Search PubMed⌕ Search

Biomedical subjects

T Pietras

Publications and source records attributed to T Pietras.

18 recordsLinked to original sources
PubMed2001

[Effects of bacterial extract IRS-19 on the concentration of hydrogen peroxide and myeloperoxidase activity in nasal washings of patients with chronic bronchitis].

AIM: To determine the effect of intranasal treatment with IRS-19, an immunomodulating agent, on the number of polymorphonuclear leukocytes (PMNL), H2O2 concentration and myeloperoxidase (MPO) activity in nasal washings. MATERIAL AND METHODS: 28 adult patients of both sexes with chronic bronchitis participated in an open study of intranasal treatment with IRS-19. RESULTS: The number of PMNL recovered from nasal spaces increased from 4460 +/- 3960 to 10,490 +/- 10,950 cells/ml (p < 0.02) after two month administration of IRS-19. It was accompanied by 2.6- and 1.4-fold increase (p < 0.001) in MPO activity and H2O2 concentration, respectively. However, no correlation was found between increments in these three variables. CONCLUSION: Since PMNL and MPO--H2O2--Cl- system are involved in the first line of defense against invading pathogens it is suggested that the above mentioned changes may represent one among mechanisms leading to enhancement of antibacterial defence in the airways in response to treatment with IRS-19.

Adjuvants, Immunologic↗
PubMed1999

Increased content of thiobarbituric acid-reactive substances and hydrogen peroxide in the expired breath condensate of patients with stable chronic obstructive pulmonary disease: no significant effect of cigarette smoking.

The imbalance between oxidants and antioxidants is known to play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cigarette smoking is the most frequent factor responsible for development of COPD by leading to oxidant overload in the lower airways, due to presence of its own oxidants and to recruitment and activation of pulmonary phagocytes. We aimed to determine whether (1) patients with stable COPD have higher thiobarbituric acid-reactive substances (TBARs, an end-product of lipid peroxidation) and H2O2 levels in expired breath condensate than healthy subjects who have never smoked; (2) COPD subjects who are current smokers exhale more TBARs and H2O2 than COPD ex-smokers and those who have never smoked; and (3) concentration of TBARs correlates with H2O2 levels in the breath condensate of COPD patients. The TBAR and H2O2 content in expired breath condensate of 17 healthy nonsmoking subjects and 44 patients (11 current smokers, 20 ex-smokers and 13 who had never smoked) with stable COPD [forced expiratory volume in 1 s (FEV1) 63.3 +/- 16.3% and FEV1 reversibility 5.2 +/- 4.3% predicted value] was measured spectrofluorimetrically by the thiobarbituric acid and homovanillic acid methods, respectively. The mean concentrations of TBARs and H2O2 in the expired breath condensate of COPD subjects were 12 (0.48-0.86 microM vs. 0.04 +/- 0.14 microM; P < 0.05) and 10 times (0.48 +/- 0.67 microM vs. 0.05 +/- 0.07 microM; P < 0.005) higher than in healthy controls. Current smokers with COPD did not exhale more H2O2 than COPD ex-smokers and those who had never smoked. TBARs levels shared only a tendency to be higher in the breath condensate of smoking COPD subjects than in that of ex-smokers (0.92 +/- 1.49 microM vs. 0.35 +/- 0.44 microM) and of COPD subjects who had never smoked (0.92 +/- 1.49 microM vs. 0.30 +/- 0.53 microM). No correlation was found between TBAR and H2O2 levels in the whole COPD group. These variables did not correlate with cigarette smoking status and the time from smoking cessation. Subjects with stable COPD exhibit increased lipid peroxidation and H2O2 generation in the airways. Current cigarette smoking does not distinguish COPD subjects with respect to TBARs and H2O2 exhalation.

Antioxidants↗
PubMed1998

Cigarette smoking does not increase hydrogen peroxide levels in expired breath condensate of patients with stable COPD.

