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Data on superoxide dismutase (SOD) activity in the cerebrospinal fluid (CSF) of patients suffering from dementia (n=32) as compared with a control group (n=58), a Parkinson disease (PD) patient group (n=12), and a group of individuals suffering from epilepsy (n=13) are presented. SOD activity was determined by electron spin resonance spectrometry using the spin trap method. No significant correlation was found between CSF SOD activity and age in the control group. In addition, CSF SOD activity was not gender dependent. One-way analysis of variance showed a highly significant between-groups effect for the CSF SOD activity and specific CSF SOD activity of the four major groups (p=0.0008). Post hoc comparison (Fisher PLSD test) revealed significant differences between the control group and the total dementia group (p < 0.001), between the dementia group and the epilepsy group (p < 0.01), and between the dementia group and the PD group (p < 0.05). The CSF of patients with PD or epilepsy showed a similar SOD activity as the CSF of control patients. In addition, CSF SOD activity levels were significantly lower in the total dementia group (p=0.002) and in the group with dementia of the Alzheimer type (DAT) (p=0.001) than in the dementia age-matched control group. No significant difference was found for CSF SOD activity levels between the control group and the non-DAT dementia group. This result corresponded with a reduction of CSF SOD activity in the total dementia group, DAT subgroup, and non-DAT subgroup of 37, 43, and 22%, respectively. No significant correlation between the Mini-Mental State Examination score and CSF SOD activity was found in DAT. The lowered CSF SOD activity in Alzheimer disease, as demonstrated here, may reflect impaired radical defense mechanisms and may have possible pathophysiological significance.

It has been recognised that the level of superoxide dismutase (SOD) significantly increases in CSF as the result of cerebral ischaemic damage. The aim of this study was to correlate the CSF levels of SOD enzymatic activity to the patterns of subarachnoid haemorrhage with regards to ischaemic complications due to vasospasm. A series of 78 patients operated on for intracranial aneurysms was studied; all patients were monitored with serial TCD measurements every second day after SAH. CSF samples were obtained at surgery by cisternal puncture of the subarachnoid cistern nearest to the aneurysm. SOD activity was assayed spectrophotometrically. Mean cisternal CSF level of SOD in 12 control cases (12.99 +/- 2.33 U/ml) is significantly higher (p < 0.01) than in 26 patients operated on between day 1 and 3 from last SAH episode (4.44 +/- 0.7 U/ml) and in 40 patients treated by delayed surgery (7.64 +/- 0.92 U/ml). In 13 patients presenting neurological deterioration related to arterial vasospasm mean cisternal SOD level was 12.23 +/- 1.86 U/ml; in 27 cases without vasospasm mean level was 5.43 +/- 0.7 U/ml (p < 001). The present results suggest that (a) cisternal CSF levels of SOD significantly decreases after SAH, probably in relation to an impaired synthesis in the brain compartment and that (b) a substantial elevation of SOD levels is evident in patients suffering ischaemic complications vasospasm-related. Biochemical events in the brain compartment could influence the expression and release of anti-oxidant enzymes in CSF after SAH.

We investigated superoxide dismutase (SOD) activity in human cerebrospinal fluid (CSF) as an index of the aging process in the central nervous system (CNS). The subjects were 61 individuals aged 21-77 years, comprising 24 men and 37 women without organic disorders of the nervous system. SOD activity in CSF was measured by the nitrite method modified by Oyanagui. The results showed that SOD activity in CSF gradually increased with age and that the values of SOD activity after the fifth decade were significantly higher than those in the third and fourth decades. It might suggest that the productivity of SOD in the CNS gradually increased with age due to stimulation of various types of oxidative stress which accumulated in vivo especially after the fifth decade.

In the pathophysiology of lumbosacral radiculopathy, inflammation of the nerve root is of critical importance. Additionally, free radicals have been shown to be associated with some inflammatory process. This study was designed to investigate whether free radicals participate in the pathophysiology of nerve root involvement. We measured superoxide dismutase (SOD) activity in cerebrospinal fluid (CSF) of 31 patients with unilateral lumbosacral radiculopathy caused by a herniated disc using electron spin resonance (ESR) spectrometry. Then SOD activity was compared with the type of nerve root compression as seen on preoperative myelography. SOD activity in the normal control group was 7U/ml, while that in the hernia group remarkably decreased. The concentration gradient of SOD activity was different between central herniation and centrolateral herniation. Our findings indicate that free radicals are generated after nerve root compression. Under severe deficiency of SOD activity in CSF, serum SOD penetrates into CSF after further compression. In addition, SOD in CSF may play an important role in protecting against nerve root involvement.

