Indole-3-Pyruvic Acid as a Direct Precursor of Kynurenic Acid

Politi, V.; Lavaggi, M. V.; Stazio, G. Di; Margonelli, Andrea

doi:10.1007/978-1-4684-5952-4_57

Cited by 28 publications

(17 citation statements)

References 6 publications

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“…KYNA is also generated from TRP via tryptophan aminotransferase and ROS (Politi et al 1991(Politi et al , 1996. In contrast with QUIN, KYNA might have a neuroprotective effect: in excitotoxic, ischaemia-induced and neuronal conditions it is able to prevent neuronal death (Smith et al 1993;Gigler et al 2007).…”

Section: Effects Of Kynurenines On Brainstem Structures Related To MImentioning

confidence: 98%

Where does a migraine attack originate? In the brainstem

et al. 2012

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Migraine is a common, paroxysmal, highly disabling primary headache disorder. The origin of migraine attacks is enigmatic. Numerous clinical and experimental results suggest that the activation of distinct brainstem nuclei is crucial in its pathogenesis, but the primary cause of this activation is not fully understood. We conclude that the initialization of a migraine attack can be explained as an altered function of the neuronal elements of the brainstem nuclei. In light of our findings and the literature data, we can assume that migraine is a subcortical disorder of a specific brainstem area.

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Section: Effects Of Kynurenines On Brainstem Structures Related To MImentioning

confidence: 98%

Where does a migraine attack originate? In the brainstem

et al. 2012

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“…It is synthesized directly from L-KYN in the astrocytes and neurones [67, 91] enzymatically by the action of kynurenine aminotransferases (KATs) [92, 93], mitochondrial aspartate aminotransferase [94] and hemoperoxidases, or non-enzymatically by reactive oxygen species (ROS) [95]. Beyond this route KYNA can be produced from TRP on an additional pathway by tryptophan aminotransferase and ROS [96, 97]. Similarly to that of QUIN, the concentration of KYNA in the human brain is in the nanomolar range [98], which changes in pathological circumstances, including neurological disorders.…”

Section: Kynurenine Metabolitesmentioning

confidence: 99%

Kynurenine Metabolites and Migraine: Experimental Studies and Therapeutic Perspectives

Fejes¹,

Párdutz²,

Toldi³

et al. 2011

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Migraine is one of the commonest neurological disorders. Despite intensive research, its exact pathomechanism is still not fully understood and effective therapy is not always available. One of the key molecules involved in migraine is glutamate, whose receptors are found on the first-, second- and third-order trigeminal neurones and are also present in the migraine generators, including the dorsal raphe nucleus, nucleus raphe magnus, locus coeruleus and periaqueductal grey matter. Glutamate receptors are important in cortical spreading depression, which may be the electrophysiological correlate of migraine aura. The kynurenine metabolites, endogenous tryptophan metabolites, include kynurenic acid (KYNA), which exerts a blocking effect on ionotropic glutamate and α7-nicotinic acetylcholine receptors. Thus, KYNA and its derivatives may act as modulators at various levels of the pathomechanism of migraine. They can give rise to antinociceptive effects at the periphery, in the trigeminal nucleus caudalis, and may also act on migraine generators and cortical spreading depression. The experimental data suggest that KYNA or its derivatives might offer a novel approach to migraine therapy.

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“…The presence of KAT I and KAT II, two main enzymes that synthesize KYNA, is well documented in the retina. 18 Other possibilities for KYNA formation are (1) transamination of tryptophan to indole-3-pyruvic acid, followed by its oxidation by free radicals, 29 and (2) nonenzymatic spontaneous deamination of kynurenine 30 followed by oxidation with H 2 O 2 and reactive oxygen species. 19 It has been documented that significant amounts of kynurenines in the lens are bound to proteins, thus forming a filter that protects the retina from UV light.…”

Section: Discussionmentioning

confidence: 99%