Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to identify mediators of brain oedema formation in experimental pneumococcal meningitis. In a rat model of pneumococcal meningitis brain water content was significantly elevated 6 hours post infection (79.69% +/- 0.24 compared to 78.94% +/- 0.16 in the control group, mean +/- SEM, p less than 0.05). Brain oedema formation was completely blocked by superoxide dismutase (132,000 U/kg i.v. per 6 hours: n = 6), pretreatment with dexamethasone (3 mg/kg i.p., n = 3), or administration of dexamethasone at two hours after pneumococcal injection (n = 5). Pretreatment with indomethacin (10 mg/kg i.v., n = 5) attenuated the brain oedema formation. These findings suggest that oxygen derived free radicals act as mediators of brain oedema formation during the early phase of experimental bacterial meningitis. Cyclooxygenase metabolites may provide one possible source for the generation of oxygen derived free radicals in bacterial meningitis.
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PMID:Superoxide dismutase inhibits brain oedema formation in experimental pneumococcal meningitis. 208 45

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.
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PMID:Elevated cerebrospinal fluid levels of manganese superoxide dismutase in bacterial meningitis. 756 47

Recent studies using a rat model of pneumococcal meningitis have shown that nitric oxide synthase (NOS) inhibitors greatly attenuated microvascular changes and brain edema formation. The site of NO production during bacterial meningitis is unknown. In this study we tested whether primary astrocyte cultures from neonatal rat cortex can be induced to release NO upon stimulation with pneumococci. NO production was assessed by measuring nitrite in the cell culture supernatant using the Griess reaction. Stimulation with heat-killed unencapsulated pneumococci (HKP) increased nitrite concentrations in astrocyte culture supernatants in a dose-dependent fashion. Administration of N-nitro-L-arginine (L-NA), aminoguanidine, L-canavanine, cycloheximide, and dexamethasone prevented the increase in nitrite concentrations. Addition of L-arginine, but not of D-arginine, partially reversed the inhibitory effect of L-NA. Administration of SOD increased nitrite accumulation. Moreover, at 72 h after stimulation with heat-killed pneumococci (10(7) cfu/ml) astrocytes showed an inducible NOS-like immunoreactivity. Accumulation of nitrite was also observed when rat cerebellar neurons and microglia were stimulated with HKP, whereas there was only a slight increase of nitrite in media of rat C6 glioma cells, but no increase of nitrite when the human glioblastoma cell line LN-229 was stimulated with HKP. There was a stronger increase in nitrite levels when astrocytes from Lewis rats were used compared to that from Wistar rats. In conclusion, our study indicates that astrocytes, neurons and microglia are inducible for NO production upon stimulation with pneumococci.
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PMID:Production of nitrite by primary rat astrocytes in response to pneumococci. 764 48

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.
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PMID:Cerebrospinal fluid levels of superoxide dismutases in neurological diseases detected by sensitive enzyme immunoassays. 793 17

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)
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PMID:[The significance of elevated Mn SOD level in cerebrospinal fluid of patients with bacterial meningitis--its relation to cytokine]. 802 25

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)
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PMID:[Superoxide dismutase in cerebrospinal fluid in patients with neurological diseases]. 833 70

Microperfusion of scala tympani with the NO donors, sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP), produced marked depression of the compound action potential (CAP) and cochlear microphonic (CM) together with severe and widespread morphological damage to hair cells and supporting cells in the organ of Corti. In addition, direct perfusion of N-methyl-D-aspartate (NMDA) into scala tympani, which probably induces excess stimulation of NMDA receptors within the cochlea and which is known to lead to the release of NO, was found to elicit similar electrophysiological and structural lesions in the cochlea. Pre-perfusion of scala tympani with L-methyl arginine (L-MA), which inhibits the release of NO, or superoxide dismutase (SOD), an O2-scavenger, conferred marked protection upon the cochlea from the lesions caused by NO donors. These observations indicate that enhanced NO production is likely to be an important factor responsible for pathological insult of the cochlea. The possibility is discussed that this factor is involved in the chain of events leading to hearing loss caused by bacterial meningitis. Such hearing loss is a major sequela of bacterial meningitis in children.
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PMID:Possible involvement of nitric oxide in the sensorineural hearing loss of bacterial meningitis. 919 17

