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Dysfunctions of kynurenine pathway of tryptophan metabolism (KPTM) are associated with multiple neuropathologies in vertebrates and invertebrates.  Drosophila  mutants with altered content of kynurenines are model objects for studying the molecular processes of neurodegeneration and senile dementia. The mutant  cardinal  ( cd 1  ) with accumulation of the redox stress inductor 3-hydroxykynurenine (3-HOK) shows age-dependent impairments of the courtship song and middle-term memory. The molecular mechanisms for 3-HOK accumulation in  cd 1   are still unknown. Here, we have studied age-dependent differences in spontaneous locomotor activity (SLA) for the wild type strain  Canton-S  ( CS ),  cd 1  , and  cinnabar  ( cn 1  ) with an excess of neuroprotective kynurenic acid (KYNA). We have also estimated the level and distribution of protein-bound 3-HOK (PB-3-HOK) in  Drosophila  brains (Br) and head tissues. The middle-age  cd 1   show the higher running speed and lower run frequency compared to  CS , for  cn 1   the situation is the opposite. There is a decrease in the index of activity for 40-day-old  cd 1   that seems to be an effect of the oxidative stress development. Surprisingly, PB-3-HOK level in  Drosophila  heads, brains, and head capsules (HC) is several times lower for  cd 1   compared to  CS . This complements the traditional hypothesis that  cd 1   phenotype results from a mutation in phenoxazinone synthase (PHS) gene governing the brown eye pigment xanthommatin synthesis. In addition to 3-HOK dimerization,  cd 1   mutation affects protein modification by 3-HOK. The accumulation of free 3-HOK in  cd 1   may result from the impairment of 3-HOK conjugation with some proteins of the brain and head tissues.

3-Hydroxykynurenine in Regulation of Drosophila Behavior: The Novel Mechanisms for Cardinal Phenotype Manifestations