Inactivation of protease nexin-1 by xanthine oxidase-derived free radicals
Identifieur interne : 001770 ( PascalFrancis/Curation ); précédent : 001769; suivant : 001771Inactivation of protease nexin-1 by xanthine oxidase-derived free radicals
Auteurs : F. N. Bolkenius [France] ; D. MonardSource :
- Neurochemistry international [ 0197-0186 ] ; 1995.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Neuronal viability is affected by reactive oxygen species. Lipid peroxidation is often defined as a major reason for cellular breakdown. Additionally, certain indispensable proteins are possible targets for excessively formed reactive oxygen species. Evidence is given here that protease nexin-1 (PN-1), an endogenous thrombin inhibitor and neurite outgrowth promoter, is inactivated by xanthine oxidase-derived free radicals. Varying protection by superoxide dismutase and catalase was observed, depending on the reaction conditions. The water-soluble α-analogues-analogues MDL 74,406 (R(+ )-3,4-dihydro-6-hydroxy-N,N,N2,5,7,8-heptamethyl-2H-1-benzopyran-2-ethanaminium 4-methylbenzenesulfonate), MDL 74,180DA (2,3dihydro-2,2,4,6,7-pentamethyl-3-(4-methyl-piperazino)-I-benzofuran-5-ol dihydro-chloride) and trolox also protected PN-I. Neurodegeneration may be triggered by oxidative inactivation of protease inhibitors such as PN-I. Protection of PN-1 in Alzheimer's or Parkinson's diseases, could be a possible target for a therapeutic function of antioxidants in these diseases.
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Pascal:95-0402708Le document en format XML
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<author><name sortKey="Bolkenius, F N" sort="Bolkenius, F N" uniqKey="Bolkenius F" first="F. N." last="Bolkenius">F. N. Bolkenius</name>
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<author><name sortKey="Monard, D" sort="Monard, D" uniqKey="Monard D" first="D." last="Monard">D. Monard</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Inactivation of protease nexin-1 by xanthine oxidase-derived free radicals</title>
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<front><div type="abstract" xml:lang="en">Neuronal viability is affected by reactive oxygen species. Lipid peroxidation is often defined as a major reason for cellular breakdown. Additionally, certain indispensable proteins are possible targets for excessively formed reactive oxygen species. Evidence is given here that protease nexin-1 (PN-1), an endogenous thrombin inhibitor and neurite outgrowth promoter, is inactivated by xanthine oxidase-derived free radicals. Varying protection by superoxide dismutase and catalase was observed, depending on the reaction conditions. The water-soluble α-analogues-analogues MDL 74,406 (R(+ )-3,4-dihydro-6-hydroxy-N,N,N2,5,7,8-heptamethyl-2H-1-benzopyran-2-ethanaminium 4-methylbenzenesulfonate), MDL 74,180DA (2,3dihydro-2,2,4,6,7-pentamethyl-3-(4-methyl-piperazino)-I-benzofuran-5-ol dihydro-chloride) and trolox also protected PN-I. Neurodegeneration may be triggered by oxidative inactivation of protease inhibitors such as PN-I. Protection of PN-1 in Alzheimer's or Parkinson's diseases, could be a possible target for a therapeutic function of antioxidants in these diseases.</div>
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