Dietary LC-O3PUFAs target the metabolism of carnosine and homocarnosine, as
evidenced by increased levels of alanine, carnosine, homocarnosine, and
4-guanidinobutanoate in the spinal cord of animals fed with LC-O3PUFAs. The diet
rich in LC-O3PUFAs also altered the glutamine-glutamate cycling. A distinctive
group of amino acid systems were affected by the diet, including threonine and
tryptophan. In particular, animals fed with LC-O3PUFAs showed dramatic increases
in the levels of kynurenines, which can regulate mitochondrial homeostasis and
oxidative stress, inflammation, and glutamate excitotoxicity through NMDA
receptor inhibition. Notably, the diet increased the levels of ornithine and
urea, while decreasing glucose and glucose-6-P levels, showing selective
alterations in the spinal cord cell bioenergetics. This support that LC-O3PUFAs
fuel energy production largely by oxidative phosphorylation via the
tricarboxylic acid (TCA) cycle and pentose phosphate pathway (PPP) rather than
glycolysis, which are essential pathways for the synthesis of necessary
macromolecules (i.e. amino acids, neurotransmitters, glutathione, nucleosides
and lipids required for assembling new cells). These pathways may represent
important mechanisms by which dietary LC-O3PUFAs confer prophylaxis against
neurodegeneration and dysfunction in SCI. This reservoir of protective molecules
and antioxidant bioavailability is expected to make neurons and glia more
resistant against calcium overload, glutamate toxicity, and cell death following
SCI. Metabolites in red increased with the dietary intervention. Features in
green decreased with the LC-O3PUFA diet when compared to controls. Putative
enzymatic/receptor targets are highlighted in red ovals. Abbreviations: AA,
amino acid (polar); GABA, gamma-aminobutyrate; NADPH, nicotinamide adenine
dinucleotide phosphate; NMDA, N-methyl-D-aspartate; PPP, pentose phosphate
pathway; R5P, ribose 5-phosphate; Thr, threonine.