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Exercise-induced sweat nitrogen excretion: evaluation of a regional collection method using gauze pads.

The exercise-induced sweat nitrogen excretion was investigated during a 45-minute run at moderate intensity on a treadmill. Sweat was collected with a regional collection technique using gauze pads and compared with the whole-body wash-down (WBW) method. In the regional collection, sweat was sampled from the upper back (UB), lower back (LB), abdomen (AB), and thigh (TH). Additionally, the relation of sweat urea, ammonia, and amino acids was investigated with the regional collection method during a second 45-minute run. Independent of the sweat collection method, a significant and positive correlation was found between sweat rate and the excretion rate of the largest nitrogen fraction urea, suggesting that the sweating response to exercise might be one of the most important factors determining absolute sweat nitrogen losses. The urea nitrogen excretion was nearly 140 mg.h-1 in the second run, representing the largest nitrogen fraction. Ammonia nitrogen and amino acid-derived nitrogen rate were approximately 30 mg.h-1 and 10 mg.h-1, respectively. The comparison of the sampling methods during the first run revealed that the urea nitrogen rate was significantly higher, but the ammonia nitrogen rate significantly lower in the WBW. After summing urea and ammonia nitrogen, no significant difference between the methods was observed anymore, except for UB. It is concluded that the regional collection method using gauze pads is a valuable approach to measure exercise-induced sweat nitrogen losses during moderate running exercise.

Adult↗

Spatial coupling of nitrogen inputs and losses in the ocean.

Nitrogen fixation is crucial for maintaining biological productivity in the oceans, because it replaces the biologically available nitrogen that is lost through denitrification. But, owing to its temporal and spatial variability, the global distribution of marine nitrogen fixation is difficult to determine from direct shipboard measurements. This uncertainty limits our understanding of the factors that influence nitrogen fixation, which may include iron, nitrogen-to-phosphorus ratios, and physical conditions such as temperature. Here we determine nitrogen fixation rates in the world's oceans through their impact on nitrate and phosphate concentrations in surface waters, using an ocean circulation model. Our results indicate that nitrogen fixation rates are highest in the Pacific Ocean, where water column denitrification rates are high but the rate of atmospheric iron deposition is low. We conclude that oceanic nitrogen fixation is closely tied to the generation of nitrogen-deficient waters in denitrification zones, supporting the view that nitrogen fixation stabilizes the oceanic inventory of fixed nitrogen over time.

Biomass↗

Sensing nitrogen limitation in Corynebacterium glutamicum: the role of glnK and glnD.

A novel nitrogen control system regulating the transcription of genes expressed in response to nitrogen starvation in Corynebacterium glutamicum was identified by us recently. In this communication, we also show that the nitrogen regulation cascade in C. glutamicum functions by a new mechanism, although components highly similar to sensor and signal transmitter proteins of Escherichia coli are used, namely uridylyltransferase and a PII-type GlnK protein. The genes encoding these key components of the nitrogen regulation cascade, glnD and glnK, are organized in an operon together with amtB, which codes for an ammonium permease. Using a combination of site-directed mutagenesis, RNA hybridization experiments, reporter gene assays, transport measurements and non-denaturing gel electrophoresis followed by immunodetection, we showed that GlnK is essential for nitrogen control and that signal transduction is transmitted by uridylylation of this protein. As a consequence of the latter, a glnD deletion strain lacking uridylyltransferase is impaired in its response to nitrogen shortage. The glnD mutant revealed a decreased growth rate in the presence of limiting amounts of ammonium or urea; additionally, changes in its protein profile were observed, as shown by in vivo labelling and two-dimensional PAGE. In contrast to E. coli, expression of glnD is upregulated upon nitrogen limitation in C. glutamicum. This indicates that the glnD gene product is probably not the primary sensor of nitrogen status in C. glutamicum as shown for enterobacteria. In accordance with this hypothesis, we found a deregulated nitrogen control as a result of the overexpression of glnD. Furthermore, quantification of cytoplasmic amino acid pools excluded the possibility that a fall in glutamine concentration is perceived as the signal for nitrogen starvation by C. glutamicum, as is found in enterobacteria. Direct measurements of the intracellular ammonium pool indicated that the concentration of this compound might indicate the cellular nitrogen status. Deduced from glnK and glnD expression patterns and the genetic organization of these genes, this regulatory mechanism is also present in Corynebacterium diphtheriae, the causative agent of diphtheria.

