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Kynurenic acid (KYNA) is a metabolite of tryptophan exerting a number of positive actions in rodents, including anti-inflammatory and antioxidative activity. In this study, an analysis of KYNA concentration in a number of honeys, including chestnut honey, as well as chestnut tree parts and products made from chestnuts, was performed.
It was found that the content of KYNA in chestnut honey is exceptionally high, in comparison both with other types of honey investigated and with selected chestnut products, such as peeled fruit, crème, puree and flour. It was also detected that the content of KYNA in chestnut tree male fl ower is several times higher than in female flower. Our results indicate that chestnut honey, which is predominantly produced in Mediterranean countries, contains very high amounts of KYNA and can be an important source of dietary KYNA.
That immediately brought to mind one of my fondest memories, involving my daughter when she was just a toddler of one: taking her with me on the short walk to check the mail. I live in a small enclave of homes in which all the mailboxes are together in a central location, less than a minute’s walk from my front door
Kynurenic acid (KYNA) is a substance whose presence was first demonstrated in urine (Liebig,1853). It is formed enzymatically via the kynurenine pathway from tryptophan. While the main end-product of kynurenine catabolism is nicotinamide adenosine dinucleotide (NAD+), KYNA is also produced, due to the activity of kynurenine aminotransferases ( Adams et al., 2012; Schwarcz et al.,2012 ). It was demonstrated that KYNA is an antagonist of ionotropic glutamate receptors ( Alt et al., 2004; Ganong and Cotman, 1986; Kem et al., 1988; Kessler et al., 1989; Mok et al., 2009 ) and an antagonist of alpha7 nicotinic receptors ( Hilmas et al., 2001). As both ionotropic glutamate receptors and alpha7 nicotinic receptors are predominantly expressed in the brain, it was stated that KYNA is present in the brain ( Moroni etal., 1988; Turski et al., 1988 ). Studies aimed at discovering KYNA’s properties and concentra-tions in the brain and very low blood–brain barrier penetration of KYNA ( Fukui et al., 1991 ) prompted researchers to concentrate on analyzing peripheral KYNA. It was found that KYNA is an agonist of G-protein coupled GPR35 receptors. Furthermore, it was stated that GPR35 receptorsare mainly present in thegastrointestinal tract ( Wang etal., 2006 ). Further analyses led to results indicating that KYNA ispresent in the gastrointestinal tract and that its concentration increases along it ( Kuc etal., 2008 ). The lowest concentration of KYNA was detected in human
saliva (0.003mM) and human gastric juice (0.0mM ) while the highest concentration of KYNA was found in rat’s middle ileum mucus (8.08mM) and rat’s distant ileum mucus(16.10mM) ( Kuc etal., 2008 ). There is, however, no explanation for a gradual increase in KYNA concentration along the digestive system (