Wyniki wyszukiwania

1

Influence of the microenvironment of thiol groups in low molecular mass thiols and protein on the reaction with methylglyoxal

100%

Acimovic J. M., Stanimirovic B. D., Todorovic N., Jovanovic V. B., Mandic L. M.

Polish Journal of Food and Nutrition Sciences

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2011

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tom 61

|

nr Suppl.1

2

New developments in the treatment of COPD: comparing the effects of inhaled corticosteroids and N-acetylcysteine

100%

Van Overveld F. J., Demkow U., Gorecka D., De Backer W. A., Zielinski J.

Journal of Physiology and Pharmacology. Supplement

|

2005

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tom 56

|

nr 4

135-142

Inhaled corticosteroids (ICS) are widely used for the treatment of COPD despite of controversial statements concerning their efficacy. The use of N-acetylcysteine (NAC), a mucolytic drug with antioxidant properties, is less clear, but it may counteract the oxidant-antioxidant imbalance in COPD. The aim of this study was to evaluate whether treatment of COPD patients with ICS or NAC is able to improve inflammatory indices and to enhance lung function. ICS treatment enhanced protective markers for oxidative stress such as glutathione peroxidase (GPx) (51.2 ±5.8 vs. 62.2 ±8.6 U/g Hb, P<0.02) and trolox-equivalent antioxidant capacity (TEAC) (1.44 ±0.05 vs. 1.52 ±0.06 mM, P<0.05). NAC decreased sputum eosinophil cationic protein (318 ±73 vs. 163 ±30 ng/ml, P<0.01) and sputum IL-8 (429 ±80 vs. 347 ±70 ng/ml, P<0.05). The increased antioxidant capacity prevented an up-regulation of adhesion molecules, since the levels of intracellular adhesion molecule 1 (ICAM-1) correlated negatively with GPx (P<0.0001) and TEAC (P<0.0001). On the other hand, expression of adhesion molecules was promoted by inflammation, reflected by a positive correlation between the levels of IL-8 and ICAM-1 (P<0.0001). The effects of treatment on lung function were only reflected in the FEV1 values. The absolute value of FEV1, both before and after salbutamol inhalation, increased from 1690 ±98 to 1764 ±110 ml, and 1818 ±106 to 1906 ±116 ml, respectively, after ICS (P<0.05) . Ten weeks after treatment, FEV1 values dropped to 1716 ±120 ml post-salbutamol (P<0.05). When followed by treatment with NAC, these values decreased even further to 1666 ±84 ml. These results suggest that ICS improved lung function in COPD patients with moderate airflow obstruction, beside a minor improvement in the oxidant-antioxidant imbalance leading to a lesser expression of ICAM-1. Treatment with NAC decreased some inflammatory parameters and had indirectly an inhibitory effect on the expression of adhesion molecules.

3

Influence of N-acetylcysteine on ICAM-1 expression and IL-8 release from endothelial and epithelial cells

100%

Radomska-Lesniewska D. M., Sadowska A. M., Van Overveld F. J., Demkow U., Zielinski J., De Backer W. A.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 4

325-334

Chronic obstructive pulmonary disease (COPD) is characterized by chronic airway inflammation. The initial step in the inflammatory process is overexpression of adhesion molecules, which leads to excessive transmigration of neutrophils. One of these adhesion molecules is ICAM-1 which is elevated in COPD patients. In this study we evaluated the influence of N-acetylcysteine (NAC) (0.01 mM-30 mM) on the cytokine-induced (TNF-alphalpha/IL-1ß) expression of the ICAM-1 adhesion molecule and on IL-8 release in endothelial (ECV-304) and bronchial epithelial (H292) cell lines. The methodology used consisted of immunochemistry for the assessment of surface ICAM-1 and ELISA method for that of soluble ICAM-1 and IL-8. NAC inhibited the TNF-alphalpha/IL-1ß-stimulated ICAM-1 expression and IL-8 release from both cell lines in a concentration dependent manner. The most effective concentrations were 30 mM and 20 mM (99 and 90% inhibition respectively, P<0.01). We conclude that NAC is an effective inhibitor of TNF-alphalpha/IL-1ß- stimulated ICAM-1 and IL-8 release in endothelial and epithelial cells. This fact highlights the anti-inflammatory potential of NAC in COPD.

4

Evaluation of selected protein biomarkers of renal function in rats with an experimental model of acute cyclophosphamide-induced cystitis treated with N-acetylcysteine

100%

Dobrek L., Nalik-Iwaniak K., Kopanska M., Arent Z., Thor P. J.