Bacterial Proteins↗

Physiological role of the GlnK signal transduction protein of Escherichia coli: survival of nitrogen starvation.

Escherichia coli contains two PII-like signal trans-duction proteins, PII and GlnK, involved in nitrogen assimilation. We examined the roles of PII and GlnK in controlling expression of glnALG, glnK and nac during the transition from growth on ammonia to nitrogen starvation and vice versa. The PII protein exclusively controlled glnALG expression in cells adapted to growth on ammonia, but was unable to limit nac and glnK expression under conditions of nitrogen starvation. Conversely, GlnK was unable to limit glnALG expression in cells adapted to growth on ammonia, but was required to limit expression of the glnK and nac promoters during nitrogen starvation. In the absence of GlnK, very high expression of the glnK and nac promoters occurred in nitrogen-starved cells, and the cells did not reduce glnK and nac expression when given ammonia. Thus, one specific role of GlnK is to regulate the expression of Ntr genes during nitrogen starvation. GlnK also had a dramatic effect on the ability of cells to survive nitrogen starvation and resume rapid growth when fed ammonia. After being nitrogen starved for as little as 10 h, cells lacking GlnK were unable to resume rapid growth when given ammonia. In contrast, wild-type cells that were starved immediately resumed rapid growth when fed ammonia. Cells lacking GlnK also showed faster loss of viability during extended nitrogen starvation relative to wild-type cells. This complex phenotype resulted partly from the requirement for GlnK to regulate nac expression; deletion of nac restored wild-type growth rates after ammonia starvation and refeeding to cells lacking GlnK, but did not improve viability during nitrogen starvation. The specific roles of GlnK during nitrogen starvation were not the result of a distinct function of the protein, as expression of PII from the glnK promoter in cells lacking GlnK restored the wild-type phenotypes.

Ammonia↗

High protein enteral feedings: a means of achieving positive nitrogen balance in head injured patients.

In an attempt to improve early enteral nitrogen replacement, nitrogen status was compared in two groups of head injured patients receiving enteral regimens of 38 to 51 kcal/kg/day with different protein concentrations. Eleven control patients received 1.5 g protein/kg/day and 10 study patients received 2.2 g protein/kg/day. Daily nitrogen excretion, corrected nitrogen balance, blood urea nitrogen changes, and enteral formula tolerance were compared between groups over a 10-day period. Those receiving 2.2 g protein/kg/day had significantly higher daily and cumulative nitrogen balances despite their higher nitrogen excretion levels. Over 10 days, the study group retained 9.2 g nitrogen. By comparison, the control group sustained a cumulative loss of 31.2 g nitrogen over 10 days, despite a mean intake of 109 g protein/day. In both groups, full strength, full rate feedings were not possible until day 10 postinjury. These data indicate that once enteral formulas are tolerated high nitrogen regimens are required to achieve positive nitrogen balance in acute severe head injury patients.

Adult↗

Effect of nitrogen intake on urea appearance in patients receiving total parenteral nutrition and hemodialysis.

Hemodialysis results in significant amino acid and protein losses and increases the patient's need for, and tolerance to, standard doses of protein. Since urea accumulation increases proportionately with increasing doses of protein in patients with normal renal function, urea accumulation may result when protein intake is increased to offset losses occurring in the dialysate. As a consequence, an increased requirement for dialysis may occur that might be poorly tolerated by the critically ill patient. This study was designed to determine the relationship between nitrogen intake and urea appearance in five patients requiring hemodialysis and total parenteral nutrition. Daily caloric and nitrogen intakes were determined. Urea appearance was calculated from measures of urine urea nitrogen excretion and daily body urea accumulation. Results of 108 measurements in treatment courses ranging from 23-79 days found that the average caloric intake (1984 +/- 55 calories/d) and nitrogen intake (11.0 +/- 0.4 g/d) resulted in a positive nitrogen balance (0.8 +/- 0.4 g/d) and a urea appearance rate of 9.4 +/- 0.8 g/d. Nitrogen intake correlated both with urea appearance (r = 0.59, p less than 0.001) and nitrogen balance (r = 0.49, p less than 0.001). Positive nitrogen balance was associated with improvements in measures of total iron binding capacity (p less than 0.05). Nitrogen intake directly relates to urea appearance, and positive nitrogen balance can be achieved without increasing dialysis requirements. In this group of patients, 28.3 calories per kg ideal body weight and 0.8 g of protein per kg ideal body weight were required to achieve nitrogen equilibrium.

