Lysine metabolism in the rat brain: Blood-brain-barrier transport, Formation of pipecolic acid and human hyperpipecolatemia.
Lysine metabolism in the human and the monkey: demonstration of pipecolic acid formation in the brain and other organs.
In vitro formation of piperidine, cadaverine and pipecolic acid in chick and mouse brain during development.
Intracerebroventricular injection of pipecolic acid inhibits food intake and induces sleeping-like behaviors in the neonatal chick.
Plasma levels of pipecolic acid, both L- and D-enantiomers, in patients with chronic liver diseases, especially hepatic encephalopathy.
Origin of D- and L-pipecolic acid in human physiological fluids: a study of the catabolic mechanism to pipecolic acid using the lysine loading test.
Quantification of pipecolic acid in plasma and urine by isotope-dilution gas chromatography/mass spectrometry.
Pipecolic acid levels in serum and urine from neonates and normal infants: comparison with values reported in Zellweger syndrome.
Determination of pipecolic acid in serum or plasma by solid-phase extraction and isotope dilution mass spectrometry.
Stable isotope dilution analysis of pipecolic acid in cerebrospinal fluid, plasma, urine and amniotic fluid using electron capture negative ion mass fragmentography.
Also, the fact that fragment ions are observed resulting in the elimination of pipecolic acid indicates that some intramolecular interactions between the C39 hydroxy group and the C16 carbonyl are possible, giving rise to a carbinolamine intermediate that is able to lose pipecolic acid, as already observed for tacrolimus [14, 15].
The fact that pipecolic acid or 2-formyl piperidine 2-ene, as also observed for tacrolimus metabolites , may be lost from the parent ion m/z = 890 confirms that intramolecular interactions of free hydroxy groups with the [C.