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1.
The Korean Journal of Internal Medicine ; : 216-223, 2013.
Article Dans Anglais | WPRIM | ID: wpr-123029

Résumé

BACKGROUND/AIMS: Ozone is an environmentally reactive oxidant, and pycnogenol is a mixture of flavonoid compounds extracted from pine tree bark that have antioxidant activity. We investigated the effects of pycnogenol on reactive nitrogen species, antioxidant responses, and airway responsiveness in BALB/c mice exposed to ozone. METHODS: Antioxidant levels were determined using high performance liquid chromatography with electrochemical detection. Nitric oxide (NO) metabolites in bronchoalveolar lavage (BAL) fluid from BALB/c mice in filtered air and 2 ppm ozone with pycnogenol pretreatment before ozone exposure (n = 6) were quantified colorimetrically using the Griess reaction. RESULTS: Uric acid and ascorbic acid concentrations were significantly higher in BAL fluid following pretreatment with pycnogenol, whereas gamma-tocopherol concentrations were higher in the ozone exposed group but were similar in the ozone and pycnogenol pretreatment groups. Retinol and gamma-tocopherol concentrations tended to increase in the ozone exposure group but were similar in the ozone and pycnogenol pretreatment groups following ozone exposure. Malonylaldehyde concentrations increased in the ozone exposure group but were similar in the ozone and pycnogenol plus ozone groups. The nitrite and total NO metabolite concentrations in BAL fluid, which parallel the in vivo generation of NO in the airways, were significantly greater in the ozone exposed group than the group exposed to filtered air, but decreased with pycnogenol pretreatment. CONCLUSIONS: Pycnogenol may increase levels of antioxidant enzymes and decrease levels of nitrogen species, suggesting that antioxidants minimize the effects of acute ozone exposure via a protective mechanism.


Sujets)
Animaux , Femelle , Souris , Antioxydants/pharmacologie , Acide ascorbique/métabolisme , Hyperréactivité bronchique/induit chimiquement , Liquide de lavage bronchoalvéolaire/composition chimique , Bronchoconstriction/effets des médicaments et des substances chimiques , Modèles animaux de maladie humaine , Flavonoïdes/pharmacologie , Exposition par inhalation , Poumon/effets des médicaments et des substances chimiques , Malonaldéhyde/métabolisme , Souris de lignée BALB C , Monoxyde d'azote/métabolisme , Stress oxydatif/effets des médicaments et des substances chimiques , Ozone , Acide urique/métabolisme , Rétinol/métabolisme , alpha-Tocophérol/métabolisme
2.
Indian J Biochem Biophys ; 2009 Aug; 46(4): 342-344
Article Dans Anglais | IMSEAR | ID: sea-135215

Résumé

Rheumatoid arthritis (RA) characterized by local and systemic effects of inflammation has a wide range of biochemical markers implicated directly or indirectly to its pathogenesis. In the present study, homocysteine, cortisol, adenosine deaminase (ADA), ferritin, malondialdehyde (MDA) and -tocopherol in serum of RA patients and healthy individuals were estimated to assess if they contribute to the disease process. The markers of disease activity such as erythrocyte sedimentation rate (ESR) and rheumatoid factor (RF) were also measured. The study group included a total of 45 subjects, including 30 RA patients and the rest being healthy individuals. RA group showed a significant increase in the levels of homocysteine, ADA and MDA, and a significant decrease in α-tocopherol compared to the healthy individuals. However, cortisol and ferritin levels did not show any significant change. Also, there was no significant correlation between the studied serum markers and markers of disease activity. Our results indicate that these biochemical markers contribute independently to the pathogenesis of RA.


Sujets)
Adenosine deaminase/métabolisme , Adulte , Sujet âgé , Polyarthrite rhumatoïde/sang , Marqueurs biologiques/métabolisme , Sédimentation du sang , Femelle , Ferritines/métabolisme , Homocystéine/métabolisme , Humains , Hydrocortisone/métabolisme , Inflammation , Mâle , Malonaldéhyde/métabolisme , Adulte d'âge moyen , alpha-Tocophérol/métabolisme
3.
Indian J Exp Biol ; 2004 Jun; 42(6): 570-4
Article Dans Anglais | IMSEAR | ID: sea-63170

Résumé

The therapeutic efficacy of chelating agents CaNa3DTPA (calcium trisodium diethylene triamine penta acetic acid) and Tiron (sodium-4,5-dihydroxy-1,3-benzene disulphonate) with and without antioxidant, alpha-Tocopherol was evaluated in the treatment of beryllium-induced toxicity in female albino rats. The animals were exposed to beryllium (as beryllium nitrate) at a dose of 1 mg/kg (ip) once a day for 28 consecutive days followed by chelation therapy by CaNa3DTPA (0.1 mM/kg, ip) and Tiron (471 mg/kg, ip) with and without alpha-Tocopherol (25 mg/kg, orally) for 5 consecutive days after toxicant administration. Tissue biochemistry revealed severe alterations in liver and kidney. A significant fall in total protein and glycogen contents, alkaline phosphatase, adenosine tri-phosphatase and succinic dehydrogenase level was noticed. On the contrary, an elevation in acid phosphatase was recorded. The significant rise in hepatic lipid peroxidation and decreased level of hepatic reduced glutathione showed toxicity due to beryllium. CaNa3DTPA with alpha-Tocopherol showed moderate therapeutic efficacy while Tiron in combination with alpha-Tocopherol exerted statistically more beneficial effects to reverse biochemical alterations in different variables altered due to beryllium intoxication.


Sujets)
1,2-Dihydroxy-benzène-3,5-disulfonate de disodium/pharmacologie , Adenosine triphosphatases/métabolisme , Phosphatase alcaline/métabolisme , Animaux , Antioxydants/pharmacologie , Béryllium/pharmacologie , Chélateurs/pharmacologie , Association de médicaments , Femelle , Glutathion/métabolisme , Glycogène/métabolisme , Rein/effets des médicaments et des substances chimiques , Peroxydation lipidique , Foie/effets des médicaments et des substances chimiques , Magnésium/métabolisme , Nitrates/pharmacologie , Acide pentétique/pharmacologie , Rats , Rat Sprague-Dawley , Succinate Dehydrogenase/métabolisme , Facteurs temps , alpha-Tocophérol/métabolisme
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