Journal of Physiology and Pharmacology

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2019

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tom 70

|

nr 5

5

Aspects of using N-acetylcysteine in aflatoxicosis and its evaluation regarding some lipid peroxidation parameters in rabbits

100%

Eraslan G., Cam Y., Eren M., Liman B. C., Atalay O., Seybek N.

Bulletin of the Veterinary Institute in Puławy

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2005

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tom 49

|

nr 2

6

N-acetylcysteine effectively diminished meconium-induced oxidative stress in adult rabbits

84%

Mokra D., Drgova A., Mokry J., Antosova M., Durdik P., Calkovska A.

Journal of Physiology and Pharmacology

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2015

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tom 66

|

nr 1

7

In vitro studies of the effect of theophylline and/or N-acetylcysteine on redox homeostasis and ketogenesis in rat hepatocytes

84%

Stec M., Kurzeja E., Gawel S., Wardas P., Maciejewska=Paszek I., Pawlowska-Goral K.

Bulletin of the Veterinary Institute in Puławy

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2011

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tom 55

|

nr 3

The examinations were conducted on hepatocvtes isolated by means of enzymatic method from the liver of three-month-old Wistar rats. The cells were incubated in medium with addition of theophylline and/or N-acetylcysteine. Significant changes in the activity of SOD, GPx, and GR in hepatocvtes incubated in the presence of the compounds in comparison with control cells demonstrated that theophylline and/or N-acetylcysteine disturb oxidative-reductive homeostasis of the cells. Changes in concentrations of ketone bodies, resulting in disturbances of acetoacetate to ß-hydroxybutyrate molar ratio, point to an unfavourable interference of theophylline into ketogenesis, which is equivalent with the disturbance of the balance between NAD⁺ and NADH+H⁺ in hepatocvtes. N-acetylcysteine simultaneously present with theophylline in incubation medium exerted a protective action on ketogenesis.

8

The oxidative status of milking goats after per os administration of N-acetylcysteine

84%

Jozwik A., Bagnicka E., Strzalkowska N., Sliwa-Jozwik A., Horbanczuk K., Cooper R. G., Pyzel B., Krzyzewski J., Swiergiel A. H., Horbanczuk J. O.

Animal Science Papers and Reports

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2010

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tom 28

|

nr 2

Investigated were changes in selected redox parameters – vitamin C, malondialdehyde (MDA) and glutathione (GSH) content of goat blood plasma – as markers of oxidative stress after per os administration the N-acetylcysteine (NAC). Used were 20 Polish White Improved goats, selected from the flock of 60 animals. Within the selected goats distinguished were four groups according to somatic cell counts (SCC) of milk: group I – below 1×106, group II – 1×106-2×106, group III – 2×106-4×106 and group IV – above 4×106/ml. Concentrations of GSH, MDA and vitamin C of blond plasma were assessed just at start of the experiment and then after 7 days of daily administration of 12 mg NAC per kg body weight to goats. After 7 days of administering NAC to goats the plasma concentration of both MDA and GSH dropped and that of vitamin C increased. It is concluded that NAC administered per os increases the anti-oxidant capacity and may reduce the content of lipid peroxidation products in blood plasma of milking goats.

9

N-acetylcysteine modulates effect of the iron isomaltoside on peritoneal mesothelial cells

84%

Misian M., Baum E., Breborowicz A.

Journal of Physiology and Pharmacology

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2020

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tom 71

|

nr 3

10

Contribution of neuronal nitric oxide (NO) synthase to N-acetylcysteine-induced increase of NO synthase activity in the brain of normotensive and hypertensive rats

84%

Pechanova O., Kunes J., Dobesova Z., Vrankova S., Zicha J.

Journal of Physiology and Pharmacology

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2009

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tom 60

|

nr 4

21-25

The goal of our study was to determine a contribution of nNOS to the increase of brain NO synthase activity induced by chronic N-acetylcysteine (NAC) treatment. Young 4-week-old male Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were subjected to treatment with NAC (1.5 g/kg/day) for 8 weeks. At the end of experiment total NOS activity was determined in the brainstem and cerebellum with and without specific nNOS inhibitor S-methyl-L-thiocitrulline (SMTC, 10-6 mol/l) by measuring the formation of L-[3H] citrulline from L-[3H] arginine. Chronic NAC treatment had no effect on blood pressure (BP) of WKY, while it attenuated BP increase in young SHR. Total NOS activity was increased in the brainstem of SHR compared to WKY, but this strain difference was abolished by SMTC. Chronic NAC treatment of SHR increased total NOS activity by 32% in the brainstem and by 67% in the cerebellum. After the incubation of brainstem and cerebellum with SMTC there were no significant differences in NOS activity of NAC-treated rats compared to strain-matched controls. Taken together, nNOS seems to be responsible for the increase of total NOS activity in the brain of SHR. SMTC inhibited 86% and 70% of NAC-induced increase of total NOS activity in the brainstem and cerebellum, respectively. Thus, nNOS is responsible not only for strain differences but also for NAC-induced increase of total NOS activity in the brain.

