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Biomedical subjects

G Piasecka

Publications and source records attributed to G Piasecka.

At least 19 recordsLinked to original sources
PubMed1997

Polymorphonuclear leukocytes from asthmatics release more calcium from intracellular stores and have enhanced calcium increase after stimulation with N-formyl-methionyl-leucyl-phenylalanine.

Polymorphonuclear leukocytes isolated from peripheral blood of asthmatics appear to be primed to release more reactive oxygen species than cells of healthy subjects. The enhanced agonist-induced rise in the intracellular free calcium concentration may be responsible for this increased respiratory burst. To test this hypothesis we studied the N-formyl-methionyl-leucyl-phenylalanine- and cyclopiazonic acid--(an inhibitor of Ca(2+)-ATPase of intracellular calcium stores) induced calcium increase in the polymorphonuclear leukocytes of 28 subjects (16 with moderate asthma, 69.6% +/- 8.3% predicted normal peak expiratory flow and 12 normal controls) using a fluorescent probe Fura-2AM at 100 nM and 1 mM extracellular calcium concentrations. In 1 mN calcium, the N-formyl-methionyl-leucyl-phenylalanine-induced calcium increase was 1.7-fold higher in asthmatics than in healthy subjects. Similarly, the contribution of calcium from intracellular stores to the calcium response to N-formyl-methionyl-leucyl-phenylalanine was higher in asthmatics (55% +/- 14% vs. 39% +/- 14%, P < 0.01). The pool of calcium released from intracellular stores by N-formyl-methinoyl-leucyl-phenylalanine and cyclopiazonic acid was 2.3- and 2.2-fold larger than in control cells. There was a correlation between maximal intracellular calcium concentration related to N-formyl-methionyl-leucyl-phenylalanine-induced calcium release from intracellular stores and forced expiratory volume in 1 s expressed as percentage predicted and reversibility in asthmatics (r = 0.63, r = -0.53, P < 0.05). In conclusion, polymorphonuclear leukocytes of asthmatics exhibit an altered calcium response that is mainly dependent on increased calcium release from intracellular stores.

Adult↗
PubMed1997

Increased hydrogen peroxide and thiobarbituric acid-reactive products in expired breath condensate of asthmatic patients.

Symptoms of bronchial asthma are a manifestation of airway inflammation. Circulatory leucocytes (predominantly eosinophils, mast cells and neutrophils), release inflammatory mediators, including reactive oxygen species, i.e. superoxide anion which is dismutated to hydrogen peroxide (H2O2). Neutrophils from asthmatics generate greater amounts of these species than those of healthy subjects. Some of the H2O2 and thiobarbituric acid-reactive products (TBARs) can evaporate from alveolar lining fluid, and could be expired from the airways of asthmatics. In this study, therefore, we determined whether asthmatic patients exhale more H2O2 and TBARs than healthy subjects. We examined 10 healthy subjects as a control group and 21 asthmatic subjects. In asthmatic subjects, forced expiratory volume in one second (FEV1), was 68+/-9% of predicted value, peak expiratory flow rate (PEFR) was 65+/-8% pred, and bronchial reversibility was 34+/-5% of prebronchodilated FEV1. The mean H2O2 level measured spectrofluorimetrically in the expired breath condensate of asthmatic subjects was 26 fold higher than that in healthy controls (0.26+/-0.29 vs 0.01+/-0.03 nM; p<0.05). The concentration of TBARs in breath condensate was also higher in asthmatic patients compared with nonasthmatics (0.073+/-0.071 vs 0.004+/-0.009 nM; p<0.05). There was a significant correlation between H2O2 level and concentration of TBARs in asthmatic patients (r=0.74; p<0.01). There was also a strong inverse correlation between H2O2 content of all asthmatics and FEV1% pred (r=-0.63; p<0.005) and PEFR% pred (r=-0.52; p<0.05). We conclude that there are elevated levels of hydrogen peroxide and thiobarbituric acid-reactive products in expired breath condensate of asthmatic patients, and that measurement of these substances in the expired breath condensate could be a simple, noninvasive method that could be used as a biochemical marker of airway inflammation.

Adult↗
PubMed1996

Effect of substance P and its precursor alpha-protachykinin on intracellular free calcium concentration in human polymorphonuclear leukocytes.

