Oksidativni stres u akutnoj blast povredi pluća je nezavisan od enzimske sinteze azot-monoksida
| Autor: | V Savic, Stojanov Marina, Cernak Ibolja, Kotur-Stevuljevic Jelena, Prokic Vera |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
chemistry.chemical_classification
0303 health sciences General Veterinary biology Superoxide Glutathione peroxidase Lung injury Pharmacology Malondialdehyde Nitric oxide Lipid peroxidation Nitric oxide synthase Superoxide dismutase 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine acute lung injury chemistry Biochemistry nitric oxide blast injury biology.protein oxidative stress 030217 neurology & neurosurgery 030304 developmental biology |
| Zdroj: | Acta veterinaria |
| ISSN: | 0567-8315 |
| Popis: | Lung trauma has been considered to be one of the vital injuries induced by explosion-generated blast overpressure. Conflicting evidence exists as to whether nitric oxide plays a crucial role in acute lung injury induced by blast. Data presented in this study demonstrate that local exposure of midthoracic region to moderate-level blast overpressure significantly enhanced lipid peroxidation product malondialdehyde and superoxide anion generation in rabbit's lungs 30 minutes after exposure, whereas the activities of antioxidant enzymes (superoxide dismutase, glutathione peroxidase) activity showed parallel increase. NG-nitro-L-arginine methyl ester, a non-specific inhibitor of nitric oxide synthase (NOS), had no effects on the measured parameters suggesting that oxidative stress induced by blast exposure might be independent from NOS. Smatra se da je povreda pluća jedna od najvažnijih povreda do kojih dolazi delovanjem blast talasa generisanog na mestu eksplozije. Do danas ne postoji definitivan stav da li azot-monoksid ima bitnu ulogu u akutnoj blast povredi pluća. Rezultati ove studije pokazuju da lokalno delovanje blast nadpritiska srednje jačine na središnji deo toraksa dovodi do povećanog stvaranja malondialdehida, produkta lipidne peroksidacije kao i povećanog generisanja superoksidnog anjona, 30 minuta posle traume. Istovremeno, dolazi do smanjenja aktivnosti antioksidativnih enzima (superoksid-dizmutaze i glutation-peroksidaze) u plućnom tkivu kunića. NG-nitro-L-arginin-metil estar (L-NAME), nespecifični inhibitor enzima azot-monoksid sintaze (NOS) nije imao efekta na određivane parametere, što ukazuje daje oskidativni stres indukovan blast povredom verovatno nezavisan od aktivnosti enzima NOS. |
| Databáze: | OpenAIRE |
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