Adult↗

Nitrogen stress causes unpredictable enrichments of 15N in two nectar-feeding bat species.

We estimated the effect of nitrogen stress on the nitrogen isotope enrichments in wing membrane and blood of two nectar-feeding bats (Glossophaga soricina and Leptonycteris curasoae) by offering a nitrogen-poor diet with a high delta(15)N and delta(13)C. Before the experiment, bats were sustained on a normal diet with a low delta(15)N and delta(13)C. Under this first food regime, the fractionation of nitrogen isotopes averaged 3.1 per thousand delta(15)N for blood and 4.4 per thousand delta(15)N for wing membrane, which was almost twice as high as the corresponding fractionation of carbon isotopes. After switching to the nitrogen-poor diet, the enrichment of heavy isotopes increased for both elements in all tissues under study. The recently published estimates of half-life of carbon isotopes indicated a low turnover rate of carbon in wing membrane and blood and an almost constant half-life over varying losses of body mass. The estimates of half-life of nitrogen were two to six times higher than those of carbon. We argue that this discrepancy was caused by the mixing of nitrogen isotopes from internal and external sources. The mixing effect was probably negligible for carbon as the amount of ingested carbon outweighed the amount of mobilized carbon from internal sources. A correlation between the estimated turnover rates of nitrogen and losses of body masses was probably obscured by the additional fractionation of nitrogen isotopes in catabolic animals. We conclude that the interpretation of nitrogen isotope data of free-ranging animals is difficult when the animal's diet is changing to a critical nitrogen content.

Analysis of Variance↗

[Effect of fasting on the concentration of amide nitrogen in the blood plasma of sheep].

The experiments with sheep starving 24, 48, 72 and 96 hrs after the last feeding showed that on the second day of starving the concentration of the total amide nitrogen in plasma increased significantly (P less than 0.01) both at a lower (7.6 g of nitrogen per day) and at a higher (24 g of nitrogen per day) nitrogen uptake before the beginning of starvation. The concentration of free amide nitrogen, unbound to plasma proteins, increased only at the lower nitrogen intake before starving. At the studied stages of fasting no significant differences in the levels of total and free amide nitrogen in plasma having a relation to nitrogen intake before starvation were found. With the increased urea level in plasma a parallel increase of the total amide nitrogen was observed only in the plasma of sheep fed before starvation the diet with a higher nitrogen content. The results confirm that a short-term starvation is one of the factors which can influence the relatively stable concentration of amide nitrogen in plasma.

Animal Feed↗

The effect of energy and nitrogen intake upon urea production in children with uremia and undernutrition.

Children with severe uremia who had anorexia were observed in a clinical study center where dietary energy and nitrogen intake could be compared with urea nitrogen production (UNPr). The children received a supplement of dextrose and amino acids at night, ate a self-selected diet and were encouraged to use carbohydrate supplements. Energy intake varied from 22 to 110 kcal/kg/day and nitrogen intake from 105 to 323 mg/kg/day. UNPr was reciprocally related to energy intake. Nitrogen intake minus UNPr, an index of nitrogen balance, was positively related to energy intake. UNPr was not related to nitrogen intake. Nitrogen intake (NI) and NI-UNPr were correlated and the slope of the regression was 1.15. We inferred from the data that low energy intakes (less than 60 kcal/kg/day) were associated with catabolic losses of body protein. Intakes above that level were associated with a low and stable rate of UNPr. The level of energy and nitrogen intake within the range observed limited the rate of nitrogen retention. Once maintenance requirements for energy and nitrogen were satisfied, the efficiency with which nitrogen was used for net protein synthesis was very high.

Adolescent↗

Nitrogen requirements in severely injured patients.