11

The influence of pretreatment with N-acetylcysteine on serum cholinesterase activity and liver glutathione levels in rats intoxicated with chlorfenvinphos

84%

Lukaszewicz-Hussain A., Moniuszko-Jakoniuk J.

Polish Journal of Environmental Studies

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2004

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tom 13

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nr 1

This study was intendent to examine if N-acetylcysteine (NAC) changes liver GSH levels and influences ChE serum activity in rats intoxicated with chlorfenvinphos. The studies were conducted on male Wistar rats of 200±20 g body weight. One group of rats was pretreated with 0.1% water solution of NAC. NAC was administered in drinking water 24h before intoxication. The control groups received oil intragastrically by stomach tube in the amount of 0.1ml/100g (I), immediately or after NAC pretreatment. The experimental groups received oil solution of chlorfenvinphos in a dose of 0.02 LD50 or 0.1 LD50 immediately or after pretreatment with NAC. One and 24 hours after intoxication with chlorfenvinphos (or after NAC pretreatment) the blood samples were collected and livers were quickly removed and placed in iced 0.9% NaCl containing 0.16 mg/ml heparin. ChE serum activity and GSH level were measured. The results of this study demonstrated the changes in serum ChE activity and liver glutathione levels in the rats after administration of chlorfenvinphos at single doses. The results reported here indicate that NAC influences a decreased level of GSH in the liver of chlorfenvinphos-intoxicated rats and does not prevent ChE inhibition.

12

Effect of ciprofloxacin and N-acetylcysteine on bacterial adherence and biofilm formation on ureteral stent surfaces

67%

El-Feky M. A., El-Rehewy M. S., Hassan M. A., Abolella H. A., Abd El-Baky R. M., Gad G. F.

Polish Journal of Microbiology

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2009

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tom 58

|

nr 3

261-267

The aim of this study was to evaluate the effect of ciprofloxacin (CIP), N-acetylcysteine (NAC) alone and in combination on biofilm production and pre-formed mature biofilms on ureteral stent surfaces. Two strains each of Staphylococcus aureus, Staphylococcus epidermidis, Escherichia coli, Klehseilla pneumoniae, Pseudomonas aeruginosa and Proteus vulgaris, recently isolated from patients undergoing ureteral stent removal and shown to be capable of biofilm production, were used in this study. The inhibitory effects of ciprofloxacin, N-acetylcysteine and ciprofloxacin/N-acetylcysteine combination were determined by static adherence assay. Ciprofloxacin (MIC and 2 MIC) and N-acetylcysteine (2 and 4 mg/ml) inhibited biofilm production by ≥60% in all tested microorganisms. Disruption of pre-formed biofilms of all tested microorganisms was found to be ≥78% in the presence of ciprofloxacin (MIC and 2 MIC) and ≥62% in the presence of N-acetylcysteine (2 and 4 mg/ml), compared to controls. Ciprofloxacin/N-acetylcysteine showed the highest inhibitory effect on biofilm production (94-100%) and the highest disruptive effect on the pre-formed biofilms (86-100%) in comparison to controls. N-acetylcysteine was found to increase the therapeutic efficacy of ciprofloxacin by degrading the extracellular polysaccharide matrix of biofilms. These data are statistically significant. The inhibitory effects of ciprofloxacin and N-acetylcysteine on biofilm production were also verified by scanning electron microscope (SEM). In conclusion, Ciprofloxacin/N-acetylcysteine combinations have the highest inhibitory effect on biofilm production and the highest ability to eradicate pre-formed mature biofilms.

13

Oral N-acetylcysteine reverses hyperoxia-related cough suppression in guinea pigs

67%

Brozmanova M., Plevkova J., Bartos V., Plank L., Javorka M., Masar J., Tatar M.

Journal of Physiology and Pharmacology. Supplement

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2007

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tom 58

|

nr 5

14

Antipyretic activity of N-acetylcysteine

67%

Wrotek S., Jedrzejewski T., Potera-Kram E., Kozak W.

