Biomedical subjects

Z Kurmanowska

Publications and source records attributed to Z Kurmanowska.

5 recordsLinked to original sources

PubMed2000

Release of hydrogen peroxide by rat type II pneumocytes in the prolonged culture.

Type II pneumocytes (T II pneumocytes) produce hydrogen peroxide (H(2)O(2)), which may be potentially dangerous for the lung. These cells in culture differentiate to type I-like pneumocytes and it may reflect the differentiation which follows the injury of alveolar epithelium. This work was undertaken to estimate the H(2)O(2) release by T II pneumocytes, freshly isolated and cultured up to 8 days. The light and electron microscopy evaluation confirmed the differentiation of T II pneumocytes to type I-like cells. The release of H(2)O(2), estimated spectrofluorimetrically as homovanillic acid oxidation product obtained in the presence of horseradish peroxidase, was significantly higher at day 4 (0.63+/-0. 68nmol/mg protein/min, P</=0.02) and 6 (0.46+/-0.31, P</=0.001) compared to fresh cells (0.15+/-0.08). Phorbol esters increased H(2)O(2) release at day 2 (0.39+/-0.22 vs 0.16+/-0.08, P</=0.02) and the inhibition of protein kinase C resulted in the decrease at day 2 (0.14+/-0.06 vs 0.07+/-0.02, P</=0.025), day 6, (0.49+/-0.25 vs 0. 15+/-0.08, P</=0.005) and 8 (0.76+/-0.63 vs 0.23+/-0.29, P</=0.02). Inhibition of intracellular catalase resulted in a significant increase only at day 2 (0.23+/-0.1 vs 0.15+/-0.09, P</=0.05). Inhibition of mitochondrial respiratory chain decreased H(2)O(2) release at day 2 (0.13+/-0.11 vs 0.07+/-0.07, P</=0.002) and 4 (0. 75+/-0.88 vs 0.61+/-0.85, P</=0.002). These results indicate that alveolar epithelium may be a source of potentially dangerous ROS and that the cell differentiation is accompanied by the increase of H(2)O(2) production. Both mitochondrial respiratory chain and membrane-bound NADPH-oxidase may be responsible for the production of H(2)O(2) by T II pneumocytes.

Animals↗

PubMed2000

Inhaled glucocorticosteroids decrease hydrogen peroxide level in expired air condensate in asthmatic patients.

H2O2 is elevated in the exhaled air condensate in several inflammatory disorders of the lung, including bronchial asthma, and thus may reflect inflammatory processes in the airways. Exhaled H2O2 may be used to guide the anti-inflammatory treatment of patients with asthma. Therefore in this study we analysed the effect of inhaled glucocorticosteroid beclomethasone for 4 weeks on H2O2 level in the exhaled air condensate. Seventeen asthmatics and 10 healthy subjects were included to the study. Eleven patients were given inhaled beclomethasone and six were given placebo (3M Health Care). In all patients pulmonary function tests were performed. H2O2 in the expired air condensate was measured spectrofluorimetically (homovanillic acid method). Inhaled beclomethasone significantly decreased H2O2 in the expired air condensate in the active-treatment group, with a fall from baseline on day 1 which remained on day 43 (follow-up) (P<0.05). Exhaled H2O2 in the active-treatment group was significantly lower than that in placebo group (P<0.05). A negative correlation between H2O2 and forced expiratory volume in 1 sec (FEV1) on day 29 was observed. The decrease in exhaled H2O2 in the active-treatment group was accompanied by an improvement in pulmonary function tests results. Inhaled glucocorticoids reduce the level of H2O2 in the expired air condensate of asthmatic patients over a 4-week period and this may reflect their anti-inflammatory activity in lung diseases.

Administration, Inhalation↗

PubMed1998

Effect of various agonists on nitric oxide generation by human polymorphonuclear leukocytes.

Nitric oxide generation is involved in a range of diseases involving polymorphonuclear leukocytes. The aim of this study was to determine whether human polymorphonuclear leukocytes are able to generate nitric oxide and to investigate the time course of its generation after stimulation with 10(-7) M N-formyl-methionyl-leucyl-phenylalanine, 60 ng/ml phorbol myristate acetate, 10(-7) M concanavalin A, and 10(-7) M platelet activating factor. Stimulation of human polymorphonuclear leukocytes with N-formyl-methionyl-leucyl-phenylalanine and phorbol myristate acetate caused sustained nitric oxide generation, reaching maximal values of 1,105 +/- 361 nM (n = 32) and 628 +/- 119 nM (n = 30), respectively. Platelet activating factor did not affect nitric oxide production (maximal value 29 +/- 7 nM, n = 8), whereas concanavalin A caused only a slight increase (102 +/- 24 nM, n = 8) when compared with resting cells control (26 +/- 6 nM, n = 8). Human polymorphonuclear leukocytes were able to respond to both consecutive and alternate N-formyl-methionyl-leucyl-phenylalanine and phorbol myristate acetate stimulation with nitric oxide generation. Nitric oxide generation was inhibited by specific inhibitors (N omega-nitro-L-arginine and N omega-monomethyl-L-arginine) and restored with L-arginine. We provide, to our knowledge, the first direct evidence that human neutrophils generate nitric oxide.

Concanavalin A↗

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↗

PubMedDate not supplied

Effect of paraquat intoxication and ambroxol treatment on hydrogen peroxide production and lipid peroxidation in selected organs of rat.

Paraquat (Pq) is a herbicide which is very toxic to all animals and to man. It generates free radicals and leads to acute or chronic lung injury and usually to death. So far, the role of lipid peroxidation of cell membranes in the mechanism of its toxicity has not been proved satisfactorily and therefore in the present study we examined the concentration of hydrogen peroxide (H2O2) and various lipid peroxidation products (LPP) such as conjugated dienes (CD), lipid hydroperoxides (LH), malonyldialdehyde (MDA) and Schiff bases in selected organs of the rat given a single intraperitoneal dose 35 mg kg-1 Pq. We also evaluated the influence of a mucolytic and probably antioxidant drug, ambroxol, on Pq-induced changes in the concentration of H2O2 and LPP. Paraquat increased the hepatic concentration of H2O2, CD, LH and MDA by approximately fourfold. Though the dose of Pq was nearly twice the LD50 dose, we did not notice any changes in the concentration of these substances in the critical organ, lung or heart and kidney. Ambroxol alleviated the increase of H2O2 in the liver but did not reduce the concentration of LPP. Moreover, the drug administered alone induced lipid peroxidation in the liver. Our results indicate that Pq dose not induce H2O2 production and lipid peroxidation in the lung but it increases the concentration of H2O2 and LPP in the liver. Ambroxol inhibits the Pq-induced increase in the concentration of H2O2 in the liver without protecting it against lipid peroxidation. Moreover, the drug alone may act as a pro-oxidant.

Ambroxol↗