The increase in intracellular free calcium concentration is an important step in signal transduction leading to phagocyte activation. The undecapeptide substance P can influence various functions of human polymorphonuclear leukocytes, including chemotaxis, phagocytosis, and respiratory burst. In this study we investigated the ability of low-concentration (that can occur in vivo) substance P (10(-7) M) and its precursor alpha-protachykinin (3 x 10(-7) M) to increase the intracellular free calcium concentration in human polymorphonuclear leukocytes. Cells isolated from ten healthy donors were incubated with substance P or alpha-protachykinin in 1 mM calcium medium for 5 min and the intracellular free calcium concentration was monitored using the fluorescent calcium indicator Fura-2am. Polymorphonuclear leukocytes from 40% of donors responded to both agonists. The substance P- and alpha-protachykinin-induced increase in intracellular free calcium concentration was 59 +/- 13 nM and 58 +/- 12 nM and the extracellular calcium influx contributed to 87 +/- 8% and 54 +/- 8% of the calcium response, respectively. alpha-Protachykinin released almost all the calcium from intracellular stores, while substance P mobilized only 24 +/- 5% of this calcium pool. Finally, cells that responded to a single challenge with substance P and alpha-protachykinin were able to increase their intracellular free calcium concentration in response to each of three consecutive stimulations with these agonists. This may be an additional mechanism by which substance P and its precursor modify the function of human polymorphonuclear leukocytes.

Calcium↗
PubMed1996

Comparison of PAF- and fMLP-induced [Ca2+]i transients in human polymorphonuclear leukocytes.

Changes of [Ca2+]i in human polymorphonuclear leukocytes (PMNL) were studied. PMNL suspension was activated three times every 5 min with 10(-7) M PAF and fMLP. Both PAF and fMLP, induced three consecutive [Ca2+]i transients in PMNL suspended in medium with 1 mM Ca2+. The first Ca2+ response was a result of Ca2+ release from internal stores and the extracellular Ca2+ influx, while the second and third responses were completely dependent on Ca2+ influx from extracellular space. The contribution of Ca2+ from intracellular stores to the first PAF-induced Ca2+ response was about 1.4-fold lower in comparison with the first fMLP induced Ca2+ response (27 +/- 1 vs 37 +/- 6% (p < 0.05). Previous addition of PAF enhanced 3-fold (p < 0.001) the PMNL response to fMLP while cells pretreated with fMLP failed to increase their [Ca2+]i after challenge with PAF. PMNL from 40% of donors did not respond to PAF in the presence of 100 nM Ca2+. However, the cells responding to PAF as the cells treated with fMLP or cyclopiazonic acid released almost the entire Ca2+ from intracellular stores after challenge. Subtraction of mean [Ca2+]i transients in the presence of 100 nM Ca2+ from that obtained in medium with 1 mM Ca2+ showed that, in PMNL stimulated with PAF in contrast to the cells treated with fMLP, the onset of Ca2+ influx from extracellular space precedes Ca2+ release from intracellular stores. These results suggest that PAF-induced Ca2+ influx from extracellular space is at least partly independent of Ca2+ release from intracellular stores.

Blood Coagulation Factors↗
PubMed1995

Effect of cytochalasin B on intracellular free calcium concentration in human polymorphonuclear leukocytes after repeated stimulation with n-formyl-methionyl-leucyl-phenylalanine.

Cytochalasin B can influence various functions of human polymorphonuclear leukocytes, including chemotaxis, lysosomal enzyme release, and reactive oxygen species generation. In this study we investigated the effect of cytochalasin B on the increase in intracellular free calcium concentration after three consecutive additions of 10(-7) M N-formyl-methionyl-leucyl-phenylalanine. The interval between stimulations was 5 min. Intracellular free calcium concentration was monitored using the fluorescent calcium indicator FURA-2AM. Cytochalasin B (3.3 micrograms/ml) added 60 s before the cell stimulation enhanced all three polymorphonuclear leukocyte calcium responses by increasing the N-formyl-methionyl-leucyl-phenylalanine-induced calcium influx from the extracellular space. Cytochalasin B increased the peak intracellular free calcium concentration and elevated the plateau phase level, but had no influence on its shape. In addition, pretreatment with cytochalasin B of polymorphonuclear leukocytes suspended in low calcium medium restored their capacity to respond to a third stimulation with N-formyl-methionyl-leucyl-phenylalanine. Finally, in resting cells cytochalasin B caused a moderate increase in intracellular free calcium concentration which was independent of extracellular calcium.

