Wyniki wyszukiwania

1

The role of reactive nitrogen species and cigarette smoke in activation of transcription factor NF-kappaB and implication to inflammatory processes

100%

Bar-Shai M., Hasnis E., Wiener-Megnazi Z., Reznick A. Z.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 4

39-44

Using the electromobility shift assay (EMSA) in the rat myoblast system, the activation of transcription factor NF-B by reactive nitrogen species was evaluated. Two distinct patterns of activation were demonstrated. Whereas NO donor, SNAP, activated NF-B in the classical pathway, which led to a transient response, NF-B activation by peroxynitrite donor, SIN-1, was mediated by an alternative pathway, which has been demonstrated in previous works to involve tyrosine nitration of the NF-B inhibitory protein I-Balpha. This led to a constitutive non-transient activation of NF-B and a prolonged inflammatory reaction. Lymphocytes exposed to mild intensity of cigarette smoke for 8 h, which activated NF-B, exhibited a decrease in the fraction of apoptotic cells from 27% to 19% compared with lymphocytes exposed to atmospheric air, using the FACS Annexin V assay. This also has been shown in previous works to be mediated by peroxynitrite. Thus, mild exposure to cigarette smoke induces NF-B activation, which can attenuate apoptosis in human lymphocytes and lead to prolonged inflammatory response. A possible proposed mechanism for induction of chronic inflammatory response may involve peroxynitrite-induced activation of NF-B.

2

Inhibition of salivary amylase activity by cigarette smoke aldehydes

100%

Weiner D., Levy Y., Khankin E. V., Reznick A. Z.

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

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nr 6

727-737

3

Cigarette smoke extract influences intracellular calcium concentration in A549 cells

100%

Yoo Y.-M., Jung E.-M., Jeon B.-H., Tran D. N., Jeung E.-B.

Journal of Physiology and Pharmacology

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2020

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tom 71

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nr 5

4

Chronic obstructive pulmonary disease: an update on nuclear signaling related to inflammation and anti-inflammatory treatment

100%

Mroz R. M., Holownia A., Chyczewska E., Braszko J. J.

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

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nr 6

35-42

5

DNA damage and alterations of gene expression in chronic-degenerative diseases

100%

Izzotti A.

Acta Biochimica Polonica

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2003

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tom 50

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nr 1

Chronic-degenerative diseases (CDD) recognise a variety of exogenous and endogenous risk factors interacting with the organism for many years before disease onset. We applied genomic and postgenomic molecular analyses in experimental models characterised by different contribution of exogenous and endogenous CDD risk factors. Exposure of mice to halogen light for 28 days resulted in induction of cyclobutane dimers and oxidative DNA damage in the skin. Evaluation of postgenomic alterations by cDNA arrays revealed upregulation of DNA repair pathways, increased cell division rate and protooncogenes transcription, resulting in skin tumors, 1 year later. Exposure of p53-/+ mutant mice to cigarette smoke (CS) for 28 days induced DNA adducts formation in the lung. Postgenomic alterations included decreased apoptosis and increased cell division, as compared to CS-exposed wild type mice. These phenomena resulted in lung tumors, 9 months later. Transplacental exposure of mouse foetuses to cigarette smoke induced DNA adduct formation in the liver. cDNA arrays analyses demonstrated decreased cell division, apoptosis increase, and tissue hypoxia. These phenomena resulted in growth retardation of the whole organism. Molecular alterations were investigated in human trabecular meshwork, the non-replicating ocular epithelia involved in the pathogenesis of chronic degenerative glaucoma. Results indicate increased oxidative DNA damage in glaucoma patients as compared to unaffected controls.

6

Low activity of the ahr gene in the ahr dd C57BL congenic mice does not prevent the depression of reproductive capacity observed as result of cigarette smoke exposure

100%

Pawlak A. L., Strauss E., Florek E.

Folia Histochemica et Cytobiologica. Supplement

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2001

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tom 39

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nr 1

7

Increased pro-inflammatory activity and impairment of human monocyte differentiation induced by in vitro exposure to cigarette smoke

80%

Lerner L., Weiner D., Katz R., Reznick A. Z., Pollack S.

