Effects of N-methyl hexanoylhydroxamic acid (NMHH) and myoglobin on endothelial damage by hydrogen peroxide
| Autor: | C A Rice Evans, Michael J. Davies, Clifford S. Collis, Wei Yang, D.P. De Bono |
|---|---|
| Rok vydání: | 1994 |
| Předmět: |
Antioxidant
Endothelium Physiology medicine.medical_treatment Hydroxamic Acids Antioxidants chemistry.chemical_compound Physiology (medical) Lactate dehydrogenase medicine Animals Drug Interactions Hydrogen peroxide Cell damage Cells Cultured Myoglobin Cell growth Hydrogen Peroxide medicine.disease Molecular biology medicine.anatomical_structure chemistry Biochemistry Cattle Endothelium Vascular Formazan Cardiology and Cardiovascular Medicine Cell Division |
| Zdroj: | Cardiovascular Research. 28:1641-1646 |
| ISSN: | 0008-6363 |
| DOI: | 10.1093/cvr/28.11.1641 |
| Popis: | Objective: The aim was to investigate the interaction of the novel antioxidant N-methyl hexanoylhydroxamic acid (NMHH) with myoglobin in protecting endothelial cells against H2O2 mediated damage. Methods: Cultured bovine aortic endothelial cells were exposed to 50–100 μM H2O2 for 10–60 min with and without NMHH and/or myoglobin, and immediate or delayed damage was assessed by lactate dehydrogenase release, 3H adenine uptake, a tetrazolium reduction assay, and microscopy. Results: Brief exposure to low concentrations of H2O2 caused cell damage, for which the tetrazolium reduction assay was the most sensitive assay, and inhibited subsequent cell division. NMHH in concentrations from 50 to 200 μM protected against damage provided it was present at the time of adding H2O2, and the effect was markedly potentiated by 10 μM oxymyoglobin, which had little protective effect alone. Conclusions: NMHH is an effective antioxidant which is markedly potentiated by low concentrations of oxymyoglobin. Oxymyoglobin may potentiate NMHH by scavenging H2O2 through the rapid formation of ferrylmyoglobin, which is then reduced by NMHH. This synergism may be particularly relevant to the protection of myoglobin-rich cells such as myocytes. Cardiovascular Research 1994; 28 :1641-1646 |
| Databáze: | OpenAIRE |
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