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 biochemical mechanisms underlying blood lymphoid cell genome destabilization in patients with HIV infection have been analyzed. Lymphocytes from HIV patients are characterized by increasing intensity of free radical oxidation together with activation of the xanthine oxidase D-form conversion into the O-form, enhanced activity of UV-endonuclease, and intensification of prooxidant-induced proteolysis. These changes increasing with the progress of the disease with a maximum at the AIDS stage form a metabolic basis for labilization of the lymph cell genome. The degree of biochemical manifestations of genome instability (levels of chromatin degradation products and intensity of formation of one-filament nicks of DNA) increase in the dynamics of HIV-infection. The data obtained are discussed in terms of the author's conception on the origin of AIDS from retroposons (retrotransposons?). A hypothesis is postulated on accumulation of autonomous genetic information on the basis of genome labilization under the influence of genotoxic factors. Clinico-biochemical data on the appearance of HIV proteins (p17, p24) in the blood of patients (previously negative for all HIV markers) in the presence of transfusions of HIV-negative blood and UV-irradiation of the autoblood are also discussed from this standpoint.
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PMID:[Genomic instability and AIDS]. 133 9

In the course of studying the effect of reactive oxygen species such as superoxide anion (O2-), hydrogen peroxide (H2O2) on oxidant-sensitive human T-lymphoblastoid cell line Molt-3, O2- has been generated by the interaction of xanthine with xanthine oxidase (XOD). To confirm that H2O2 is a key intermediate for inducing DNA single-strand breaks in Molt-3 cells, studies have been carried out with pure H2O2. In the presence of xanthine + XOD or H2O2 the amount of DNA single-strand breaks has been found to increase as a function of the O2- and H2O2 concentration. Data from studies with antioxidants such as superoxide dismutase and catalase supports a mechanism of DNA damage dependent on the presence of H2O2 in Molt-3 cells. Molt-3 cells are CD4+ and sensitive to reactive oxygen stress and therefore, could be an ideal cell line for determining the relationship between oxidative stress and various diseases such as acquired immunodeficiency syndrome (AIDS).
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PMID:DNA damage in human T-lymphoblastoid cell line Molt-3 induced by reactive oxygen species. 767 95

Sera of patients with various inflammatory and autoimmune rheumatic diseases were screened for the presence of xanthine oxidase (XOD) and compared to sera from healthy donors and patients with nonrheumatic diseases including AIDS, internal diseases, and different carcinomas. Up to 50-fold higher levels of XOD were detected in rheumatic sera (P < 0.001). In addition, serum sulfhydryls (SH) were determined as sensitive markers of oxidative stress. The SH status in rheumatic patients was diminished by 45-75% (P < 0.001) and inversely correlated to the concentration of serum XOD (R = 0.73), suggesting a causal interrelation. The depletion of serum sulfhydryls by the oxyradical-producing XOD/acetaldehyde system was mimicked successfully ex vivo in human serum from healthy donors. Cortisone treatment of patients suffering from systemic lupus erythematosus and rheumatoid arthritis impressively normalized elevated XOD concentrations in rheumatic sera to those of healthy controls. The participation of xanthine oxidase in the depletion of serum antioxidants in rheumatic patients is discussed in the light of substrate availability and Km values.
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PMID:Elevated levels of xanthine oxidase in serum of patients with inflammatory and autoimmune rheumatic diseases. 822 62

Neurodegenerative diseases of the human brain comprise a variety of disorders that affect an increasing percentage of the population. Some of these are age dependent (e.g. Alzheimer's and Parkinson's diseases) and some are infection dependent, e.g. human immunodeficiency virus (HIV/AIDS). The vulnerable brain regions in HIV/AIDS individuals include the dentate nucleus in the cerebellum, the red nucleus, substantia nigra (SN) in the mid-brain, the subthalamic nucleus, thalamic fasciculus in the diencephalons, the globus pallidus and striatum (or neostriatum, which consists of caudate and putamen) in the forebrain. Lesion in these regions may lead to progressive dementia, which is similar to what is observed in Alzheimer's disease and Parkinson's disease. The entry of calcium into the cytoplasm of cells at concentrations that can activate oxidative enzymes such as phospholipase A(2) and xanthine oxidase, deplete cells of cysteine and glutathione, cause mitochondrial release of free radicals and cell death. Glutamate and its receptors are key molecular elements at the interface between neurons and glia. Dietary factors can modulate physiological functions (including brain function) thereby increasing the economic productivity of a population as a function of health. A greater understanding of the molecular mechanisms of neuroprotection, oxidative stress and immune function will facilitate definition of the prophylactic potentials of diet, nutritional/food supplements, medicinal plants and herbal extracts.
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PMID:Neuroprotection by bioactive components in medicinal and food plant extracts. 1464 22