Journal of Physiology and Pharmacology. Supplement

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2009

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tom 60

|

nr 5

8

A low vitamin A status increases the susceptibility to cigarette smoke-induced lung emphysema in C57BL/6J mice

80%

Van Eijl S., Mortaz E., Versluis C., Nijkamp F. P., Folkerts G., Bloksma N.

Journal of Physiology and Pharmacology

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2011

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tom 62

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nr 2

Chronic obstructive pulmonary disease (COPD) is characterized by chronic airway inflammation. Cigarette smoke has been considered a major player in the pathogenesis of COPD. The inflamed airways of COPD patients contain several inflammatory cells. Vitamin A metabolites have been implicated in the repair of lung damage. Exposure to cigarette smoke has been shown to depress levels of retinol in lungs of rats. The purpose of this study was to investigate if a low, but not deficient, vitamin A status potentiated susceptibility to the development of cigarette smoke-induced lung emphysema in mice. Mice were bred that were the offspring’s of 3 generations of mice that were fed a purified diet containing low levels of vitamin A and exposed to cigarette smoke for 3 months, every weekday. Then, levels of 9-cis, 13-cis, and all-trans retinoic acid, retinol and retinyl palmitate were measured in plasma, liver and right lung lobe. The left lung lobe was used to assess mean linear intercept (Lm), as a measure of smoke-induced lung damage. Average feed intakes were not different between treatment groups. We show that both retinol and retinyl palmitate levels were dramatically decreased in the storage organs of mice on the low vitamin A diet (retinol 2-fold in both lung and liver, and retinyl palmitate 5- fold in lung) which shows that the depletion was successful. However, this treatment did not result in the development of lung emphysema. However, smoke exposure led to a significant increase in Lm in mice with a low vitamin A status compared to the room air-breathing controls. Lung levels of acid retinoids were similar in all mice, irrespective of diet or smoke exposure. Concluding, a low vitamin A status increases the susceptibility to the development of cigarette smoke-induced lung emphysema, possibly because of decreased anti-oxidant capacity in the lungs due to locally reduced retinol and retinyl palmitate levels. These observations indicate that human populations with a low vitamin A status and a high prevalence of smoking may be at increased risk of developing lung emphysema.

9

Mechanisms underlying cigarette smoke-induced NF-kappaB activation in human lymphocytes: the role of reactive nitrogen species

80%

Hasnis E., Bar-Shai M., Burbea Z., Reznick A. Z.

Journal of Physiology and Pharmacology. Supplement

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2007

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tom 58

|

nr 5

10

Effects of cigarette smoke on the lung and systemic immunity

80%

Domagala-Kulawik J.

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

|

nr 6

19-34

11

Distribution of selected metals in pregnant and foetal rat tissues under exposure to cigarette smoke

80%

Czekaj P., Palasz A., Donica E., Florek E.

Acta Poloniae Toxicologica

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2002

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tom 10

|

nr 2

12

An assessment of the selected morphometric parameters and levels of nicotine and cotinine in placentae of smoking mothers

80%

Wielgus E., Celinski R., Pawlicki K., Sybirska H., Kaminski M.

Acta Toxicologica

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2003

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tom 11

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nr 2

13

Effect of passive smoking on blood antioxidant status in school children

80%

Jendryczko A., Szpyrka G., Gruszczynski J., Kozowicz M.

Polish Journal of Environmental Studies

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1992

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tom 01

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nr 3

Despite similar vitamin E concentrations, erythrocytes in children of smoking parents have an increased tendency to peroxidize in vitro compared with children of nonsmoking parents. The increased susceptibility to erythrocyte peroxidation in children of smoking parents may reflect lower erythrocyte glucose-6-phosphate dehydrogenase, glutathione peroxidase and superoxide dimutase activities. Children of smoking parents seem to be under sustained oxidant stress with increased plasma-conjugated dienes, dehydroascorbate and oxidized glutathione concentrations. Infections of the lower respiratory tract were more frequent in children of smoking parents.