Journal of Physiology and Pharmacology

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2011

|

tom 62

|

nr 6

15

Nanoparticle carbon black driven DNA damage induces growth arrest and AP-1 and NFkappaB DNA binding in lung epithelial A549 cell line

67%

Mroz R. M., Schins R. P. F., Li H., Drost E. M., Macnee W., Donaldson K.

Journal of Physiology and Pharmacology. Supplement

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2007

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tom 58

|

nr 5

16

New therapeutic approaches to sickle cell disease: targeting RBC membrane oxidative damage

67%

Goodman S. R., Pace B. S., Shartava A.

Cellular and Molecular Biology Letters

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1998

|

tom 03

|

nr 4

In this brief review, we discuss evidence leading to the conclusion that diminished levels of reduced glutathione combined with increased oxygen radical production leads to oxidative damage to membrane proteins in sickle cell disease erythrocytes. Among these oxidatively damaged proteins are K+-channels (Gardos channel and K+-Cl--channel) and β-actin. Oxidative damage to the K+-channels leads to K+ leakage and H2O loss from light density reversibly sickled cells (RSCs). The resulting dense RSCs are primarily sickled in shape due to increased [HbS] and increased polymerization. The oxidation of β-actin converts the dense RSCs to dense irreversibly sickled cells (ISCs) as explained in our two step model. Furthermore, we discuss recent in vitro evidence that N-acetylcysteine (NAC) can block the formation of dense cells and ISCs by protecting the K+-channels and β-actin respectively from oxidative damage. Finally we describe an ongoing Phase II human trial to determine whether NAC can also lower dense cells and ISCs in vivo and, if so, result in fewer painful vasooclusive episodes.

17

N-acetycysteine effects on microsomal monooxygenase system and glutathione levels in rats after paracetamol and-or trichloroethylene single oral intoxication

67%

Plewka A., Nowaczyk G., Plewka D., Zielinska-Psuja B., Kowalowka-Zawieja J., Gawlik T., Garczorz W., Kaminski M., Orlowski J.

Acta Toxicologica

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2003

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tom 11

|

nr 2

18

Ochronny wplyw N-acetylocysteiny na prooksydacyjne i proapoptotyczne dzialanie tiuramu w komorkach V79 chomika chinskiego

59%

Kurpios-Piec D., Grosicka-Maciag E., Czeczot H., Szumilo M., Grzela T., Rahden-Staron I.

Bromatologia i Chemia Toksykologiczna

|

2010

|

tom 43

|

nr 3

354-361

Ograniczanie wyników

Influence of the microenvironment of thiol groups in low molecular mass thiols and protein on the reaction with methylglyoxal

New developments in the treatment of COPD: comparing the effects of inhaled corticosteroids and N-acetylcysteine

Influence of N-acetylcysteine on ICAM-1 expression and IL-8 release from endothelial and epithelial cells

Evaluation of selected protein biomarkers of renal function in rats with an experimental model of acute cyclophosphamide-induced cystitis treated with N-acetylcysteine

Aspects of using N-acetylcysteine in aflatoxicosis and its evaluation regarding some lipid peroxidation parameters in rabbits

N-acetylcysteine effectively diminished meconium-induced oxidative stress in adult rabbits

In vitro studies of the effect of theophylline and/or N-acetylcysteine on redox homeostasis and ketogenesis in rat hepatocytes

The oxidative status of milking goats after per os administration of N-acetylcysteine

N-acetylcysteine modulates effect of the iron isomaltoside on peritoneal mesothelial cells

Contribution of neuronal nitric oxide (NO) synthase to N-acetylcysteine-induced increase of NO synthase activity in the brain of normotensive and hypertensive rats

The influence of pretreatment with N-acetylcysteine on serum cholinesterase activity and liver glutathione levels in rats intoxicated with chlorfenvinphos

Effect of ciprofloxacin and N-acetylcysteine on bacterial adherence and biofilm formation on ureteral stent surfaces

Oral N-acetylcysteine reverses hyperoxia-related cough suppression in guinea pigs

Antipyretic activity of N-acetylcysteine

Nanoparticle carbon black driven DNA damage induces growth arrest and AP-1 and NFkappaB DNA binding in lung epithelial A549 cell line

New therapeutic approaches to sickle cell disease: targeting RBC membrane oxidative damage

N-acetycysteine effects on microsomal monooxygenase system and glutathione levels in rats after paracetamol and-or trichloroethylene single oral intoxication

Ochronny wplyw N-acetylocysteiny na prooksydacyjne i proapoptotyczne dzialanie tiuramu w komorkach V79 chomika chinskiego