Detection of N‐acetyl methionine in human and murine brain and neuronal and glial derived cell lines

• Published in: Journal of neurochemistry Vol. 118; no. 2; pp. 187 - 194
• Main Authors: Smith, Tara, Ghandour, M. Said, Wood, Paul L.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.07.2011; Wiley-Blackwell
• Subjects: Acetaminophen; Acetic acid; acetylation; Amino acids; Aminoacylase; aminoacylase 1; Animals; Biological and medical sciences; Brain; Brain - cytology; Brain - metabolism; Brain Chemistry - physiology; Cell culture; Cell Line; Cells, Cultured; Cellular biology; Fundamental and applied biological sciences. Psychology; HEK293 Cells; Human subjects; Humans; Isolated neuron and nerve. Neuroglia; Life Sciences; Liver; Medical sciences; Metabolism; Methionine; Methionine - analogs & derivatives; Methionine - analysis; Mice; Mutation; Neurochemistry; Neuroglia - chemistry; Neuroglia - metabolism; Neurological diseases; Neurology; Neuronal-glial interactions; Neurons; Neurons - chemistry; Neurons - metabolism; Neurons and Cognition; N‐acetyl aspartic acid; N‐acetyl methionine; oligodendroglioma cells; Overdose; Rodents; Supplementation; Toxicity; Tumors of the nervous system. Phacomatoses; Vertebrates: nervous system and sense organs; Cell culture; Toxicity; Neuroglia; Liver; Overdosing; Central nervous system; Tissue culture; aminoacylase 1; N-acetyl methionine; Encephalon; acetylation; Malignant glioma; Endogenous; Neurological disorder; N-acetyl aspartic acid; Human; Nervous system diseases; Glial cell; Digestive system; Deficiency; Rodentia; Malignant tumor; Metabolism; Oligodendroglioma; Vertebrata; Mammalia; Cell line; Mouse; Central nervous system disease; Cancer
• ISSN: 0022-3042; 1471-4159; 1471-4159
• DOI: 10.1111/j.1471-4159.2011.07305.x

J. Neurochem. (2011) 118, 187–194. Despite the fact that N‐acetyl methionine (NAM) supplementation has long been reported as a bioavailable source of methionine in humans, and known to reduce liver toxicity after acetaminophen overdose, its cellular endogenous presence has never been investigated. We demonstrate for the first time that NAM is present in both human and mouse tissues and cells in culture. A wide variety of cultured cells, including a number of brain derived cell types, as well as mouse and human brain tissue all have clearly detectable levels of NAM. Methionine is rapidly acetylated to form NAM in cultured human oligodendroglioma cells with an initial rate of 0.44 ± 0.064 atom percent excess per minute. The presence of measurable quantities of NAM in brain cells in combination with its rapid formation point to a potential physiological role for N‐acetylated methionine in the brain. Aminoacylase 1 is responsible for metabolism of NAM to methionine and acetate. Deficiencies in aminoacylase 1 have been linked to a variety of neurological disorders; however, it is unclear whether and how the brain is affected by this defect. The reported presence of NAM in the human brain may provide an invaluable key to discovering the link between aminoacylase 1 mutations and neurological problems.