DL-Homocysteine is a weak neurotoxin, and can affect the production of kynurenic acid in the brain.

DL-Homocysteine (0.1-0.5 mM) significantly enhances kynurenic acid (KYNA) production in rat cortical slices, and diministes the production of at 3.0, 5.0, and 10.0 mM, with the estimated IC50 of 6.4 (5.5-7.5) mM. DL-Homocysteine dose-dependently inhibits kynurenine aminotransferases I (KATI) activity at concentrations ≥0.2 mM, with an IC50 of 0.566 (0.442-0.724) mM, and the activity of KAT II with IC50 value of 8.046 (5.804-11.154) mM[1].

DL-Homocysteine (1.3 mmol/kg, i.p.) increases KYNA content (pmol/g tissue) from 8.47 ± 1.57 to 13.04 ± 2.86 and 11.4 ± 1.72 in cortex, and from 4.11 ± 1.54 to 10.02 ± 3.08 in rat hippocampus[1].

[1]. DL-Homocysteine, et al. Dual effect of DL-homocysteine and S-adenosylhomocysteine on brain synthesis of the glutamate receptor antagonist, kynurenic acid. J Neurosci Res. 2005 Feb 1;79(3):375-82.

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