Cigarette smoking is the most common factor responsible for the development of chronic obstructive pulmonary disease (COPD) leading to oxidant overload in the lower airways because of the presence of oxidants in cigarette smoke and recruitment and activation of pulmonary phagocytes. In this study we intended to determine whether: 1) patients with stable COPD have higher H2O2 levels in expired breath condensate than healthy nonsmoking subjects and 2) whether cigarette smoking increases H2O2 exhalation in patients with stable COPD. The H2O2 content of the expired breath condensate of 17 healthy nonsmoking subjects and 38 patients (10 current smokers, 17 exsmokers and 11 who have never smoked) with stable COPD (forced expiratory volume in one second (FEV1) 63.3 +/- 15.5% of predicted value) was measured spectrofluorimetrically (homovanillic acid method). The mean H2O2 concentration in the expired breath condensate of COPD subjects was 10-times higher than that found in healthy controls (0.55 +/- 0.69 microM versus 0.05 +/- 0.07 microM, p < 0.005). There were no significant differences between H2O2 levels found in current smokers with COPD (0.44 +/- 0.56 microM) and COPD subjects who have never smoked (0.49 +/- 0.70 microM). No correlation was found between expired H2O2 and daily cigarette consumption or cumulative cigarette consumption in current smokers or exsmokers with COPD. These findings demonstrate that subjects with stable chronic obstructive pulmonary disease exhibit increased H2O2 generation in the airways and that cigarette smoking does not increase H2O2 production.

Breath Tests↗
PubMed1997

Effect of bacterial extract, IRS-19, on the concentration of hydrogen peroxide and myeloperoxidase activity in nasal washings of patients with chronic bronchitis.

Twenty eight adult patients of both sexes with chronic bronchitis participated in an open study to determine the effect of intranasal treatment with IRS-19, an immunomodulating agent, on the number of polymorphonuclear leukocytes (PMNL), H2O2 concentration and myeloperoxidase (MPO) activity in nasal washings. The number of PMNL recovered from nasal spaces increased from 4460 +/- 3960 to 10,490 +/- 10,950 cells/ml (p < 0.02) after two month administration of IRS-19. It was accompanied by 2.6- and 1.4-fold increase (p < 0.001) in MPO activity and H2O2 concentration, respectively. However, no correlation was found between increments in these three variables. Since PMNL and MPO-H2O2-Cl- system are involved in the first line of defense against invading pathogens it is suggested that above mentioned changes may represent one among mechanisms leading to enhancement of antibacterial defence in the airways in response to treatment with IRS-19.

Adjuvants, Immunologic↗
PubMed1997

Severe haemorrhagic diathesis in an adult patient with cystic fibrosis after long-term antibiotic treatment of pulmonary infection.

We describe the case of a 22 yr old male patient with cystic fibrosis, who, after long-term antibiotic treatment of pulmonary infection, developed a haemorrhagic diathesis with severe bleeding from the mucus membrane of the mouth, and haematuria. Rapid recovery was observed after infusion of vitamin K. During 8 months of follow-up, no evidence of recurrence of the clotting disturbances and anaemia were noted. The combination of impaired absorption of vitamin K due to underlying disease with the antibiotic-induced suppression of vitamin K synthesis by intestinal bacteria could be a possible explanation for this disorder.

Adult↗
PubMed1997

The newly synthetized pyridobenzoxazocynone inhibits HIV-1 reverse transcriptase activity.

We synthetized pyridobenzoxazocynone that differs in the enlarged eight-membered heterocyclic system from the basic structure of pyridobenzoxazepinones a known class of non-nucleoside HIV-1 reverse transcriptase inhibitors. Pyridobenzoxazocynone hydrochloride was found to inhibit HIV-1 reverse transcriptase activity. At concentration 0.35 microM the enzyme activity decreased by 64 +/- 14%. Higher concentrations of pyridobenzoxazocynone hydrochloride completely abolished the enzyme activity expressed as radioactivity of acid insoluble products. These results suggest that pyridobenzoxazocynones may represent a new class of HIV-1 reverse transcriptase inhibitors.

Gene Products, pol↗
PubMed1996

Increased content of hydrogen peroxide in the expired breath of cigarette smokers.

Cigarette smoking causes an influx of mononuclear phagocytes and polymorphonuclear leucocytes into the lower airways. These cells have altered oxygen metabolism and release more H2O2 than phagocytes from nonsmokers. In this study, we intended to determine whether asymptomatic cigarette smokers exhale more H2O2 than healthy nonsmokers. The content of H2O2 in the expired condensate of 27 nonsmokers and 33 cigarette smokers was measured spectrofluorimetrically (homovanillic acid method). The mean H2O2 level in the expired breath condensate of all cigarette smokers was about fivefold higher than that found in the whole nonsmoker group (0.24 +/- 0.32 versus 0.05 +/- 0.11 nM). However, only 16 smokers (49%) and 6 nonsmokers (22%) had detectable levels of H2O2 in expired breath that reached values 0.49 +/- 0.28 and 0.23 +/- 0.10 nM, respectively. Although the cigarette smoking status was similar for both male and female smokers, females expired 2.5 fold less H2O2 than males (0.15 +/- 0.24 (n = 21) versus 0.38 +/- 0.39 (n = 12) nM. No correlation was found between expired H2O2 levels and cigarette smoking status expressed as the daily cigarette consumption, cumulative cigarette consumption and urinary cotinine concentration. It is suggested that in some smokers, expressed H2O2 can be a noninvasive marker of oxidant overload in the lower airways related to cigarette smoking.