The study was designed to evaluate nitrogen needs in severely injured patients during the first week after trauma. Thirty-nine patients aged from 18 to 65 years with a burn or fractures of more than two long bones were studied. Energy requirements were given parenterally as fat and glucose in isocaloric amounts. The patients were randomized into five groups receiving different amounts of nitrogen from zero to 0.3 g kg body-weight-1 24 h-1. Daily and cumulative nitrogen balance, urinary 3-methylhistidine excretion and nitrogen retention were calculated on days 2-8 after trauma. With no nitrogen, the mean(s.e.m.) daily nitrogen balance after the trauma was -13.8(0.5) gN. The balance improved markedly in groups with a nitrogen intake of up to 0.2 g kg body-weight-1 (P less than 0.001) compared with the no-nitrogen group. The 3-methylhistidine excretion increased because of the trauma in all groups with no statistically significant difference between the groups. Nitrogen retention decreased with increase in nitrogen supply and with time after injury. It is suggested that a nitrogen supply of 0.20 kg bodyweight-1 24 h-1 is optimal for severely injured patients during the first week after trauma.

Adolescent↗

Ecological and toxicological effects of inorganic nitrogen pollution in aquatic ecosystems: A global assessment.

We provide a global assessment, with detailed multi-scale data, of the ecological and toxicological effects generated by inorganic nitrogen pollution in aquatic ecosystems. Our synthesis of the published scientific literature shows three major environmental problems: (1) it can increase the concentration of hydrogen ions in freshwater ecosystems without much acid-neutralizing capacity, resulting in acidification of those systems; (2) it can stimulate or enhance the development, maintenance and proliferation of primary producers, resulting in eutrophication of aquatic ecosystems; (3) it can reach toxic levels that impair the ability of aquatic animals to survive, grow and reproduce. Inorganic nitrogen pollution of ground and surface waters can also induce adverse effects on human health and economy. Because reductions in SO2 emissions have reduced the atmospheric deposition of H2SO4 across large portions of North America and Europe, while emissions of NOx have gone unchecked, HNO3 is now playing an increasing role in the acidification of freshwater ecosystems. This acidification process has caused several adverse effects on primary and secondary producers, with significant biotic impoverishments, particularly concerning invertebrates and fishes, in many atmospherically acidified lakes and streams. The cultural eutrophication of freshwater, estuarine, and coastal marine ecosystems can cause ecological and toxicological effects that are either directly or indirectly related to the proliferation of primary producers. Extensive kills of both invertebrates and fishes are probably the most dramatic manifestation of hypoxia (or anoxia) in eutrophic and hypereutrophic aquatic ecosystems with low water turnover rates. The decline in dissolved oxygen concentrations can also promote the formation of reduced compounds, such as hydrogen sulphide, resulting in higher adverse (toxic) effects on aquatic animals. Additionally, the occurrence of toxic algae can significantly contribute to the extensive kills of aquatic animals. Cyanobacteria, dinoflagellates and diatoms appear to be major responsible that may be stimulated by inorganic nitrogen pollution. Among the different inorganic nitrogenous compounds (NH4+, NH3, NO2-, HNO2NO3-) that aquatic animals can take up directly from the ambient water, unionized ammonia is the most toxic, while ammonium and nitrate ions are the least toxic. In general, seawater animals seem to be more tolerant to the toxicity of inorganic nitrogenous compounds than freshwater animals, probably because of the ameliorating effect of water salinity (sodium, chloride, calcium and other ions) on the tolerance of aquatic animals. Ingested nitrites and nitrates from polluted drinking waters can induce methemoglobinemia in humans, particularly in young infants, by blocking the oxygen-carrying capacity of hemoglobin. Ingested nitrites and nitrates also have a potential role in developing cancers of the digestive tract through their contribution to the formation of nitrosamines. In addition, some scientific evidences suggest that ingested nitrites and nitrates might result in mutagenicity, teratogenicity and birth defects, contribute to the risks of non-Hodgkin's lymphoma and bladder and ovarian cancers, play a role in the etiology of insulin-dependent diabetes mellitus and in the development of thyroid hypertrophy, or cause spontaneous abortions and respiratory tract infections. Indirect health hazards can occur as a consequence of algal toxins, causing nausea, vomiting, diarrhoea, pneumonia, gastroenteritis, hepatoenteritis, muscular cramps, and several poisoning syndromes (paralytic shellfish poisoning, neurotoxic shellfish poisoning, amnesic shellfish poisoning). Other indirect health hazards can also come from the potential relationship between inorganic nitrogen pollution and human infectious diseases (malaria, cholera). Human sickness and death, extensive kills of aquatic animals, and other negative effects, can have elevated costs on human economy, with the recreation and tourism industry suffering the most important economic impacts, at least locally. It is concluded that levels of total nitrogen lower than 0.5-1.0 mg TN/L could prevent aquatic ecosystems (excluding those ecosystems with naturally high N levels) from developing acidification and eutrophication, at least by inorganic nitrogen pollution. Those relatively low TN levels could also protect aquatic animals against the toxicity of inorganic nitrogenous compounds since, in the absence of eutrophication, surface waters usually present relatively high concentrations of dissolved oxygen, most inorganic reactive nitrogen being in the form of nitrate. Additionally, human health and economy would be safer from the adverse effects of inorganic nitrogen pollution.

