Perspectives of Adenylate Kinase Activity and Glutathione Concentration in Cerebrospinal Fluid of Patients with Ischemic and Neoplastic Brain Lesions

Abstract

Adenylate kinase (AK) activity and glutathione concentration were measured in cerebrospinal fluid (CSF) on three different occasions after the ictus in 16 patients with cerebral infarction. All patients displayed an unambiguous AK activity in their CSF within 48 h after the ictus while glutathione was present in 10 of the 16 patients. The mean AK activity among these patients was reduced by about 60% after 1 week and an additional smaller reduction took place after 3–4 weeks. The glutathione concentration in CSF of these patients showed a similar curve profile with time. The 9 patients who showed clinical signs of improvement had significantly lower values on all occasions for both AK and glutathione than those who did not improve or deteriorated. A corresponding reduction in AK activity with time was not observed in 3 patients with cerebral malignancies. The possibility was excluded that the enhanced AK activity in CSF was the result of an increased transfer of the enzyme from the plasma compartment. Instead a causal relationship was suggested between the appearance of AK in CSF and a disturbed brain cell metabolism. Repeated analyses revealed different curve profiles for ischemic and neoplastic brain lesions. The importance of sampling and handling the CSF material under standardized conditions is emphasized.

Effect of Cardiac Glycosides on the Release of Adenylate Kinase into Cerebrospinal Fluid of Patients with Cerebral Arteriosclerosis

“…This finding is in agreement with a previous report [3]. The sampling and handling of CSF were performed under strictly standardized conditions, and the influence of irrelevant factors on the AK results were under such conditions negligible [4], This assumption was also corroborated by the absence of any correlation between AK activity and red cells (before centrifugation twice) as well as be tween AK activity and protein in CSF of any of the two groups of patients with arterioscle rosis. We therefore conclude that the consis tent finding of AK activity in CSF (lacking hemoglobin and hemoglobin derivatives in all cases except one) of patients with arterio sclerosis was the result of a pathological re lease of this marker enzyme from brain tissue into CSF.…”

“…Hence, no sig nificant rise in the albumin concentration in CSF took place during the first fortnight after the ictus in patients with stroke [16], and no correlation existed between hemoglobin [15] or erythrocytes [4] and AK in CSF in isch emic lesions of the brain. A causal relation ship between the ischemic lesion of the brain cells and the release of AK into CSF was instead proposed to exist [4,15,16]. The molecular mechanisms for such a release have been hypothetically discussed elsewhere [12,15,16].…”

“…The release of adenylate kinase (AK, ATP: AMP phosphotransferase, EC 2.7.4.3) into cerebrospinal fluid (CSF) was studied in isch emic lesions of the brain [3,4,12,15,16], A paraphenomenological appearance of AK in CSF in these conditions was less probably like an enhanced transfer of AK from the blood plasma compartment to the CSF com partment or leakage of AK from possible contaminating erythrocytes. Hence, no sig nificant rise in the albumin concentration in CSF took place during the first fortnight after the ictus in patients with stroke [16], and no correlation existed between hemoglobin [15] or erythrocytes [4] and AK in CSF in isch emic lesions of the brain.…”

Occurrence of Adenylate Kinase in Cerebrospinal Fluid after Isoflurane Anaesthesia and Orthognathic Surgery

“…Under other circumstances such an increase would indicate brain injury, since normally the CSF-AK activity is low, and it should not exceed 0.040 U/L (8,10,24,25,28,30,32,33). The most, A serious objection to the result would be that the definition of the lower limit for normotension, MAP >65 mmHg, was set too low.…”

Glutamate transporters in the biology of malignant gliomas

“…Glutathione is an important antioxidant present in most cells, and its levels are known to be increased in a number of human cancers, including brain tumors [82,139]. The ability of tumor cells to increase intracellular GSH synthesis provides growth and survival advantages against both intrinsic and extrinsic factors.…”