4-Hydroxynonenal induces oxidative stress and death of cultured spinal cord neurons.
作者： Andrzej Malecki , Rosario Garrido , Mark P. Mattson , Bernhard Hennig , Michal Toborek
DOI: 10.1046/J.1471-4159.2000.0742278.X
关键词: Viability assay 、 Spinal cord 、 Internal medicine 、 Anesthesia 、 4-Hydroxynonenal 、 Endocrinology 、 Lipid peroxidation 、 Arachidonic acid 、 Central nervous system 、 Chemistry 、 Oxidative stress 、 Calcium in biology
摘要: Primary spinal cord trauma can trigger a cascade of secondary processes leading to delayed and amplified injury neurons. Release fatty acids, in particular arachidonic acid, from cell membranes is believed contribute significantly these events. Mechanisms acid-induced neurons may include lipid peroxidation. One the major biologically active products acid peroxidation 4-hydroxynonenal (HNE). The levels HNE-protein conjugates cultured increased dose-dependent manner after 24-h exposure acid. To study cellular effects HNE, were treated with different doses oxidative stress, intracellular calcium, viability determined. A 3-h 10 microM HNE caused approximately 80% increase stress 30% elevation calcium. Exposure dramatic loss viability, indicated by decrease MTS [3-(4, 5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-s ulfophenyl)- 2H-tetrazolium, inner salt] conversion. cytotoxic effect was diminished pretreating ebselen or N-acetylcysteine. These data support hypothesis that formation be responsible, at least part, for membrane-released
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