Acid Rain↗

Nitrogen mass balance across pilot-scale algae and duckweed-based wastewater stabilisation ponds.

Nitrogen removal processes and nitrogen mass balances in algae-based ponds (ABPs) and duckweed (Lemna gibba)-based ponds (DBPs) were assessed during periods of 4 months, each under different operational conditions. During periods 1 and 2, the effect of cold and warm temperature was studied. During periods 2 and 3, the effect of low- and high-system organic loading (OL) was studied in warm seasons operation. The pilot-scale systems consisted of four similar ponds in series fed with domestic sewage with hydraulic retention time of 7 days in each pond. Overall nitrogen removal was higher during warm temperature in both ABPs and DBPs, but similar during periods 2 and 3. Nitrogen removal in DBPs was lower than in ABPs by 20%, 12% and 8% during cold temperature, warm temperature and high-OL periods, respectively. Depending on temperature and OL rate, ABPs showed higher nitrogen removal via sedimentation (46-245% higher) compared to DBPs. Also, ABPs also showed higher nitrogen removal via denitrification (7-37% higher) compared to DBPs. Ammonia volatilisation in both systems did not exceed 1.1% of influent total nitrogen during the entire experimental period. N uptake by duckweed corresponds to 30% of the influent nitrogen during warm/low OL period and decreased to 10% and 19% during the cold and warm/high OL period, respectively. Predictive models for nitrogen removal presented a good reflection of nitrogen fluxes on overall nitrogen balance under the prevailing experimental conditions.

Araceae↗

Effects of long-term growth hormone (GH) and triiodothyronine (T3) administration on functional hepatic nitrogen clearance in normal man.

BACKGROUND/AIMS: A decline in urea excretion is seen following long-term growth hormone administration, reflecting overall protein anabolism. Conversely, hyperthyroidism is characterized by increased urea synthesis and negative nitrogen metabolism. These seemingly opposite effects are presumed to reflect different actions on peripheral protein metabolism. The extent to which these hormonal systems have different direct effects on hepatic urea genesis has not been fully characterized. METHODS: We measured urea nitrogen synthesis rates and blood alanine levels concomitantly before, during, and after a 4-h constant intravenous infusion of alanine (2 mmol.kg bw-1.h-1). Urea nitrogen synthesis rate was estimated hourly as urinary excretion corrected for gut hydrolysis and accumulation in body water. The slope of the linear relationship between urea nitrogen synthesis rate and alanine concentration represents the liver function as to conversion of amino-N, and is denoted the functional hepatic nitrogen clearance. Eight normal male subjects (age 21-27 years; body mass index 22.4-27.0 kg/m2) were randomly studied four times: 1) after 10 days of subcutaneous saline injections, 2) after 10 days of subcutaneous growth hormone injections (0.1 IU/kg per day), 3) after 10 days of triiodothyronine administration (40 micrograms on even dates, 20 micrograms on uneven dates) and 4) after 10 days given 2)+3). All injections were given at 20 00 h. RESULTS: Growth hormone decreased functional hepatic nitrogen clearance (l/h) by 30% (from 33.8 +/- 3.2 l/h (control) to 23.8 +/- 1.5 l/h (10 days growth hormone) (mean +/- SE) (ANOVA; p < 0.01)). Triiodothyronine did not change functional hepatic nitrogen clearance (36.7 +/- 3.2 l/h), but triiodothyronine given together with growth hormone abolished the effect of growth hormone functional hepatic nitrogen clearance (38.8 +/- 4.8 l/h). CONCLUSIONS: The results show that long-term growth hormone administration acts on liver by decreasing functional hepatic nitrogen clearance, thereby retaining amino-N in the body. Triiodothyronine has no effect on functional hepatic nitrogen clearance, but given together with growth hormone, it abolishes the effect of growth hormone on functional hepatic nitrogen clearance. A possible mechanism is the known effect of thyroid hormones in reducing the bioavailability of insulin-like growth factor-I. Thus, the effects of growth hormone and triiodothyronine on amino-N homeostasis are interdependent and to some extent exerted via interplay in their regulation of liver function as to amino-N conversion.

