High-pressure synthesis of Ruddlesden-Popper nitrides.

Layered perovskites with Ruddlesden-Popper-type structures are fundamentally important for low-dimensional properties, for example, photovoltaic hybrid iodides and superconducting copper oxides. Many such halides and oxides are known, but analogous nitrides are difficult to stabilize due to the high cation oxidation states required to balance the anion charges. Here we report the high-pressure synthesis of three single-layer Ruddlesden-Popper (K2NiF4 type) nitrides-Pr2ReN4, Nd2ReN4 and Ce2TaN4-along with their structural characterization and properties. The R2ReN4 materials (R = Pr and Nd) are metallic, and Nd2ReN4 has a ferromagnetic Nd3+ spin order below 15 K. Thermal decomposition gives R2ReN3 with a Peierls-type distortion and chains of Re-Re multiply bonded dimers. Ce2TaN4 has a structural transition driven by octahedral tilting, with local distortions and canted magnetic Ce3+ order evidencing two-dimensional Ce3+/Ce4+ charge ordering correlations. Our work demonstrates that Ruddlesden-Popper nitrides with varied structural, electronic and magnetic properties can be prepared from high-pressure synthesis, opening the door to related layered nitride materials.

[Enhancing monitoring of disease progression-remote sensoring in multiple sclerosis]. / Remote-Sensoring ­ neue Optionen des Progressionsmonitorings bei Multipler Sklerose.

BACKGROUND: As a result of innovations in the digitalization of healthcare new technologies, such as remote sensoring are gaining in importance for the collection of real-life data in addition to the regular medical examination. This enables a closer view into the daily lives of patients with multiple sclerosis and a more detailed monitoring of disease progression. OBJECTIVE: This article gives a summary of sensor-based measurement technologies in the field of multiple sclerosis RESULTS: A wide variety of sensor-based measurement technologies are already available, which largely focus on gait analysis and mobility. Furthermore, there are many innovative approaches for a sensor-based collation of the multifocal symptoms of multiple sclerosis, for example technologies focus on the area of stress surveillance, the autonomic nervous system, GPS tracking and sleep monitoring. DISCUSSION: Despite the existence of many already available technologies, the aim is now to find a practical way to integrate them into the daily routine of patient monitoring, which includes standardized data collection, evaluation and interpretation. Only at this point a perspective benefit for treating physicians and patients can be achieved.

Neutrophil oxidative activity is differentially affected by exercise intensity and type.

The differential effects of exercise intensity and type on neutrophil activation were assessed in eight well-trained male runners. Each subject undertook, on different days, three separate 40 min interval (8 x 5 min) treadmill bouts: an intense uphill run (90% VO2 max), a moderate-intensity near-level run and an eccentrically-biased downhill run (both at 52% VO2 max). Blood granulocyte count increased (p< 0.05) after all three treadmill bouts (range 25-108%). Chemiluminescence activity of isolated neutrophils decreased (p< 0.05) immediately after (-58%) and 1-h after (-72%) uphill running, but became significantly elevated (p< 0.05) at 6-h after the near-level (+71%) and downhill (+84%) runs. The ability of neutrophils to release the superoxide anion radical was reduced (p< 0.05) immediately after near-level (-29%) and uphill (-21%) running in cells stimulated with opsonized zymosan. Epinephrine concentration increased by 430% (p=0.01) after uphill but not with near-level or downhill running. The plasma concentration of elastase increased (p< 0.05) immediately after uphill and near-level running, and one hour after uphill running. These results suggest that a population of neutrophils mobilised into the circulation became directly activated in response to exercise, and that neutrophil oxidative activity is affected differentially by both the intensity and type of exercise undertaken.

Lactate/H+ uptake by red blood cells during exercise alters their physical properties.

We investigated whether uptake of lactate anions by red blood cells (RBC) during maximal exercise altered certain cellular physical properties including volume, density and osmotic fragility. Irrespective of whether individuals undertook 1 min of exercise at maximal effort or a progressive exercise test to exhaustion, whole-blood lactate concentration increased about tenfold relative to pre-exercise values (P < 0.001). The plasma and cellular concentrations of lactate increased uniformly, which maintained a constant plasma-to-cell gradient. Exercise-induced increases in RBC osmotic fragility (P < 0.001) and mean cell volume (MCV; P < 0.05), and decreases in mean cell haemoglobin concentration (MCHC; P < 0.05) and cell density (P < 0.005) also occurred. These exercise-induced cellular responses could be simulated in vitro by treating blood with L-lactic acid (15 mM), but not by low pH (7.1) or L-lactate alone. The uptake of lactate by RBCs during vigorous exercise alters certain cellular properties. Although the physiological implications of these changes are unclear, the traditional view that the lactate anion has no known harmful effects should be reconsidered.