Animal studies of experimental bacterial meningitis have provided evidence for an involvement of reactive oxygen species (ROS) in the pathophysiology of this disease. Using a lucigenin-enhanced chemiluminescence (CL) method, we tested whether primary rat cerebral endothelial cells can be induced to release ROS upon stimulation with pneumococci. In addition, we determined CSF levels of two markers of lipid peroxidation in patients with bacterial meningitis, compared to patients with viral meningitis and noninflammatory neurological disorders. Malondialdehyde/4-hydroxynonenal concentrations were significantly elevated in CSF samples obtained from patients with bacterial meningitis (23.12+/-5.47 microM), as compared to both control groups (5.43+/-0.18 microM and 7.80+/-0.33 microM, respectively). Cerebromicrovascular endothelial cells, granulocytes, and the macrophage cell line RAW 264.7 (but not astrocytes and neuron-like cells) produced an increase in CL intensity after stimulation with pneumococci. The peak value produced by endothelial cells (500+/-83 cpm) was significantly lower than the maximum CL response in macrophages (1386+/-142 cpm; p<0.05). After addition of superoxide dismutase (SOD), the CL signal returned to baseline values. Equal to the CL technique, nitroblue tetrazolium (NBT) staining of RAW 264.7 showed SOD-inhibitable formazan precipitation when stimulated with pneumococci. In conclusion, this study suggests an important role of endothelial cells in the pathophysiology of bacterial meningitis-namely as a source for ROS production.
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PMID:Superoxide production by primary rat cerebral endothelial cells in response to pneumococci. 1033 17

The study was undertaken to investigate the possible role of free radicals and antioxidants in childhood meningitis. Sixty children suffering from acute bacterial meningitis (ABM) or tuberculous meningitis (TBM) according to their clinical and laboratory findings were enrolled in the study. The production of superoxide anions (O2.-), hydrogen peroxide (H2O2) and malondialdehyde (MDA) and the activities of xanthine oxidase (XO), superoxide dismutase (SOD) and glutathione peroxidase (GPx) were monitored in the study groups and findings compared with those in 20 age-matched controls. Children with ABM and TBM who died registered significant increases in the production of O2.- and MDA and in the activities of SOD and CPK compared with survivors. The rate of production of oxidants and MDA and the activities of XO, SOD and CPK were of a much higher magnitude in deceased ABM and in ABM survivors than in fatal TBM and survivors, respectively. The abnormalities in most of the biochemical parameters investigated were more marked in the children with ABM than in TBM and controls (p < 0.001). Increased MDA production and creatine phosphokinase (CPK) activity of different magnitudes in the two study groups suggest varying degrees of tissue damage. The alterations observed in 20 children who died (14 from ABM, 6 from TBM) revealed elevated levels of oxidants, antioxidants and toxicity markers, particularly in ABM patients, which suggests the possibility that natural or synthetic antioxidants might prevent disease progression and tissue damage in childhood meningitis.
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PMID:Evaluation of free radical status in CSF in childhood meningitis. 1094 61

Antioxidant status was investigated in children with acute bacterial meningitis and encephalitis to investigate the possible role of free radicals in children with meningitis and encephalitis. Our study included 16 children with acute bacterial meningitis, 13 with encephalitis, and 17 control subjects. Serum ceruloplasmin, uric acid, albumin, bilirubin superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) levels were studied in all subjects within 6 h of admission. There was a statistically significant difference between the groups for all parameters except for serum uric acid. All antioxidant activities except for albumin level were increased in the study groups. Albumin level was higher in the control group than those of meningitis and encephalitis groups. When the values of meningitis and encephalitis were compared, there was a statistically significant difference between the groups for serum SOD, GPx, ceruloplasmin, and albumin. In conclusion, our study showed that serum SOD, GPx, catalase, and ceruloplasmin were higher in children with acute bacterial meningitis and serum SOD, GPx, catalase, ceruloplasmin, and total bilirubin levels were increased in children with encephalitis. These findings suggest that antioxidant status was almost similar in both acute bacterial meningitis and encephalitis conditions in childhood.
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PMID:Evaluation of antioxidant status in children with acute bacterial meningitis and encephalitis. 1458 50


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