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Published on: June 3, 2018
Tryptophan Pathway Abnormalities in a Murine Model of Hereditary Glaucoma
Michal Fiedorowicz1, Tomasz Choragiewicz2, Waldemar A Turski3
1Mossakowski Medical Research Centre, Polish Academy of Sciences, 02-106 Warsaw, Poland.
Background:
It has been shown that a possible pathogenetic mechanism of neurodegeneration in the mouse model of glaucoma (DBA/2J) may be an alteration of kynurenic acid (KYNA) in the retina. This study aimed to verify the hypothesis that alterations of tryptophan (TRP) metabolism in DBA/2J mice is not limited to the retina.
Methods:
Samples of the retinal tissue and serum were collected from DBA/2J mice (6 and 10 months old) and control C57Bl/6 mice of the same age. The concentration of TRP, KYNA, kynurenine (KYN), and 3-hydroxykynurenine (3OH-K) was measured by HPLC. The activity of indoleamine 2,3-dioxygenase (IDO) was also determined as a KYN/TRP ratio.
Results:
TRP, KYNA, L-KYN, and 3OH-K concentration were significantly lower in the retinas of DBA/2J mice than in C57Bl/6 mice. 3OH-K concentration was higher in older mice in both strains. Serum TRP, L-KYN, and KYNA concentrations were lower in DBA/2J than in age-matched controls. However, serum IDO activity did not differ significantly between compared groups and strains.
Conclusions:
Alterations of the TRP pathway seem not to be limited to the retina in the murine model of hereditary glaucoma.

