Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.17.3.2 (xanthine oxidase)
 8,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Experimental bacterial meningitis due to Streptococcus pneumoniae in infant rats was associated with a time-dependent increase in CSF and cortical urate that was approximately 30-fold elevated at 22 h after infection compared to baseline. This increase was mirrored by a 20-fold rise in cortical xanthine oxidoreductase activity. The relative proportion of the oxidant-producing xanthine oxidase to total activity did not increase, however. Blood plasma levels of urate also increased during infection, but part of this was as a consequence of dehydration, as reflected by elevated ascorbate concentrations in the plasma. Administration of the radical scavenger alpha-phenyl-tert-butyl nitrone, previously shown to be neuroprotective in the present model, did not significantly affect either xanthine dehydrogenase or xanthine oxidase activity, and increased even further cortical accumulation of urate. Treatment with the xanthine oxidoreductase inhibitor allopurinol inhibited CSF urate levels earlier than those in blood plasma, supporting the notion that urate was produced within the brain. However, this treatment did not prevent the loss of ascorbate and reduced glutathione in the cortex and CSF. Together with data from the literature, the results strongly suggest that xanthine oxidase is not a major cause of oxidative stress in bacterial meningitis and that urate formation due to induction of xanthine oxidoreductase in the brain may in fact represent a protective response.
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PMID:Marked elevation in cortical urate and xanthine oxidoreductase activity in experimental bacterial meningitis. 1133 4

Reactive oxygen and nitrogen species are produced by the human immune system in response to infection. Methods to detoxify these reactive species are vital to the survival of human pathogens, such as Neisseria meningitidis, which is the major aetiological agent of bacterial meningitis. Following activation, macrophages produce superoxide (O(2)(-)), hydrogen peroxide (H(2)O(2)) and nitric oxide (NO). The toxicity of O(2)(-), generated using X/Xo (xanthine/xanthine oxidase), and H(2)O(2) was investigated in the presence and absence of the NO donor DEA-NONOate [2-(N,N-diethylamino)-diazenolate-2-oxide diethylammonium salt]. Most of the toxicity from X/Xo was due to H(2)O(2). In N. meningitidis, NO decreased the toxicity of the H(2)O(2). In contrast, in the enteric bacterium Escherichia coli, NO increased the toxicity of the H(2)O(2).
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PMID:Effect of combined oxidative and nitrosative stress on Neisseria meningitidis. 1641 21