14

Sesbania grandiflora diminishes oxidative stress and ameliorates antioxidant capacity in liver and kidney of rats exposed to cigarette smoke

71%

Ramesh T., Sureka C., Bhuvana S., Hazeena Begum V.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 4

467-476

Cigarette smoke is a major risk factor for many chronic diseases. However, it may be possible to relieve the smoke-induced damage by increasing the defensive system. In this study, we planned to evaluate the protective mechanism of Sesbania grandiflora (S. grandiflora) leaves against cigarette smoke-induced oxidative damage in liver and kidney of rats. Adult male Wistar-Kyoto rats were exposed to cigarette smoke for a period of 90 days and consecutively treated with S. grandiflora aqueous suspension (SGAS, 1000 mg/kg body weight per day by oral gavage) for a period of 3 weeks. Hepatic marker enzymes like aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP), as well as renal markers such as urea and creatinine were analysed in serum. Lipid peroxidation marker mainly thiobarbituric acid reactive substances (TBARS) and antioxidant enzymes namely superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST) and glucose-6-phosphate dehydrogenase (G6PDH) activities and non-enzymatic antioxidants such as reduced glutathione, ascorbic acid and a-tocopherol levels were studied. In addition, micronutrients mainly copper (Cu), zinc (Zn), manganese (Mn) and selenium (Se) levels were analyzed in liver and kidney of rats exposed to cigarette smoke. The results indicated that SGAS significantly decreased the elevated hepatic, renal and lipid peroxidation markers and ameliorated the diminished antioxidant levels while restored the hepatic and renal architecture in cigarette smoke-exposed rats. This study concludes that S. grandiflora leaves restrain cigarette smoke-induced oxidative damage in liver and kidney of rats.

15

Cigarette smoke-induced NF-kappaB activation in human lymphocytes: the effect of low and high exposure to gas phase of cigarette smoke

71%

Hasnis E., Bar-Shai M., Burbea Z., Reznick A. Z.

Journal of Physiology and Pharmacology. Supplement

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2007

|

tom 58

|

nr 5

16

Wplyw indywidualnego sposobu palenia papierosow na retencje tlenku wegla w ukladzie oddechowym palaczy czynnych i jej ocena w swietle kryteriow srodowiskowych

71%

Czogala J.

Roczniki Państwowego Zakładu Higieny

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2003

|

tom 54

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nr 4

383-392

Oznaczano tlenek węgla w dymie papierosowym wdychanym przez indywidualnych palaczy i w powietrzu przez nich wydychanym, wyznaczając bezwzględną i względną retencję tego związku w ich ustroju. Wielkość pobieranych przez nich dawek tlenku węgla oceniano w kategoriach narażenia środowiskowego.

17

Effect of smoking on concentrations of cadmium, copper, iron and zinc in early transitional human milk

70%

Milnerowicz H., Chmarek M.

Acta Toxicologica

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2003

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tom 11

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nr 2

Ograniczanie wyników

The role of reactive nitrogen species and cigarette smoke in activation of transcription factor NF-kappaB and implication to inflammatory processes

Inhibition of salivary amylase activity by cigarette smoke aldehydes

Cigarette smoke extract influences intracellular calcium concentration in A549 cells

Chronic obstructive pulmonary disease: an update on nuclear signaling related to inflammation and anti-inflammatory treatment

DNA damage and alterations of gene expression in chronic-degenerative diseases

Low activity of the ahr gene in the ahr dd C57BL congenic mice does not prevent the depression of reproductive capacity observed as result of cigarette smoke exposure

Increased pro-inflammatory activity and impairment of human monocyte differentiation induced by in vitro exposure to cigarette smoke

A low vitamin A status increases the susceptibility to cigarette smoke-induced lung emphysema in C57BL/6J mice

Mechanisms underlying cigarette smoke-induced NF-kappaB activation in human lymphocytes: the role of reactive nitrogen species

Effects of cigarette smoke on the lung and systemic immunity

Distribution of selected metals in pregnant and foetal rat tissues under exposure to cigarette smoke

An assessment of the selected morphometric parameters and levels of nicotine and cotinine in placentae of smoking mothers

Effect of passive smoking on blood antioxidant status in school children

Sesbania grandiflora diminishes oxidative stress and ameliorates antioxidant capacity in liver and kidney of rats exposed to cigarette smoke

Cigarette smoke-induced NF-kappaB activation in human lymphocytes: the effect of low and high exposure to gas phase of cigarette smoke

Wplyw indywidualnego sposobu palenia papierosow na retencje tlenku wegla w ukladzie oddechowym palaczy czynnych i jej ocena w swietle kryteriow srodowiskowych

Effect of smoking on concentrations of cadmium, copper, iron and zinc in early transitional human milk