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Increase in the Content of Quinolinic Acid in Cerebrospinal Fluid and Frontal Cortex of Patients with Hepatic Failure
Author(s) -
Moroni F.,
Lombardi G.,
Carlá V.,
Lal S.,
Etienne P.,
Nair N. P. V.
Publication year - 1986
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1986.tb13071.x
Subject(s) - quinolinic acid , hepatic encephalopathy , cerebrospinal fluid , coma (optics) , metabolite , medicine , encephalopathy , cerebral cortex , endocrinology , autopsy , cortex (anatomy) , frontal cortex , tryptophan , chemistry , pathology , anesthesia , biology , biochemistry , cirrhosis , neuroscience , amino acid , physics , optics
Quinolinic acid (QUIN), an excitotoxic tryptophan metabolite, has been identified and measured in human cerebrospinal fluid (CSF) using a mass‐fragmentographic method. Furthermore, its content has been evaluated in frontal cortex obtained at autopsy from the cadavers of patients who died after hepatic coma. During the coma, the concentration of QUIN in the CSF was 152 ± 38 pmol ml ‐1 . In contrast, the concentration in control patients affected by different pathologies was 22 ± 7 pmol ml ‐1 . In the frontal cortex of patients who died after episodes of hepatic encephalopathy, the content of QUIN was three times higher than in controls (2.6 ± 0.6 versus 0.80 ± 0.08 nmol/g wet weight). As a result of these investigations we are now able to extend our previous observations on the increase of QUIN in the brains of rats used as experimental models of hepatic encephalopathy to man. QUIN should therefore be added to the list of compounds possibly involved in the pathogenesis and symptomatology of brain disorders associated with liver failure.