Metabolomics analysis implies noninvolvement of the kynurenine pathway neurotoxins in the interferon-gamma- induced neurotoxicity of adult human astrocytes

Emerging evidence indicates that the kynurenine pathway (KP) contributes to neurodegenerative diseases associated with glial activation. Interferon (IFN)-γ is a potent activator of indole-2,3-dioxygenase, the first and rate-limiting enzyme of the KP. Our previous studies have shown that adult human astrocytes become neurotoxic when activated by IFN-γ. We now used high performance liquid chromatographymass spectrometry in both the positive- and negative- ionization mode of electrospray interface, to examine whether the IFN-γ-activated adult human astrocytes secrete neurotoxic KP metabolites, such as quinolinic acid (QUIN), 3-hydroxykynurenine (3-HK) and 3-hydroxyanthranilic acid (3-HAA). Kynurenine was detected in cell culture supernatants of IFN-γ-stimulated astrocytes, but not in supernatants of unstimulated astrocytes. On the other hand, QUIN, 3-HK and 3-HAA were not detected in samples from either IFN-γ- stimulated or unstimulated cells. These results indicate that the KP may not be involved in the IFN-γ-induced neurotoxicity of adult human astrocytes. Therefore, neurotoxins other than KP metabolites could be responsible for the IFN-γ-induced astrocyte neurotoxicity.


For more details Abstract: http://www.jneuropsychiatry.org/abstract/metabolomics-analysis-implies-noninvolvement-of-the-kynurenine-pathway-neurotoxins-in-the-interferongamma-induced-neurot-11917.html

Full Text Link: http://www.jneuropsychiatry.org/peer-review/metabolomics-analysis-implies-noninvolvement-of-the-kynurenine-pathway-neurotoxins-in-the-interferongamma-induced-neurotoxicity-of.html

PDF Link: http://www.jneuropsychiatry.org/peer-review/metabolomics-analysis-implies-noninvolvement-of-the-kynurenine-pathway-neurotoxins-in-the-interferongamma-induced-neurot.pdf

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