Double-enzymic assay for determination of glutamine and glutamic acids in cerebrospinal fluid and plasma

Pye, I F; Stonier, C.; Hf, McGale

doi:10.1021/ac50029a031

Cited by 19 publications

(8 citation statements)

References 11 publications

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“…Secondly, previous studies from this department and elsewhere done on patients with meningitis have shown that the large increase in CSF protein and amino acid concentrations are most likely to result from a breakdown of the blood-CSF barrier.) 14 In the Guillain-Barre syndrome it is possible that the breakdown of the barrier might occur at the nerve roots where there is evidence that a protein-rich oedema fluid collects'5 and protein leakage occurs.¢ Alternatively, an inflammatory reaction might occur in the choroid plexus and disturb the transport processes at this site.1 [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] Evidence for this latter mechanism is based on the morphological, molecular and functional similarities between the choroid plexus and the renal glomerulus2' and the presence of immunological cross-reactivity between these tissues. 22 Since glomerulonephritis has been shown to occur commonly in patients with the Guillain-Barre syndrome26 and since there has been histological confirmation of immune-complex nephritis in patients with this syndrome27 28 it would seem reasonable to infer that immunological damage might also occur in the choroid plexus.…”

Section: Discussionmentioning

confidence: 99%

Abnormalities of cerebrospinal fluid amino acids in patients with the Guillain-Barre syndrome.

Corston¹,

McGale²,

Stonier³

et al. 1981

Journal of Neurology, Neurosurgery & Psychiatry

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SUMMARY Measurements of cerebrospinal fluid (CSF) and plasma amino acid concentrations have been made in 12 patients with the Guillain-Barre syndrome. The CSF protein concentration was normal in seven specimens and raised in 13. Abnormalities of the CSF amino acid profile were found in all specimens but were more marked in those with a raised CSF protein concentration. The possible causes and diagnostic significance of these changes are discussed.

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Section: Discussionmentioning

confidence: 99%

Abnormalities of cerebrospinal fluid amino acids in patients with the Guillain-Barre syndrome.

Corston¹,

McGale²,

Stonier³

et al. 1981

Journal of Neurology, Neurosurgery & Psychiatry

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show abstract

“…After centrifugation (4000 g, 10 min, 40C), specimens were deproteinised, stored, and analysed for their free amino-acid content as described previously (McGale et al, 1977). Glutamine and glutamic acid concentrations were measured on an aliquot of the same specimens by an enzymatic procedure (Pye et al, 1978). An aliquot of CSF was cultured and examined by microscopy.…”

Section: Methodsmentioning

confidence: 99%

Abnormalities of cerebrospinal fluid amino-acids in purulent meningitis

Corston¹,

McGale²,

Stonier³

et al. 1979

Journal of Neurology, Neurosurgery & Psychiatry

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“…Glutamate and glutamine were determined using the method described by Pye et al [27]. Each microdialysate was divided into two equal parts: the first (''Glu'' sample) for determination of glutamate, and second (''Glu + Gln'' sample) for determination of the sum of glutamate and glutamine.…”

Section: Glutamate and Glutamine Assaymentioning

confidence: 99%

Effect of Glutamine Synthesis Inhibition with Methionine Sulfoximine on the Nitric Oxide–Cyclic GMP Pathway in the Rat Striatum Treated Acutely with Ammonia: A Microdialysis Study

Hilgier

Węgrzynowicz

Mączewski³

et al. 2007

Neurochem Res

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Ammonia neurotoxicity is associated with overactivation of N-methyl-D-aspartate (NMDA) receptors leading to enhanced nitric oxide and cyclic GMP synthesis and to accumulation of reactive oxygen and nitrogen species. Ammonia is detoxified in the brain via synthesis of glutamine, which if accumulated in excess contributes to astrocytic swelling, mitochondrial dysfunction and cerebral edema. This study was aimed at testing the hypothesis that the activity of the NMDA/NO/cGMP pathway is controlled by the ammonia-induced production of Gln in the brain. Ammonium chloride (final concentration 5 mM), infused for 40 min to the rat striatum via a microdialysis probe, caused a significant increase in Gln (by 40%), NO oxidation products (nitrite+nitrate=NOx) (by 35%) and cGMP (by 50%) concentration in the microdialysate. A Gln synthetase inhibitor, methionine sulfoximine (MSO, 5 mM), added directly to the microdialysate, completely prevented ammonia-mediated production of Gln, and paradoxically, it increased ammonia-mediated production of NOx and cGMP by 230% and 250%, respectively. Of note, MSO given alone significantly reduced basal Gln concentration in the rat striatum, had no effect on the basal NOx concentration, and attenuated basal concentration of cGMP in the microdialysate by 50%. The results of the present study suggest that Gln, at physiological concentrations, may ameliorate excessive activation of the NO-cGMP pathway by neurotoxic concentrations of ammonia. However, in view of potential direct interference of MSO with the pathway, exogenously added Gln and less toxic modulators of Gln content and/or transport will have to be employed in further studies on the underlying mechanisms.

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Double-enzymic assay for determination of glutamine and glutamic acids in cerebrospinal fluid and plasma

Cited by 19 publications

References 11 publications

Abnormalities of cerebrospinal fluid amino acids in patients with the Guillain-Barre syndrome.

Abnormalities of cerebrospinal fluid amino acids in patients with the Guillain-Barre syndrome.

Abnormalities of cerebrospinal fluid amino-acids in purulent meningitis

Effect of Glutamine Synthesis Inhibition with Methionine Sulfoximine on the Nitric Oxide–Cyclic GMP Pathway in the Rat Striatum Treated Acutely with Ammonia: A Microdialysis Study

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