Moderate exercise triggers both priming and activation of neutrophil subpopulations.

We investigated how moderate exercise affects neutrophil microbicidal activity and whether exercise-induced responses are associated with changes in growth hormone (GH) secretion. Biological fluctuations were controlled for and GH secretion was manipulated by glucose ingestion. In eight men, 1 h of moderate exercise increased intracellular H2O2 generation in response to phorbol 12-myristate 13-acetate stimulation by threefold (P = 0.025) and complement receptor expression by 20% (P = 0.045). These responses were accompanied by a twofold increase in the plasma concentration of elastase, a marker of neutrophil activation in vivo. The plasma concentration of GH increased 10-fold after exercise, but this was reduced to 3-fold by glucose ingestion (P < 0.001), which also blunted elastase release (P < 0.001). Although the magnitude of H2O2 generation increased in proportion to the increase in plasma GH concentration, it declined progressively once this exceeded 20 ng/ml. The net response of neutrophils to exercise may represent a balance between the individual responses of subpopulations that are unaffected, primed, or fully activated by circulating mediators that respond to exercise and to dietary glucose intake.

Interaction of reactive nitrogen and oxygen intermediates in HL60 and dimethylsulphoxide-differentiated HL60 cells.

The interaction of reactive nitrogen intermediates (RNI) with reactive oxygen intermediates (ROI) was inferred from the effect of added L-arginine on luminol-dependent chemiluminescence (LCL) and cytochrome C reduction in HL60 cells, dimethylsulphoxide (DMSO)-differentiated HL60 cells and human neutrophils. Phorbol myristate acetate (PMA)-stimulated HL60 cells had no effect on LCL and a decreased rate of cytochrome C reduction in the presence of increasing concentrations of L-arginine. Inhibition of L-arginine-mediated cytochrome C reduction was relieved by L-N(G)-monomethyl arginine (L-NMMA), an inhibitor of nitric oxide synthesis, in a concentration-dependent manner. In contrast, DMSO-differentiated cells and human neutrophils separated from blood showed decreased rates of LCL and cytochrome C reduction with increasing concentrations Of L-arginine, which were relieved to some extent by L-NMMA in a dose-dependent manner. These results are consistent with a 40% increase in the production of nitrate following stimulation of DMSO-differentiated cells and human neutrophils by PMA compared with only a 6% rise in undifferentiated HL60 cells. Possible inhibition of NADPH oxidase has been suggested to explain the responses of LCL, cytochrome C reduction and nitrate production by nitric oxide in the presence of L-arginine.

Exercise and the neutrophil oxidative burst: biological and experimental variability.

The effect of acute bouts of moderate-intensity running and cycling on the neutrophil oxidative burst was examined. Eight well-trained male runners in group 1 each undertook, on different days, either two 40-min bouts of running (run 1 and run 2) separated by a 1-h recovery period, or 40 min of moderate cycling. Blood leucocyte (+49%) and granulocyte (+57%) counts increased (P < 0.05) with moderate running, but only the leucocyte count (+27%) was elevated significantly during moderate cycling. Chemiluminescence activity and superoxide anion release decreased after run 1 (-61%, P < 0.05) and after 30 min of cycling (-53%, P < 0.05), with no significant changes in the intracellular release of hydrogen peroxide. The same measures were also assessed at rest in a group of eight male volunteers (group 2) with no significant difference in neutrophil activity for samples treated in parallel or 1 h apart. These data suggest that while neutrophils are mobilised into the circulation in the first few hours following moderate exercise, their oxidative burst is temporarily inhibited. These effects were due to exercise per se and not to temporal variability or intra-assay variation.

Effects of an intensive 12-wk training program by elite swimmers on neutrophil oxidative activity.