Adult↗
PubMed1994

Antioxidant properties of Ambroxol.

We tested whether Ambroxol, a drug which stimulates the release of surfactant by pneumocytes type II, may also possess antioxidant properties. To assess the reactivity of Ambroxol with reactive oxygen species, we analysed its ability to decompose hydrogen peroxide (H2O2) and to inhibit the superoxide (O2.-)-dependent autooxidation of pyrogallol, hydroxyl radical (.OH)-mediated deoxyribose oxidation, and hypochlorous acid (HClO-induced chlorination of monochlorodimedon. Ambroxol was found to be a sufficient scavenger of HClO and .OH and also revealed the capacity to decompose H2O2. At concentrations of 25 and 70 microM, it inhibited HClO-induced chlorination of monochlorodimedon by 22 +/- 13 and 59 +/- 14%, respectively. Similarly, at concentrations of 1, 2, and 10 mM, Ambroxol decreased .OH-mediated deoxyribose oxidation by 47 +/- 11, 75 +/- 9, and 89 +/- 4%. In addition, at concentrations of 1 to 5 mM, it completely protected linoleic acid from .OH-induced peroxidative damage. Ambroxol had a weak effect on O2.(-)-dependent autooxidation of pyrogallol. Our results indicate that Ambroxol has antioxidant activity, which may have clinical significance in protecting lung tissue from oxidant-induced injury.

Ambroxol↗
PubMed1994

Protective effect of ambroxol against heat- and hydrogen peroxide-induced damage to lung lipids in mice.

We wanted to determine whether ambroxol, a drug which stimulates the release of surfactant by type II pneumocytes, can protect lung lipids from peroxidative damage in mice. Animals were injected intraperitoneally with ambroxol, 0.169 mmol.kg-1, or 1 ml buffer once a day for three consecutive days. Lipid peroxidation was then induced in lung homogenates either by means of heat, 50 degrees C, or H2O2, 10 mmol.l-1. The lung homogenates from ambroxol-treated animals revealed decreased lipid peroxidation in response to both stimuli. The heat- and H2O2-induced generation of conjugated dienes (a first lipid peroxidation product) in ambroxol-treated lung homogenates was 3.7 and 3.1 fold lower than in the lungs from buffer-injected mice. Ambroxol, as an inhibitor of heat- and H2O2-induced lipid peroxidation, was equipotent to and stronger than the two antioxidants, N-acetylcysteine and methionine, respectively. Ambroxol was not able to protect heart and liver lipids. These results suggest that ambroxol can sufficiently enhance the antioxidant defence in lung tissue and can act as a lung lipid antioxidant.

Acetylcysteine↗
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

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

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↗
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↗
PubMedDate not supplied

Ascorbic acid did not alter the content of conjugated dienes and malondialdehyde in organs of mice.

The aim of this study was to explore whether ip administration of ascorbic acid (AA) in a dose of 500 mg/kg, once a day for 3 following days, affected the content of lipid peroxidation products: malondialdehyde (MDA) and conjugated dienes (CD) in organs of mice. Injection of AA caused 2.1-, 1.3- and 1.8-fold increase in the concentration of this vitamin in liver, spleen and lungs, respectively, while the content of MDA and CD in these organs did not differ from values found in animals treated with 0.9% NaCl. It suggests that in our animal model AA did not act as a prooxidant enhancing the lipid peroxidation in various tissues.

Animals↗
PubMedDate not supplied

Ambroxol inhibits endotoxin-induced lipid peroxidation in mice.

Administration of ambroxol (70 mg/kg ip) once a day for 3 days protected lung and heart lipids from lipopolysaccharide (LPS, 17 mg/kg)-induced oxidative stress in mice. Ambroxol as a lipid peroxidation inhibitor was almost as active as an equivalent dose of N-acetylcysteine (27.6 mg/kg), a well known antioxidant. The lung and heart levels of conjugated dienes in animals pretreated with ambroxol were 3.3- and 1.7-times lower (p < 0.05 and p < 0.01) than those observed in the control group which received only buffer and subsequently LPS. These results indicate that ambroxol can sufficiently inhibit the harmful process of lipid peroxidation in vivo.

Ambroxol↗