Adult↗
PubMed1995

Changes of intracellular free calcium concentration in human polymorphonuclear leukocytes after repeated stimulations with N-formyl-methionyl-leucyl-phenylalanine.

A rapid transient rise in the intracellular free calcium concentration ( Ca2+]i) is an important step in human polymorphonuclear leukocytes (PMNL) activation. This can be caused by many inflammatory mediators and has been implicated in the regulation of various cellular reactions. In this study we investigated the changes of [Ca2+]i in human PMNL activated three times with 10(-7)M n-formyl-methionyl-leucyl-phenylalanine (FMLP). PMNL in the presence of 1 mM Ca2+ were able to respond to three consecutive stimulations with FMLP. The first Ca2+ response was the highest one and was a result of Ca2+ release from internal stores (which was responsible for about 30% of maximal increment in [Ca2+]i) and the extracellular Ca2+ influx. Experiments with PMNL suspended in a medium containing 100 nM Ca2+ and pretreated with 1 nM Ni2+ (an inorganic calcium channel blocker) revealed that the second and third response is completely dependent on the extracellular Ca2+ influx. Changes of the time interval between stimulations had no influence on the occurrence of extracellular Ca2+ influx related to second addition of FMLP. Elongation of the time interval up to 30 min did not restore the release of Ca2+ from internal stores. It indicates the occurrence of dissociation of Ca2+ release from intracellular stores and extracellular Ca2+ influx during the second and third PMNL response to FMLP.

Calcium↗
PubMed1993

Effect of bacterial lipopolysaccharide on the content of lipid peroxidation products in lungs and other organs of mice.

The influence of lipopolysaccharide from Escherichia coli (LPS, 17 mg/kg body weight) on the lipid peroxidation process in organs of mice was studied. The content of conjugated dienes (CD), lipid peroxides (LP), malondialdehyde (MDA) (all three lipid peroxidation by-products), peroxidase (PO) activity and wet-to-dry weight ratio in lungs, heart, spleen, kidneys and liver were determined 1.5 h after intravenous injection of LPS. Animals observed at this time-point had reduced activity and decreased body temperature by about 2 degrees C, however, all analysed organs did not reveal any changes of wet-to-dry weight ratio comparing to organs from mice injected with sterile, pyrogen free 0.9% NaCl. Only extracts from heart and lungs showed significant increase in the tissue level of at least two lipid peroxidation products. The heart content of CD, MDA, and LP was about 1.5-, 1.3-, and 2.4-fold higher than in control group. In lungs CD and MDA increased 3.3- and 1.3-times but in spleen only content of LP was elevated. In these organs the suppression of PO activity was also observed. Liver and kidneys did not reveal any convincing enhancement of lipid peroxidation process and alterations of PO activity. Since free radical reactions are involved in lipid peroxidation process and inactivation of PO these results suggest that heart, lungs and spleen are the organs mostly exposed to oxidative stress during the first 1.5 h after single injection of LPS in mice.

Animals↗
PubMed1993

Ascorbic acid enhances the decrease in peroxidase activity in inflamed tissues of mice.

The aim of this study was to explore whether intraperitoneal administration of ascorbic acid (AA) at a dose of 500 mg/kg, once a day for 3 following days, affected the peroxidase (PO) activity in inflamed feet of mice. The foot inflammatory reaction induced by the carrageenan (CAR), n-formyl-methionyl-leucyl-phenylalanine (FMLP) and xanthine-xanthine oxidase was accompanied by suppression of PO activity. Administration of AA, having no effect on the degree of foot oedema, skin temperature and microscopic picture of tissue specimens significantly enhanced the decline in PO activity provoked by inflammatory agents. This activity decreased 2.0-, 1.6- and 1.9-fold (p < 0.001, p < 0.01, p < 0.05) when inflammatory response was induced with FMLP, CAR and X-XO, respectively. Also in vitro AA (50-100 micrograms/ml) inhibited PO activity of leukocyte lysate and foot extract obtained from untreated animals. In conclusion we found that AA, having no effect on inflammatory response, significantly enhanced inhibition of PO activity in inflamed tissues in mice which could be a result of direct action of AA on the enzyme molecule.

Animals↗
PubMed1991

Erythrocytes protect alpha-1-proteinase inhibitor from oxidative inactivation induced by chemicals, the myeloperoxidase-H2O2-halide system and stimulated polymorphonuclear leukocytes.