The effects of an intensive 12-wk training program by 12 national-level swimmers on neutrophil oxidative activity were studied. Eleven sedentary (untrained) subjects (6 males and 5 females) served as environmental controls. Blood samples (10 ml) were taken at rest from an antecubital vein and neutrophils isolated by standard separation techniques. The oxidative burst activity of isolated neutrophils was assessed with an in vitro flow cytometric assay that used the fluorescent probe dihydrorhodamine 123. Two-way ANOVA (repeated measures) showed that oxidative activity was lower (P < 0.05) in the elite swimmers compared with the sedentary control group across the 12-wk period. Analysis of cells from swimmers in training was made: repeated measures ANOVA provided evidence of a significant decline (P < 0.05) in the number of cells responding positively ito in vitro challenge. Despite this decline, there was no significant difference in self-reported upper respiratory tract infection rate between the swimmers and sedentary individuals. These data show that: (i) elite swimmers undertaking intensive training have a significantly lower neutrophil oxidative activity at rest than do age- and sex-matched sedentary individuals; (ii) aspects of oxidative activity in swimmers are further suppressed during periods of strenuous training, and (iii) the extent of the suppression does not appear to be of clinical significance.

Biochemical effect of three different inhibitors of purine/pyrimidine metabolism on differentiation in HL60 cells.

The effects of three different nucleotide biosynthesis inhibitors were tested on differentiation and purine/pyrimidine metabolism in HL60 cells. On the three nucleotide biosynthesis inhibitors, acivicin and mycophenolic acid were able to differentiate HL60 cells, while alanosine failed to do so. Differentiation of HL60 cells by acivicin and mycophenolic acid was associated with substantial decreases in both the guanylate and adenylate pools and appeared to be dependent on the state of depletion of intracellular GTP. Simultaneous addition of guanosine or guanine to mycophenolic acid-treated cells restored the GTP pool and prevented differentiation from occurring. Adenine or adenosine had no such effect, while hypoxanthine and inosine partially reversed the differentiation. In acivicin-treated cells, simultaneous addition of guanine caused partial prevention of differentiation. Even though treatment of HL60 cells with alanosine resulted in the depletion of guanylates, this effect was secondary to the depletion of adenylates and developed only upon prolonged exposure. In all the inhibitor-treated cells the activities of the key regulatory enzymes of de novo purine biosynthesis were affected. Even though the measurable activity of hypoxanthine/guanine phosphoribosyl transferase was enhanced in inhibitor-treated cells, the activity of the salvage pathway was inhibited in mycophenolic acid and alanosine-treated cells. Besides de novo purine nucleotide biosynthesis, de novo pyrimidine nucleotide biosynthesis was also inhibited in inhibitor-treated cells. The inhibition of purine and pyrimidine nucleotide biosynthesis in mycophenolic acid, acivicin and alanosine-treated cells resulted in an increase in the steady-state concentration of PRPP. Since purine and pyrimidine nucleotides play an important role in the synthesis of important macromolecules, it can be suggested that depletion of guanine ribonucleotide as a result of inhibition of early de novo purine biosynthesis, or due to specific inhibition of de novo guanine nucleotide biosynthesis, may be an obligatory step in the initiation of differentiation in mycophenolic acid and acivicin-treated HL60 cells.

Changes in the susceptibility of red blood cells to oxidative and osmotic stress following submaximal exercise.

Red blood cell (RBC) susceptibility to oxidative and osmotic stress in vitro was investigated in cells from trained and untrained men before and after submaximal exercise. Whilst no significant change in peroxidative haemolysis occurred immediately after 1 h of cycling at 60% of maximal aerobic capacity (VO2max), a 20% increase was found 6h later in both groups (P < 0.05). The RBC osmotic fragility decreased by 15% immediately after exercise (P < 0.001) and this was maintained for 6h (P < 0.001). There was an associated decrease in mean cell volume (P < 0.05). Training decreased RBC susceptibility to peroxidative haemolysis (P < 0.025) but it did not influence any other parameter. These exercise-induced changes were smaller in magnitude but qualitatively similar to those found in haemopathological states involving haem-iron incorporation into membrane lipids and the short-circuiting of antioxidant protection. To explore this similarity, a more strenuous and mechanically stressful exercise test was used. Running at 75% VO2max for 45 min reduced the induction time of O2 uptake (peroxidation), consistent with reduced antioxidation capacity, and increased the maximal rate of O2 uptake in RBC challenged with cumene hydroperoxide (P < 0.001). The proportion of high-density RBC increased by 10% immediately after running (P < 0.001) but no change in membrane-incorporated haem-iron occurred. In contrast, treatment of RBC with oxidants (20-50 mumol.l-1) in vitro increased cell density and membrane incorporation of haem-iron substantially. These results showed that single episodes of submaximal exercise caused significant changes in RBC susceptibility to oxidative and osmotic stress. Such responses may account for the increase in RBC turnover found in athletes undertaking strenuous endurance training.

Purine metabolism in promyelocytic HL60 and dimethylsulphoxide-differentiated HL60 cells.