Adult↗

Effects of geographical location and land use on atmospheric deposition of nitrogen in the State of Connecticut.

A network of eight monitoring stations was established to study the atmospheric nitrogen concentration and deposition in the State of Connecticut. The stations were classified into urban, rural, coastal and inland categories to represent the geographical location and land use characteristics surrounding the monitoring sites. Nitrogen species including nitrate, ammonium, nitric acid vapor and organic nitrogen in the air and precipitation were collected, analyzed and used to infer nitrogen concentrations and dry and wet deposition flux densities for the sampling period from 1997 through 1999, with independently collected meteorological data. Statistical analyses were conducted to evaluate the spatial variations of atmospheric concentration and deposition fluxes of total nitrogen in Connecticut. A slightly higher atmospheric concentration of total nitrogen was observed along the Connecticut coastline of Long Island Sound compared to inland areas, while the differences of nitrogen deposition fluxes were insignificant between coastal and inland sites. The land use characteristics surrounding the monitoring sites had profound effects on the atmospheric nitrogen concentration and dry deposition flux. The ambient nitrogen concentration over the four urban sites was averaged 38.9% higher than that over the rural sites, resulting a 58.0% higher dry deposition flux in these sites compared to their rural counterparts. The local industrial activities and traffic emissions of nitrogen at urban areas had significant effects on the spatial distribution of atmospheric nitrogen concentration and dry deposition flux in the State. Wet and total deposition fluxes appeared to be invariant between the monitoring sites, except for high flux densities measured at Old Greenwich, a monitoring station near to and downwind of the New York and New Jersey industrial complexes.

Agriculture↗

A yeast glutamine tRNA signals nitrogen status for regulation of dimorphic growth and sporulation.

Dimorphic growth of the budding yeast Saccharomyces cerevisiae is regulated by the quality of the nitrogen supply. On a preferred nitrogen source diploid cells grow as ellipsoidal cells by using a bipolar pattern of budding, whereas on a poor nitrogen source a unipolar pattern of budding is adopted, resulting in extended pseudohyphal chains of filamentous cells. Here we report that the quality of the nitrogen source is signaled by the glutamine tRNA isoform with a 5'-CUG anticodon (tRNACUG). Mutations that alter this tRNA impair assessment of the nitrogen supply without measurably affecting protein synthesis, so that mutant cells display pseudohyphal growth even on a preferred nitrogen source. The nitrogen status for other nitrogen-responsive processes such as catabolic gene expression and sporulation also is signaled by this tRNA: mutant cells inappropriately induce the nitrogen-repressed gene CAR1 and undergo precocious sporulation in nitrogen-rich media. Therefore, in addition to its role in mRNA translation, this tRNA also transduces nitrogen signals that regulate development.

Base Sequence↗

Toxicity of ozone and nitrogen dioxide to alveolar macrophages: comparative study revealing differences in their mechanism of toxic action.

The toxicity of ozone and nitrogen dioxide is generally ascribed to their oxidative potential. In this study their toxic mechanism of action was compared using an intact cell model. Rat alveolar macrophages were exposed by means of gas diffusion through a Teflon film. In this in vitro system, ozone appeared to be 10 times more toxic than nitrogen dioxide. alpha-Tocopherol protected equally well against ozone and nitrogen dioxide. It was demonstrated that alpha-tocopherol provided its protection by its action as a radical scavenger and not by its stabilizing structural membrane effect, as (1) concentrations of alpha-tocopherol that already provided optimal protection against ozone and nitrogen dioxide did not influence the membrane fluidity of alveolar macrophages and (2) neither one of the structural alpha-tocopherol analogs tested (phytol and the methyl ether of alpha-tocopherol) could provide a protection against ozone or nitrogen dioxide comparable to the one provided by alpha-tocopherol. It was concluded that reactive intermediates scavenged by alpha-tocopherol are important in the toxic mechanism of both ozone and nitrogen dioxide induced cell damage. However, further results presented strongly confirmed that the kind of radicals and/or reactive intermediates, and thus the toxic reaction mechanism involved, must be different in ozone- and nitrogen dioxide-induced cell damage. This was concluded from the observations that showed that (1) vitamin C provided significantly better protection against nitrogen dioxide than against an equally toxic dose of ozone, (2) glutathione depletion affected the cellular sensitivity toward ozone to a significantly greater extent than the sensitivity towards nitrogen dioxide, and (3) the scavenging action of alpha-tocopherol was accompanied by a significantly greater reduction in its cellular level during nitrogen dioxide exposure than during exposure to ozone. One of the possibilities compatible with the results presented in this study might be that lipid (peroxyl) free radicals formed in a radical-mediated peroxidative pathway, resulting in a substantial breakdown of cellular alpha-tocopherol, are involved in nitrogen dioxide-induced cell damage, and that lipid ozonides, scavenged by alpha-tocopherol as well, are involved in ozone-induced cell damage.