The oxidative inactivation of the alpha-1-proteinase inhibitor (alpha 1PI) is one of the mechanisms responsible for creating the elastase/antielastase imbalance during inflammation in the lower respiratory tract. Chronic supremacy of elastase may cause degradation of elastin fibers leading to the pulmonary emphysema. In this study we have investigated the effect of erythrocytes (RBC, concentrations 0.125 to 1.5%) on the oxidative inactivation of alpha 1PI by the phorbol myristate acetate-stimulated polymorphonuclear leukocytes (PMNL) and PMNL myeloperoxidase-H2O2-halide system. During exposure of alpha 1PI to both systems in the presence of RBC the significant protection (p less than 0.001) of alpha 1PI was found for all RBC concentrations, e.g. at RBC concentration of 1% the elastase inhibitory capacity (EIC) of alpha 1PI increased from 0 to 60 +/- 6 and 88 +/- 9% of the control value (untreated alpha 1PI), n = 5, respectively. The preincubation of RBC with chloramine-T (1 mM), inhibition of RBC catalase or depletion of RBC reduced glutathione alone did not diminish the capacity of RBC to protect alpha 1PI. However, these treatments together completely deprived RBC of their protective properties. Moreover, we have compared the decrease in the EIC of human blood and its plasma after incubation with H2O2 (0.1 mM to 0.1 M) or chloramine-T (1 microM to 1 mM). For the incubation with H2O2 no decrease in blood EIC was found whereas in plasma the loss of EIC was already visible at a H2O2 concentration of 0.1 mM. Also for the incubation with chloramine-T the EIC of blood was more resistant to oxidant damage than EIC of plasma. It is suggested that RBC contaminations present in the phagocyte inflammatory infiltration in the lower airways may protect alpha 1PI from oxidative inactivation and thus indirectly diminish proteolytic lung injury related to inflammation.

Chloramines↗
PubMed1991

Effect of ascorbic acid on hydroxyl radical generation by chemical, enzymatic and cellular systems. Importance for antioxidant prevention of pulmonary emphysema.

The ability of ascorbic acid (AA) (25 to 500 microM) to increase OH production by a chemical (Fe(2+)-EDTA-H2O2), an enzymatic (xanthine-xanthine oxidase-Fe(2+)-EDTA) and a cellular system (3.10(6) human polymorphonuclear leukocytes (PMNL) or murine peritoneal macrophages (PM) activated with 7.2 ng PMA/ml) was studied. At all concentrations used AA strongly enhanced OH generation by the chemical and the enzymatic systems. However, the maximal increase of about 14-fold was found for incomplete chemical system (10 microM Fe(2+)-20 microM EDTA) and 500 microM AA. In the case of phorbol-myristate-acetate-activated-PMNL and macrophages, the moderate increase in OH formation was only caused by low AA concentrations. At 50 microM AA, the OH formation was 112 +/- 3 and 117 +/- 4% of control, respectively. Higher AA concentrations had no influence or even decreased OH formation by phagocytes. It is suggested that administration of AA will not significantly enhance OH generation from pulmonary phagocytes and could be useful for prevention of the oxidant-mediated lung injury related to inflammation.

Animals↗
PubMed1991

The main serum protease inhibitors; alpha-1-proteinase inhibitor and alpha-2-macroglobulin inhibit H2O2 release from human polymorphonuclear leukocytes stimulated with phorbol myristate acetate.

Since various functions of phagocytes can be affected by protease inhibitors, the ability of alpha-1-proteinase inhibitor (alpha 1PI) and alpha-2-macroglobulin (alpha 2M) to modulate the H2O2 production by human polymorphonuclear leukocytes (PMNL) was studied. The preincubation of PMNL for 30 min with these protease inhibitors at concentrations which may occur in human blood diminished in a dose dependent manner their H2O2 generation induced with phorbol myristate acetate. At alpha 1PI 600 mg/dl and alpha 2M 800 mg/dl the H2O2 response decreased to 61 +/- 2 and 58 + 3% (p less than 0.001, n = 4) of the control value obtained with cells preincubated in phosphate buffered saline with glucose, respectively. Autologous serum alone and with addition of pure alpha 1 PI or alpha 2M also suppressed H2O2 release from PMNL. It is suggested that inhibition of H2O2 generation from PMNL may be another additional way by which these serum protease inhibitors may protect tissues (especially lungs) from acute injury related to inflammation.

Dianisidine↗
PubMed1991

Effect of ascorbic acid on killing of lymphocytes and macrophages by hydrogen peroxide.