Purine metabolism was studied in the human promyelocytic leukaemic cell line HL60 both before and after differentiation by dimethylsulphoxide (DMSO) treatment in vitro. DMSO-induced differentiation had no effect on the steady-state concentration of 5-phosphoribosylpyrophosphate (PRPP), even though the activity of the oxidative segment of the pentose phosphate pathway (OPP) increased two-fold and the activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase were enhanced 3-6 times. [14C]-formate incorporation, on the other hand, showed that undifferentiated HL60 cells produced purines by the de novo pathway at six-fold the rate of the differentiated cells and at three times the rate measured in polymorphonuclear leukocytes (PMNs) separated from human blood. This is consistent with significantly higher activities (two to five-fold) of the key regulatory enzymes of the de novo purine synthesis pathway (PRPP synthetase, amido-phosphoribosyl transferase and adenylosuccinate synthase) in the undifferentiated cells. Labelling the cells with [14C]-hypoxanthine showed that there was an active salvage pathway in the HL60 cells which remained unaltered by differentiation. The activities of the salvage enzymes were also the same, although hypoxanthine was taken up at twice the rate by the undifferentiated cells. Human PMNs had an active salvage pathway, but their rate was five times lower than that of the HL60 cells, consistent with much lower activities (three to eight-fold) of the salvage pathway enzymes. These observations suggest that regulation of the synthesis and activities of the purine nucleotide synthesis enzymes may play an important role in the regulation of differentiation of myeloid cells.

The response of leukocyte subsets and plasma hormones to interval exercise.

Aerobic exercise has an established role in modulation of peripheral leukocyte concentrations. However, the effects of intense interval exercise, as employed by athletes in a range of sports, has been given little attention. Eight trained male athletes of mean age (SD) = 31.5 (4.5) yr; VO2max = 64.3 (3.8) ml.kg-1.min-1 undertook an intense interval exercise protocol (treadmill running) to exhaustion. Subjects completed an average of 15.6 1-min efforts. The protocol produced a biphasic leukocytosis: an initial (immediately posttest) leukocytosis resulting from mobilization of lymphocytes (CD3+, CD4+, CD8+, CD16+/56+, CD3+HLA/DR+) (all P < 0.01), with the later (6 h) leukocytosis resulting from mobilization of granulocytes and monocytes (both P < 0.01). This protocol modified significantly the peripheral blood concentration of the hormones cortisol (both total and free), norepinephrine, DHPG, and dopamine (all P < 0.01). Modulation of peripheral leukocyte subsets induced by interval exercise correlated with both the number of exercise efforts performed and the concomitant changes in peripheral hormone concentrations. Sustained alterations in plasma catecholamine levels in the posttest period may have important metabolic and immunological implications for athletes undertaking regular interval training.

The effect of intense interval exercise on iron status parameters in trained men.

Iron and iron-binding proteins play a critical role in the physiology of many human systems, including the immune system. Intense interval exercise in trained men (mean [SD] age = 31.5 [4.5] yr; VO2max = 64.3 [3.8] ml.kg-1.min-1) is associated with significant modulation of iron status parameters. The concentration of red blood cells, hemoglobin, and transferrin all increased significantly immediately post-test (P < 0.01), increases which can largely be attributed to hemoconcentration. Serum iron was elevated by approximately 25% both immediately and 1 h post-test (P < 0.08). Maximum post-test serum iron values (either immediately or 1 h post-test) were significantly elevated with respect to rest (P < 0.01). Transferrin concentration was also significantly elevated at 24 h post-test (P < 0.05). Transferrin saturation was not significantly altered by this protocol (P > 0.10). Despite a trend toward elevation at 24 h post-test, ferritin concentration was not significantly different from the resting value at any sampling point. Intense interval exercise appears to be associated with significant modulation of iron status, the biological importance of which remains to be determined.

Further characterization of the neutrophil oxidative burst by flow cytometry.

