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NO-Mediated Neurotoxicity

Because glutamate acting via NMDA receptors stimulates NO formation, it would be logical to expect that NOS neurons would be the first cells to succumb to excess NMDA receptor stimulation. However, NOS neurons are resistant to NMDA and NO neurotoxicity (Dawson and Snyder, 1994). It is unknown why NOS neurons are resistant to NMDA and NO neurotoxicity, but they probably possess protective factors that render them relatively resistant to the toxic NO environment they create. NOS neurons within the striatum are enriched in manganese SOD, and SOD in these neurons may [Pg.334]

Although nNOS is constitutively expressed, under some pathological insults nNOS can be induced in certain cells and is expressed after new protein synthesis (Wu et al., 1994). In spinal cord motoneurons nNOS is [Pg.335]


NO, in large amounts, also causes the autoribosylation of glyceralde-hyde-3-phosphate dehydrogenase, which inactivates this glycolytic enzyme (Dimmeler et al.,1992). Moreover, NO activates ADP-ribosyltransferases, this process being enhanced by previous nitrosylation of the enzyme by NO (Briine and Lapetina, 1989 Dimmeler et al., 1992). This pathway may be involved in the NO-mediated neurotoxic actions (Zhang et al., 1994). [Pg.115]


See other pages where NO-Mediated Neurotoxicity is mentioned: [Pg.515]    [Pg.331]    [Pg.334]   


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