The ability of ascorbic acid (AA) to modify the H2O2 (0.6 to 9 mM) toxic activity for human lymphocytes (PBMC) and murine peritoneal macrophages (PM) was studied in vitro. 100 microM AA added simultaneously with H2O2 to the cell medium enhanced the killing of PBMC but not of PM independently of the presence of Fe(2+)-EDTA. Similarly, preincubation of PBMC with 500 microM AA that resulted in a 2.5-fold rise in the intracellular level of AA increased their susceptibility to both H2O2 and H2O2-Fe(2+)-EDTA. On the contrary, PM preincubated with AA were more resistant to the toxic action of the H2O2-Fe(2+)-EDTA system and did not reveal any changes of the susceptibility to H2O2 alone. It is suggested that AA under certain conditions may have opposite effects on the H2O2-induced cell damage related to inflammation.

Animals↗
PubMed1990

Nicotine increases human polymorphonuclear leukocytes chemotactic response--a possible additional mechanism of lung injury in cigarette smokers.

Human polymorphonuclear leukocytes (PMNL) which are a potential source of proteolytic enzymes and reactive oxidant species contribute to the development of pulmonary emphysema in cigarette smokers. We found that nicotine at concentrations that occur in smokers' plasma enhances human PMNL chemotactic response to zymosan-activated serum (ZAS) and n-formyl-methionyl-leucyl-phenylalanine (FMLP). Maximal increase in chemotactic migration was at nicotine concentration 1 mumol/l. Higher concentrations, above 0.1 mmol/l inhibited PMNL chemotactic response and spontaneous migration. Nicotine also enhanced PMNL influx to the place of inflammation developed in the mouse pleural cavity after injection of ZAS. The number of PMNL found in the pleural cavity was 1.9-fold higher (p less than 0.001, n = 5) when animals were pretreated with 0.15 mg of nicotine. However, this drug itself (concentrations of 0.1 mumol/l to 10 mmol/l) had weak chemotactic activity for PMNL. It seems that the stimulatory action of nicotine on PMNL chemotaxis may be partly responsible for increased PMNL numbers in the lower airways of cigarette smokers and following formation of the elastase/antielastase imbalance in lung tissue.

Animals↗
PubMed1990

Chemotactic activity of histones for human polymorphonuclear leukocytes.

The chemotactic activity of histones for human polymorphonuclear leukocytes (PMNL) was investigated using the under-agarose method. Total histone and histone fractions H1, H2a, H2b, H3, H4 were prepared from calf thymus and dissolved in phosphate buffered saline (PBS) pH 7.4. At concentrations of 1 and 0.1 mg/ml all histone preparations were chemotactic for PMNL. The PMNL migration (expressed as a chemotactic index) to total histone (1 mg/ml) was 1.5 +/- 0.2 (n = 8) and to histone fractions it ranged from 1.2 to 1.4. The injection of total histone (50 micrograms) to the mouse pleural cavity induced cell influx. The mean PMNL number found in this cavity (0.33 +/- 0.15 X 10(6] was 3.6-fold higher in this group as compared to PBS-treated animals. Human PMNL during 60 min incubation with total histone (10 micrograms/ml) or with total histone and cytochalasin B (CB, 4.8 micrograms/ml) released 12.9 +/- 2.5 (n = 9) and 40.6 +/- 4.9 (n = 4) % of the total myeloperoxidase cell activity. Total histone (1 to 10 micrograms/ml) did not stimulate hydrogen peroxide generation independently of the presence of CB and had no influence on its production induced by phorbol myristate acetate. Our results suggest that histones released from cell debris in the place of inflammation could secondarily modulate to some extent its course by enhancing PMNL influx and their activation. These findings may be important for the course of inflammatory response in lungs especially in the light of their susceptibility to proteolytic injury.

Chemotaxis, Leukocyte↗
PubMed1990

DNA activates human polymorphonuclear leukocytes--a new importance of DNA presented in the inflammatory tracheobronchial secretion.