The ability to generate reactive oxygen species is essential for neutrophils to kill infectious micro-organisms. We have investigated the 'oxidative burst' in human neutrophils stimulated in vitro with either opsonized zymosan (OZ) or phorbol myristate acetate (PMA) at the single cell level by flow cytometry using dichlorofluorescein diacetate (DCFH-DA) and dihydrorhodamine 123 (DHR) as oxidative probes. These responses have been compared to results obtained with chemiluminescence and spectrophotometric assays. DHR was the most sensitive oxidative probe and PMA the more potent stimulus. The magnitude of the intracellular fluorescence generated with both probes was increased substantially by inhibiting the activities of H2O2-consuming enzymes with a relatively low concentration of azide, which also influenced the distribution of neutrophil subpopulations that expressed fluorescence differentially. Positive correlations between the DCFH-DA and DHR assays were found with both stimuli, and between these assays and ferricytochrome c reduction with OZ-stimulated cells only. We conclude that the DHR flow cytometric assay is the most sensitive technique available for investigating changes that may occur in the oxidative activities and distribution patterns of active neutrophil subpopulations in response to a variety of physiological and pathological conditions.

Granulocyte activation induced by intense interval running.

Activation of granulocytes has been associated with normal immune function, inflammation, and exercise-induced muscle damage. The effect of intense interval running on granulocyte activation was examined by use of flow cytometry, monoclonal antibodies, and spectrophotometric techniques. Eight trained males [maximal oxygen uptake VO2max, mean (SD) = 64.4 (3.6) ml/kg/min; age 30.1 (4.8) years] undertook an intense interval exercise (treadmill running) protocol to exhaustion. Subjects completed an average of 16.5 one-minute runs. Granulocyte expression of CR3 (CD11b), receptor for complement component C3bi (6 and 24 h post-test), and Fc gamma RIII (CD16) (24 h post-test) and the plasma concentration of elastase-inhibitor complex (1 h post-test) increased significantly (all P < .05). Subjects (8 of 8) exhibited a post-test decrease at either 1 or 6 h (P < .01) and a 24-h post-test significant increase (7 of 8; P < .05) in granulocyte 90 degrees light scattering (LS). Plasma lactoferrin (Lf) concentration, although increased by 17% at 6 h post-test, was not significantly different from resting values at any sampling point. Changes in plasma Lf and median channel 90 degrees LS were significantly correlated (r = -.43, P = .04), raising the possibility of monitoring exercise-induced granulocyte activation (degranulation) by flow cytometry. Intense interval exercise appears to induce granulocyte activation, as manifested by release of granule proteins and changes in 90 degrees LS and expression of both Fc and complement receptors.

Glycolytic, glutaminolytic and pentose-phosphate pathways in promyelocytic HL60 and DMSO-differentiated HL60 cells.

The human leukaemic cell line HL60 undergoes differentiation to granulocyte-like cells in response to dimethylsulphoxide (DMSO). The rates of glucose and glutamine utilization were studied in HL60 cells that were either undifferentiated or fully differentiated by 9 days exposure to DMSO. Differentiation did not alter the rate of utilization of exogenous glucose, approximately 75% of which was converted to lactate in each case. The activities of hexokinase, phosphofructokinase, pyruvate kinase and citrate synthase were similarly unaffected. In contrast, the activity of the oxidative segment of the pentose-phosphate pathway was enhanced by differentiation, and no glycogen synthase activity could be detected. These observations are consistent with the significantly lower content of glycogen, the increased activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase and the increased oxidation of [1-14C] glucose relative to [6-14C] glucose in the differentiated cells. Glucose utilization was depressed by exogenous glutamine but, at the same time, glutamine utilization was enhanced by glucose in both cell types; these reciprocal effects were more pronounced in the undifferentiated HL60 cells. Glucose utilization may be depressed in the presence of glutamine as a result of the allosteric inhibition of a rate-limiting step of glycolysis (eg. phosphofructokinase). In spite of having glutaminase activity twice that of their differentiated counterparts, the uptake of glutamine by undifferentiated HL60 cells was low, especially when it was the sole substrate. The stimulation of glutaminolysis by glucose may be due to activation of mitochondrial glutamine transport. A large proportion of the glutamine utilized by both cells contributed to a net accumulation of glutamate, aspartate and alanine, whilst up to 35% was oxidized to CO2. In contrast, almost all of the glucose utilized was converted to lactate and very little was oxidized. The high rates of glycolysis and glutaminolysis observed before and after differentiation may not contribute primarily to energy production but may supply, in undifferentiated cells, substrates for biosynthetic processes that generate nucleic acid precursors or, in the case of differentiated cells which synthesize reactive oxygen intermediates, substrates that maintain NADP in a reduced state.

Endocrine response to intense interval exercise.