Animals↗

Onset of and recovery from nitrogen stress during reproductive growth of soybean.

Photosynthetic rates and allocation of dry matter, nitrogen, and nonstructural carbohydrates were determined during onset of and recovery from a nitrogen stress for reproductive soybean (Glycine max [L.] Merrill cv Ransom) plants. Until the beginning of seed fill, non-nodulated plants were grown in flowing solution culture with 1.0 mM NO3- in a complete nutrient solution. One set of plants then was transferred to minus-nitrogen solution for 24 d of seed fill; a second set was transferred to a minus-nitrogen solution for 14 d followed by return to the complete solution with 1.0 mM NO3- for the remaining 10 d of seed fill; and a third set was continued on the complete solution. Net CO2 exchange rates of individual leaves, which remained nearly constant during seed fill for nonstressed plants, declined at an accelerated rate during onset of nitrogen stress as the specific content of reduced nitrogen in the leaves was decreased by remobilization of nitrogen to support pod growth. The rate of nitrogen remobilization out of leaves initially was relatively greater than the decrease in photosynthetic rate. While rate of pod growth declined in response to the developing nitrogen stress, photosynthetic assimilation of carbon exceeded reproductive demand and nonstructural carbohydrates accumulated within tissues. Following resupply of exogenous NO3-, specific rate of NO3- uptake by roots was enhanced relative to nonstressed plants. While there was little increase in content of reduced nitrogen in leaves, net remobilization of nitrogen out of leaves ceased, and the decline in photosynthetic rate stabilized at about 51% of that for nonstressed plants. This level of photosynthesis, combined with the availability of elevated pools of carbohydrates accumulated during stress, was sufficient to support the increases in both the specific rates of NO3- uptake and the rate of pod growth during recovery.

Carbohydrate Metabolism↗

Consumption of retrograded (RS3) but not uncooked (RS2) resistant starch shifts nitrogen excretion from urine to feces in cannulated piglets.

To study the effect of resistant starch (RS) on the route of nitrogen excretion, we fed three groups of six cannulated piglets each a diet containing either uncooked resistant starch (RS2 ), retrograded resistant starch (RS3 ) or glucose. The use of piglets with a cannula at the end of the ileum allowed measurement of the amount of nitrogen that entered the colon. Ileal digesta, urine and feces were collected quantitatively and weighed, and dry matter, starch and nitrogen content were determined. We hypothesized that RS2 would lower colonic absorption of nitrogen when compared with RS3 , because RS2 may be more fermentable than RS3 , thus trapping more nitrogen in bacteria. The piglets fed RS3 had a significantly higher production of ileal digesta and feces than the piglets fed glucose or RS2 . In the piglets fed RS2 , 44% of the amount of RS fed was recovered in the ileal digesta; in the piglets fed RS3 , 71% was recovered. Thus, more fermentable material entered the colon in the RS3 -fed piglets than in the RS2 -fed piglets. Virtually no starch was recovered in the feces of any dietary group. Replacement of glucose by either RS2 or RS3 did not affect nitrogen retention but increased fecal nitrogen excretion. Compared with glucose, RS3 but not RS2 reduced urinary nitrogen excretion, mainly in the form of urea, and reduced the amount of nitrogen absorbed by the colon when expressed as a percentage of the amount of nitrogen entering the colon. This study provides evidence that RS3 , but not RS2 , shifts nitrogen excretion from urine to feces in cannulated piglets.

Animals↗