DNA from calf thymus (1 to 10 micrograms/ml) was shown to stimulate the release of myeloperoxidase (MPO) and low amounts of H2O2 (about 1.5 nmoles/10(6) cells) from human polymorphonuclear leukocytes (PMNL). PMNL during 60 min incubation with DNA (10 micrograms/ml) and with DNA and cytochalasin B (4.8 micrograms/ml) released 14.4 +/- 3.4 and 25.5 +/- 4.8% (n = 7) of the total MPO cell activity, respectively. Higher DNA concentrations (0.25 to 1mg/ml) were chemotactic for PMNL as assayed under agarose method. At DNA concentration 1mg/ml the chemotactic index reached 1.5 +/- 0.2 and was approximate to value 1.7 +/- 0.2 (n = 7) obtained with zymosan-activated serum. However, the introduction of DNA to the mouse pleural cavity caused insignificant increase in the number of PMNL and lymphocytes recovered from the cavity at 3 h after injection, comparing it to material obtained from buffer-treated animals. The yield of DNA preparation from purulent sputum (about 10 micrograms/ml) indicates that DNA concentrations which activate PMNL in vitro occur in the inflammatory tracheobronchial secretion. The DNA from sputum electrophoresed on the 0.6% agarose gel reveal pattern which could be the result of nucleosomal DNA degradation. These results suggest that DNA released from nuclear debris in the place of inflammation, especially in the lower respiratory tract could secondarily modulate its course by PMNL activation. This novel role of DNA may be important for pulmonary pathology since lungs are susceptible to proteolytic and oxidant mediated injury.

Animals↗
PubMed1989

Chemotactic activity of elastin-derived peptides for human polymorphonuclear leukocytes and their effect on hydrogen peroxide and myeloperoxidase release.

The chemotactic activity of elastin-derived peptides (EP) for human polymorphonuclear leukocytes (PMNL) was investigated using the under agarose method. The EP were produced by digesting the bovine ligament elastin with porcine pancreatic elastase. Thus prepared digest had weak chemotactic activity for PMNL. The mean chemotactic index for all tested EP concentrations did not exceed 1.30 and was lower than that obtained with zymosan-activated serum (ZAS, n-formyl-methionyl-leucyl-phenylalanine (FMLP) 2.2 +/- 0.40, 3.1 +/- 0.32, (n = 10) respectively. However, EP (50 micrograms) after injection to the mouse pleural cavity induced PMNL influx. The mean PMNL number found in this cavity was 0.09 +/- 0.03 x 10(6) for PBS and 0.18 +/- 0.03 +/- 10(6) for EP injection (p less than 0.01 n = 6). Human PMNL during 60 min incubation with EP (1 to 10 micrograms/ml) or with EP and cytochalasin B (CB 4.8 micrograms/ml) released myeloperoxidase and low amounts of hydrogen peroxide. At 1 micrograms/ml and in presence of CB elastin digest was nearly as active in myeloperoxidase release as FMLP (300 ng/ml). The values reached 17.1 +/- 2.5 and 19.7 +/- 2.1% of the total activity of whole cell lysate, respectively. The obtained results suggest that EP produced in vivo in the site of inflammation could modulate to some extent its course by enhancing PMNL influx and their activation. It seems that such mechanism of enhancement of the inflammatory response may occur in the lungs which are rich in elastin fibers.

Animals↗
PubMed1989

Ascorbic acid inhibits polymorphonuclear leukocytes influx to the place of inflammation--possible protection of lung from phagocyte-mediated injury.

Ascorbic acid as a scavenger of oxidants derived from human polymorphonuclear leukocytes (PMNL) may have clinical significance in antioxidant prevention of emphysema. However, there is a risk relevant to its administration because this drug was reported to enhance PMNL chemotactic response and thus could create protease burden in the lower airways. In this study we have investigated the effect of ascorbic acid on the PMNL influx to the place of inflammation developed in the mouse pleural cavity after injection of zymosan-activated serum (ZAS). We also evaluated the influence of ascorbic acid on human PMNL spontaneous migration, chemotaxis to ZAS and n-formyl-methionyl-leucyl-phenylalanine (FMLP) under agarose. The previous ascorbic acid intraperitoneal administration (single dose 10 mg per day for 3 following days) inhibited leukocyte influx. Total number of cells found in the cavity, number of PMNL and lymphocytes was 2.4, 3.5, 1.7-fold lower than in animals without ascorbic acid, respectively. In vitro ascorbic acid (concentrations of 1 to 10 mg/dl) enhanced PMNL spontaneous migration, concentrations 10 mg/dl and higher inhibited PMNL chemotaxis to ZAS and had no influence on migration of the cells toward FMLP. These results suggest that ascorbic acid may be useful for prevention of lung oxidant injury not only as oxidant scavenger but also as an inhibitor of PMNL influx to the pulmonary tissue.

Animals↗