This investigation provides an insight into the physiological changes produced, and processes operating, during and after a typical interval exercise training regime. The role of interval exercise in the modulation of the plasma concentration of sex hormone binding globulin (SHBG) and the hormones beta-oestradiol, testosterone, prolactin and growth hormone was assessed. Eight trained male athletes [mean maximal oxygen uptake (VO2max) 64.3 (SD 3.8) ml.kg-1 x min-1, mean age 31.5 (SD 4.5) years] undertook an intense interval exercise (treadmill running) protocol to exhaustion. Subjects completed an average of 15.6 x 1-min runs. This interval protocol produced significant increase in the plasma concentration of SHBG and all four hormones (all P < 0.01) in the immediate post-test period. The plasma concentration of the hormones increased as indicated: beta-oestradiol (45%), testosterone (38%), prolactin (230%), growth hormone (2000%). These hormones have an established capacity to interact with components of many physiological systems and, as such, may provide a mechanism for the changes induced by intense exercise in many of these systems.

Anaerobic exercise causes transient changes in leukocyte subsets and IL-2R expression.

There is evidence that the stress of intense athletic competition and training depresses cellular immunity and predisposes athletes to increased infection. This paper reports changes in circulating leukocyte subsets of trained (group I: VO2max = 67.2 +/- 5.4 ml.kg-1min-1; age = 22.0 +/- 6.2 yr) and untrained (group II: VO2max = 55.0 +/- 4.9 ml.kg-1min-1; age = 21.4 +/- 2.0 yr) males following 1 min of bicycle ergometry at maximum effort. Significant post-exercise increases in concentrations of total leukocytes, monocytes, lymphocytes, CD3+, CD4+, CD8+ lymphocytes were observed in both groups (all P < 0.01). The CD4/CD8 ratio decreased significantly (P < 0.01) but the granulocyte concentration was not altered (P > 0.05). Despite groups I and II not differing in either peak power or total work performed during the exercise test (P > 0.05), group II had a significantly greater concentration and percentage of CD8+ lymphocytes immediately after exercise (P < 0.01). All of the early changes were transient, with normalization occurring within 1 h. Only trained subjects showed a significant decrease in the percentage of CD25+ lymphocytes following PHA stimulation of whole blood obtained 6 h post-exercise. Alterations in leukocyte subpopulations found in response to predominantly anaerobic exercise appear to be associated with a significant, but possibly transient, alteration in the mitogenic responsiveness of lymphocytes that is restricted to aerobically trained subjects.

Free radical generation in hydroperoxide-treated erythrocytes monitored continuously by luminol-amplified chemiluminescence.

Organic hydroperoxides induce oxidative damage to mammalian cells. We describe how luminol-amplified chemiluminescence can be used to monitor free radical generation (following treatment of erythrocytes in vitro with organic hydroperoxides) throughout the entire time-course of oxidative stress. Enrichment of erythrocyte alpha-tocopherol levels increased the induction time by 25% and led peak chemiluminescence fall of 30%. Furthermore, ascorbate loading reduced the signal four-fold during the induction period. The catalytic role of haemoglobin was shown by the abolition of chemiluminescence by azide and a low (but detectable) signal in haemoglobin-depleted erythrocyte ghosts. Luminol-amplified chemiluminescence enables the kinetics of free radical generation to be monitored continuously. Furthermore, it may enable features of the mechanism of interaction between cellular antioxidants and antioxidant enzymes to be elucidated.

Cytokine immunoreactivity in plasma does not change after moderate endurance exercise.

We investigated whether increased concentrations of circulating cytokines may be responsible for exercise-induced priming of blood neutrophils (J. A. Smith et al. Int. J. Sports Med. 11: 179-187, 1990). The plasma concentrations of tumor necrosis factor-alpha, interleukin- (IL) 1 beta, IL-6, granulocyte-macrophage colony-stimulating factor, and neopterin in trained and untrained human subjects were measured by immunoassay before and after 1 h of cycling at 60% of maximal oxygen uptake. C-reactive protein and creatine kinase (CK) were also measured before and 24 h after exercise as markers of the "acute-phase response" and muscle damage (C. Taylor et al. J. Appl. Physiol. 62: 464-469, 1987), respectively. The small changes in the plasma concentrations of cytokines or neopterin observed after exercise in both trained and untrained subjects were not significantly different to those found in a control group of nonexercised subjects. However, untrained subjects did exhibit an acute-phase response (P = 0.04) 24 h after exercise without additional release of CK into plasma. Baseline training differences were confined to a twofold elevation in CK activity (P = 0.04). The results show that circulating cytokines are unlikely to be responsible for the priming of neutrophil microbicidal activity observed after moderate endurance exercise (J. A. Smith et al. Int. J. Sports Med. 11: 179-187, 1990).