We examined the mechanism of increase of manganese superoxide dismutase (Mn SOD) in the cerebrospinal fluid (CSF) in bacterial meningitis (BM). The elevated levels of Mn SOD in the CSF in BM, measured with an enzyme immunoassay method, were more prominent than those in aseptic meningitis (AM) and encephalitis (EN). In AM and EN Mn SOD levels well correlated with levels of neuron-specific enolase and S-100b protein, which are markers of damages to nervous tissues, but did not with any of them in BM. CSF concentrations of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 alpha (IL-1 alpha) were higher in BM than in AM and EN. From the serial measurements in BM, the peak values of these cytokines chronologically preceded or corresponded to those of Mn SOD. Immunohistochemically, a large number of the glial cells were stained for Mn SOD in the cerebral cortex from a patient with BM. By contrast, in the normal cerebral cortex, the glial cells were negative for Mn SOD staining. These results suggest that the marked increase of Mn SOD in the CSF in BM may be related to the increase of such cytokines as TNF-alpha and IL-1 alpha and that these cytokines may play a role in the induction of Mn SOD in nervous tissues.

Cu, Zn superoxide dismutase (SOD) levels in the serum, cerebrospinal fluid (CSF) and skin fibroblasts of patients with dementia of the Alzheimer type (DAT) were estimated using enzyme immunoassay. The SOD mRNA level in the skin fibroblasts was also determined by the Northern blot analysis. As compared with the age-matched control groups of neurological patients without dementia, the AD group consisting of patients with DAT at ages under 65 years of age as well as the SDAT group of patients with DAT at ages over 65 years of age showed no significant changes in serum or CSF SOD levels. However, the skin fibroblast SOD- and SOD mRNA levels, which were correlate each other, were significantly higher in the AD group (p < 0.05), while lower in the SDAT group (p < 0.05). These results suggest that the determination of the SOD level of skin fibroblast may be useful for diagnosis of DAT and that the abnormality of SOD may play an important role in developing DAT.

Ten patients with SDAT received the ECP therapy. The examination of Hasegawa's Dementia Scale (HDS), single photor emission computed tomography (SPECT) brain imaging, and some biochemical parameters in blood and CSF were selected to evaluate the effect of ECP for SDAT. After ECP treatment, the average HDS score of the patients increased, the value of P was close to 0.05; and the cortical cerebellar ratios of SPECT brain scan, the superoxide dismutase (SOD) activity and the concentrations of somatostatin-like immunoreactivity (SLI), dynorphin AL-13 (Dyn Al-13) in blood and/or CSF were significantly elevated. The results indicated that ECP could not only improve cerebral blood flow, but also make a notable impact on biological active substances in blood and CSF. It is suggested that ECP is beneficial to SDAT patients.

We measured cerebrospinal fluid (CSF) levels of Cu/Zn superoxide dismutase (Cu/Zn SOD) and Mn superoxide dismutase (Mn SOD) using enzyme immunoassays in 196 neurological patients and 44 controls. The mean Cu/Zn SOD level was 55.8 +/- 27.6 (SD) ng/ml and the Mn SOD, 8.0 +/- 2.5 ng/ml in the controls. Cu/Zn SOD or Mn SOD levels showed neither age-nor sex-related differences in the controls. Both SODs were markedly elevated in cerebrovascular diseases, bacterial meningitis and encephalitis. Mn SOD alone was significantly elevated in neurodegenerative diseases. We compared SODs with CSF levels of neuron-specific enolase (NSE) and S-100b protein (S-100b) in cerebral infarction and bacterial meningitis. Both SODs were correlated with NSE and S-100b in patients with cerebral infarction, but not in those with bacterial meningitis. This means that elevations of SODs in CSF may not only be due to leakage from damaged nervous tissues, but also to the induction of SOD in lesions. We conclude that the mean SOD levels were elevated in various neurological diseases, and their varied magnitudes may be associated with the underlying diseases.

