and 0.3% CO₂. In addition, apoptosis was increased, while cell numbers were decreased in the CA1 regions of hippocampus and PFC after 0.3% CO₂ air exposure in adolescent rats. A positive correlation was found between the blood IGF-1 level and apoptosis in the PFC. We found that chronic exposure to 0.3% CO₂ air decreased IGF-1 levels in the serum, hippocampus and PFC, and increased oxidative stress. These findings were associated with increased anxiety behavior, and impaired memory and learning.     

Spin trapping of nitrogen dioxide and of radicals generated from nitrous acid

Spin trapping of nitrogen dioxide radical by several nitrones has been studied. The reaction results in the formation of persistent acyl nitroxides, after the oxidation of the intermediate spin adducts having an -ONO group on C-2 atom. The intermediate is effectively detected when DEPMPO is used as the spin trap. The reaction between PBN or 5,7-di-tert-butyl-3,3-dimethyl indoline N-oxide with nitrous acid gives the corresponding acyl nitroxide only when oxygen is present in the reaction milieu.

On the other hand, nitroso spin traps do not trap ^⋅NO₂ confirming that the unpaired electron of nitrogen dioxide is localized on the oxygen atom.     

The interaction between elevated carbon dioxide and nitrogen nutrition: the physiological and molecular background

AGPase, ADP glucose pyrophosphorylase
GS, glutamine synthetase
GOGAT, glutamate : oxoglutarate amino transferase
NADP-ICDH, NADP-dependent isocitrate dehydrogenase
NR, nitrate reductase
OPPP, oxidative pentose phosphate pathway
3PGA, glycerate-3-phosphate
PEPCase, phosphoenolpyruvate carboxylase
Rubisco, ribulose-1,5-bisphosphate carboxylase/oxygenase
SPS, sucrose phosphate-synthase

This review first summarizes the numerous studies that have described the interaction between the nitrogen supply and the response of photosynthesis, metabolism and growth to elevated [CO₂]. The initial stimulation of photosynthesis in elevated [CO₂] is often followed by a decline of photosynthesis, that is typically accompanied by a decrease of ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco), an accumulation of carbohydrate especially starch, and a decrease of the nitrogen concentration in the plant. These changes are particularly marked when the nitrogen supply is low, whereas when the nitrogen supply is adequate there is no acclimation of photosynthesis, no major decrease in the internal concentration of nitrogen or the levels of nitrogen metabolites, and growth is stimulated markedly. Second, emerging evidence is discussed that signals derived from nitrate and nitrogen metabolites such as glutamine act to regulate the expression of genes involved in nitrate and ammonium uptake and assimilation, organic acid synthesis and starch accumulation, to modulate the sugar-mediated repression of the expression of genes involved in photosynthesis, and to modulate whole plant events including shoot–root allocation, root architecture and flowering. Third, increased rates of growth in elevated [CO₂] will require higher rates of inorganic nitrogen uptake and assimilation. Recent evidence is discussed that an increased supply of sugars can increase the rates of nitrate and ammonium uptake and assimilation, the synthesis of organic acid acceptors, and the synthesis of amino acids. Fourth, interpretation of experiments in elevated [CO₂] requires that the nitrogen status of the plants is monitored. The suitability of different criteria to assess the plant nitrogen status is critically discussed. Finally the review returns to experiments with elevated [CO₂] and discusses the following topics: is, and if so how, are nitrate and ammonium uptake and metabolism stimulated in elevated [CO₂], and does the result depend on the nitrogen supply? Is acclimation of photosynthesis the result of sugar-mediated repression of gene expression, end-product feedback of photosynthesis, nitrogen-induced senescence, or ontogenetic drift? Is the accumulation of starch a passive response to increased carbohydrate formation, or is it triggered by changes in the nutrient status? How do changes in sugar production and inorganic nitrogen assimilation interact in different conditions and at different stages of the life history to determine the response of whole plant growth and allocation to elevated [CO₂]?