We measured cerebrospinal fluid (CSF) levels of manganese superoxide dismutase (Mn SOD) using an enzyme immunoassay method in 19 patients with bacterial meningitis (BM), 33 with aseptic meningitis (AM) and 13 with encephalitis (EN), and examined the significance of their elevations, especially in BM. 1) In BM, the Mn SOD levels were obviously high, ranging from 10.4 to 1179.2 ng/ml. The mean level of Mn SOD was 234.6 +/- 306.7 (SD) ng/ml and 18 patients showed abnormal levels of Mn SOD (more than 13.1 ng/ml). On the other hand, in the remaining 2 diseases, the elevation of SOD levels was not remarkable: the mean levels of Mn SOD in AM and EN were 20.6 +/- 11.6 ng/ml and 41.9 +/- 23.6 ng/ml, respectively. 2) In AM and EN, Mn SOD levels well correlated with NSE or S-100b levels which are the markers of nervous tissue damages. But there was no correlation between the Mn SOD levels in BM and these markers. 3) In BM, there was a positive relationship between Mn SOD and total protein levels, but the disease days showing peak levels were different between them. In addition, Mn SOD levels showed no correlation with cell counts in CSF. 4) In BM, CSF levels of TNF-alpha and IL-1 alpha were remarkably high, whereas in AM and EN, the increases of these cytokines were not marked. And these cytokines in BM showed the peak values in the disease day before or when Mn SOD reached the peak levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Superoxide dismutase (SOD), neuron specific enolase (NSE) and lactic dehydrogenase (LDH) were measured in the serum and cerebrospinal fluid (CSF) of ischemic cerebrovascular patients, other neurological patients and in age-matched healthy controls (serum only). The levels of SOD in the CSF or serum of the ischemic patients in the first 24 hrs after stroke were similar to the control groups. However, SOD levels in the ischemic patients increased after two days, reaching their peak values after one week (2-3 fold of the initial values). NSE showed a similar kinetics while LDH showed no change. These results suggest that oxygen radicals are formed in the ischemic patients and the increased synthesis of SOD may protect the patients from the potential damage of such radicals.

To evaluate significance of superoxide dismutase in neurological diseases, we measured cerebrospinal fluid (CSF) levels of copper-zinc superoxide dismutase (Cu/Zn SOD) and manganese superoxide dismutase (Mn SOD) using enzyme immunoassay methods in 181 neurological patients and 43 controls. The mean level of Cu/Zn SOD in CSF of controls was 54.4 +/- 28.7 ng/ml, and that of Mn SOD 8.1 +/- 2.5 ng/ml, although other methods have reported that Mn SOD is undetectable in CSF. Cu/Zn SOD or Mn SOD showed no statistical difference in age or sex of the controls. The elevation of both SOD levels was marked in acute diseases such as cerebrovascular diseases (CVD), bacterial meningitis and encephalitis, but mild in aseptic meningitis. The elevation of Cu/Zn SOD level was more prominent than that of Mn SOD in CVD, whereas vice versa in bacterial meningitis and encephalitis. In neurodegenerative diseases and cervical spondylosis, only Mn SOD level was significantly elevated. To examine the source of CSF SOD, we compared it with CSF levels of neuron-specific enolase (NSE) and S-100b protein (S-100b) in cerebral infarction and bacterial meningitis. Both SOD levels were correlated with NSE and S-100b levels in patients with cerebral infarction, but in bacterial meningitis no significant relationship was found among SOD levels, NSE and S-100b levels. This means that elevations of SODs in CSF may be due to not only damage of the nervous tissues but also the other mechanisms, as induction of SOD in the lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral vasospasm may result from lipid peroxidation induced by oxyhemoglobin in the subarachnoid space after subarachnoid hemorrhage. To test this theory, vasospasm was induced in monkeys by intrathecal injections of oxyhemoglobin or supernatant fluid from autologous blood incubated in vitro. Concentration of malondialdehyde (MDA), a product of lipid peroxidation, was elevated in cerebrospinal fluid (CSF) in association with vasospasm caused by oxyhemoglobin and supernatant fluid. Intrathecal injections of methemoglobin or bilirubin did not cause vasospasm or increased CSF MDA. Activity of glutathione peroxidase in CSF increased significantly after injection of oxyhemoglobin and methemoglobin. There were no significant changes in CSF superoxide dismutase activity although there was a trend towards higher activities in animals treated with oxyhemoglobin, methemoglobin, bilirubin, and supernatant fluid. These results show oxyhemoglobin-induced vasospasm is associated with MDA and lipid peroxidation in the subarachnoid space. Furthermore, detection of peroxidation products after injection of oxyhemoglobin in the absence of erythrocyte membranes indicates that oxyhemoglobin may directly damage cerebral arteries and brain by inducing lipid peroxidation in these structures. Depletion of free-radical scavenging enzymes in CSF did not seem necessary for development of vasospasm. In fact, there was a tendency for vasospasm to elevate enzyme activities, as if production of scavengers was induced by excess free radicals in the subarachnoid space.

Background and Purpose: Evaluation of biochemical patterns in cerebrospinal fluid may add diagnostic and prognostic information. We tested to determine whether the concentration of superoxide dismutase in cerebrospinal fluid is a marker of brain tissue damage in acute ischemic stroke., Methods: We investigated 36 acute ischemic stroke patients for cerebrospinal fluid activity of the enzyme superoxide dismutase on two occasions shortly after symptom onset (average, day 1 and day 4)., Results: In 75% of the patients, the first of two lumbar punctures revealed the maximal superoxide dismutase value. The amount in the cerebrospinal fluid was significantly correlated with the size of infarction on computed tomographic scan (p less than 0.001 by analysis of variance) and to functional impairment and stroke-related mortality during initial hospital stay (p less than 0.002). The correlation of initial superoxide dismutase concentration with the need for long-term institutional care and mortality at 3 months after the stroke was also significant (p less than 0.03)., Conclusions: We conclude that superoxide dismutase in cerebrospinal fluid is a marker of an acute brain lesion and has some value as a prognostic predictor. This small enzyme leaks rapidly from ischemically injured cells.

Activity of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase as well as content of diene conjugates and malonic dialdehyde were studied in blood serum and cerebrospinal fluid of patients with transitory ischemia, small ischemic insult, ischemic insult of middle severity and with severe ischemic insult without lethality within 1-2, 7-8 and 14-15 days of diseases. Content of lipid peroxidation products and activity of antioxidant enzymes were decreased in the biological fluids studied in all the forms of brain circulation impairments within early periods of pathology. These patterns tend to normalization within 14-15 days. The rate of biochemical alterations corresponded highly to severity of impairments developed and these patterns may be used for diagnostic and prognostic purposes.

Superoxide dismutase (SOD) activity in CSF of patients was determined by electron spin resonance spectrometry using the spin trap method. Variation in SOD activity was found among patients. SOD activity in CSF of subjects increased with age and this was identified as Cu,Zn-SOD activity by electrophoresis. In addition, animal experiments showed that SOD activities were higher in mitochondrial and cytosol fractions of aged rats than in those of adult rats. This finding on aged rat brain validates the increase of SOD activity in aged human CSF.

We determined the concentration of copper zinc superoxide dismutase (CuZnSOD) in cerebrospinal fluid (CSF) and plasma of 36 persons without neurological illness or with various central and peripheral nervous system disorders not supposed to generate abnormal radical formation. The CuZnSOD concentration in CSF was significantly higher compared with plasma, suggesting the presence of a high oxygen-radical load on the central nervous system. Our data may be considered to reflect normal values.

The activity of the superoxide dismutase was measured by the polarographic method of catalytic currents in the cerebrospinal fluid of patients with age-related neurologic degenerative diseases, namely, amyotrophic lateral sclerosis and Alzheimer's disease, and of a reference group of normal subjects. The superoxide dismutase activity was found to increase with age in reference subjects (r = 0.81) while no significant correlation was found in amyotrophic lateral sclerosis and Alzheimer's disease patients. The activity mean values were significantly lower (P less than 0.01) in patients with neurologic degenerative diseases than in the reference subjects. The changes of superoxide dismutase activity in the aging brain and in age-related neurologic degenerative diseases are discussed.

We examined the relationship between the biological protective mechanisms of scavengers and free radicals that are elicited by subarachnoid hemorrhage (SAH) in the pathogenesis of prolonged vasospasm following ruptured intracranial aneurysm. The study included 25 patients treated by early surgery (within 72 hours after SAH). Lipid peroxides concentrations and the activities of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH-px) in the cerebrospinal fluid (CSF) were measured. The concentration of lipid peroxides increased significantly more (p less than 0.05) during the first 4 days after SAH in patients with symptomatic vasospasm than in those without. Patients with symptomatic vasospasm had a marked decrease in SOD activity on Days 3 and 4 followed by a gradual decrease, whereas the patients without spasm showed little change (difference between the groups, p less than 0.05). There was a significant difference in catalase activity reversal to SOD activity, but no difference in GSH-px activity. Thus, correlation was close between the increased lipid peroxides concentration and the decrease in SOD activity in CSF (p less than 0.05), suggesting an important mechanism in the pathogenesis of vasospasm.

The neuronal ceroid-lipofuscinoses is a group of diseases characterized by a widespread accumulation in the body of pigments believed to be end-products of lipid-peroxidation damaged organelles. It was recently shown that cerebrospinal fluid from patients with infantile and juvenile neuronal ceroid-lipofuscinosis were less protective against superoxide radical-induced hydroxyl radical formation compared with controls. The content of superoxide dismutase isoenzymes in cerebrospinal fluid and in plasma from patients with different forms of neuronal ceroid-lipofuscinosis was analysed. No significant difference from controls could be demonstrated in samples from patients with juvenile neuronal ceroid-lipofuscinosis. The few samples from patients with infantile and late infantile neuronal ceroid-lipofuscinosis analysed all fell within the range defined by the controls.