Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to evaluate the activity of glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R) and superoxide dysmutase (SOD-1) in the single brain metastases. The activity of the GSH-Px was evaluated with the use of spectrophotometry, GSSG-R was evaluated basing on the method of Mize and Langdon and SOD-1 with Sykes et al. method. The examinations were carried out in 36 specimens (10 specimens of healthy brain tissue, 12 specimens of brain metastases, 14 specimens of glioma multiforme). The statistical analysis revealed significant increase (p < 0.001) of GSH-Px and GSSG-R activity within the single brain metastases in comparison with the healthy brain tissue.
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PMID:[Activity of glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R) and superoxide dismutase (SOD-1) in single brain metastasis]. 1223 89

Protective effects of quinic acids from Aster scaber on tetrahydropapaveroline (THP)-induced cell toxicity were evaluated in rat C6 glioma cells. Among 4 quinic acid derivatives tested, (-) 4,5-dicaffeoyl quinic acid (QA3) exhibited the highest protective effect against THP-induced cell toxicity. C6 cells treated with THP exhibited the decrease in the survival rate and activities of glutathione peroxidase and catalase, but increased the level of malondialdehyde and superoxide dismutase activity. Staining C6 cells with propidium iodide and Hoechst 33342 revealed that 10 microM of THP treatment caused to necrotic and apoptotic cell death. However, preincubation of cells with QA3 prior to THP exposure recovered the cell survival rate and activities of antioxidant enzymes to control level. Taken together, the results indicate that QA3 might be a potential agent for treating or preventing diseases with oxidative stress.
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PMID:Protective effects of quinic acid derivatives on tetrahydropapaveroline-induced cell death in C6 glioma cells. 1280 90

Gardenia, the fruit of Gardenia jasminoides Ellis, has been widely used to treat liver and gall bladder disorders in Chinese medicine. It has been shown recently that geniposide, the main ingredient of Gardenia Fructus, exhibits the anti-tumor effect. In this review, we discuss the anti-tumor effect and possible mechanisms of a derivative from Gardenia Fructus, penta-acetyl geniposide ((Ac)5GP). It has been demonstrated that (Ac)5GP plays more potent roles than geniposide in chemoprevention. (Ac)5GP decreased DNA damage and hepatocarcinogenesis induced by aflatoxin B1 (AFB1) by activating the phase II enzymes glutathione S-transferase (GST) and GSH peroxidase (GSH-Px). It reduced the growth and development of inoculated C6 glioma cells especially in pre-treated rats. In addition to the preventive effect, (Ac)5GP exerts its actions on apoptosis and growth arrest. Treatment of (Ac)5GP caused DNA fragmentation of glioma cells. (Ac)5GP induced sub- G1 peak through the activation of apoptotic cascades PKCdelta/JNK/Fas/caspase8 and caspase 3. Besides, p53/Bax signaling was suggested to be involved in (Ac)5GP-induced apoptosis, though its downstream cascades needs further clarified. (Ac)5GP has also been shown to inhibit DNA synthesis of tumor cells. It arrested cell cycle at G0/ G1 by inducing the expression of p21, thus suppressing the cyclin D1/cdk4 complex formation and the phosphorylation of E2F. The phosphorylation status of p53 on serine 392 correlated with the process of growth arrest. Evidences from the in vivo experiments showed that (Ac)5GP is not harmful to liver, heart and kidney. In conclusion, (Ac)5GP is highly suggested to be an anti-tumor agent for development in the future.
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PMID:The anti-tumor effect and mechanisms of action of penta-acetyl geniposide. 1597 50

NMDA class of glutamate receptors plays an important role in regulating toxic and plastic responses in CNS. Astrocytes are the predominant cell type in the adult CNS and recent studies have suggested their role in many aspects of CNS function and dysfunction. We report here the protective effect of a subtoxic dose of NMDA in retinoic acid differentiated C6 glioma cell cultures. C6 glioma cell cultures differentiated with retinoic acid (10 microM) were exposed to NMDA (100 microM) or to antagonist MK-801 (200 nM) alone as well as with NMDA and cells were harvested after 24h of treatment to study the expression of HSP70 and for biochemical assay of free radical scavenger system. The protection imparted by a subtoxic dose of NMDA was checked by challenging the differentiated controls as well as NMDA treated and MK-801 treated cultures with a toxic dose of glutamate and subsequently estimating the free radical scavenger system profile. Biochemical analysis revealed a significant increase in the activities of glutathione peroxidase (GPx), copper zinc-superoxide dismutase (CuZnSOD) and reduced glutathione (GSH) content upon exposure to NMDA. No significant change was observed in the level of lipid peroxidation (LPx). A significant increase was observed in HSP70 expression as seen by Western blotting and immunocytofluorescent studies in NMDA treated cultures. Treatment of cultures with MK-801 alone, a non-competitive NMDA receptor antagonist, or pretreatment with MK-801 prior to NMDA exposure prevented the NMDA mediated changes indicating the involvement of NMDA receptors mediated mechanism. The results illustrate the protective effect of a subtoxic dose of NMDA in RA differentiated C6 glioma cell line.
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PMID:HSP70 induction and oxidative stress protection mediated by a subtoxic dose of NMDA in the retinoic acid-differentiated C6 glioma cell line. 1646 83

Maple syrup urine disease (MSUD) is an inherited neurometabolic disorder biochemically characterized by the accumulation of the branched-chain alpha-keto acids (BCKA) alpha-ketoisocaproic (KIC), alpha-keto-beta-methylvaleric (KMV) and alpha-ketoisovaleric (KIV) and their respective branched-chain alpha-amino acids in body fluids and tissues. Affected MSUD patients have predominantly neurological features, including cerebral edema and atrophy whose pathophysiology is not well established. In the present study we investigated the effects of KIC, KMV and KIV on cell morphology, cytoskeleton reorganization, actin immunocontent and on various parameters of oxidative stress, namely total antioxidant reactivity (TAR), glutathione (GSH) and nitric oxide concentrations, and on the activities of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) in C6 glioma cells. We initially observed that C6 cultivated cells exposed for 3 h to the BCKA (1 and 10 mM) changed their usual rounded morphology to a fusiform or process-bearing cell appearance, while 24 h exposure to these organic acids elicited massive cell death. Rhodamine-labelled phalloidin analysis revealed that these organic acids induced reorganization of the actin cytoskeleton with no modifications on total actin content. It was also observed that 3h cell exposure to low doses of all BCKA (1 mM) resulted in a marked reduction of the non-enzymatic antioxidant defenses, as determined by TAR and GSH measurements. In addition, KIC provoked a reduced activity of SOD and GPx, whereas KMV caused a diminution of SOD activity. In contrast, CAT activity was not modified by the metabolites. Furthermore, nitric oxide production was significantly increased by all BCKA. Finally, we observed that the morphological features caused by BCKA on C6 cells were prevented by the use of the antioxidants GSH (1.0 mM), alpha-tocopherol (trolox; 10 microM) and Nomega-nitro-L-arginine methyl ester (L-NAME; 500 microM). These results strongly indicate that oxidative stress might be involved in the cell morphological alterations and death, as well as in the cytoskeletal reorganization elicited by the BCKA. It is presumed that these findings are possibly implicated in the neuropathological features observed in patients affected by MSUD.
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PMID:Morphological alterations and induction of oxidative stress in glial cells caused by the branched-chain alpha-keto acids accumulating in maple syrup urine disease. 1682 90

Molecular and genetic signatures may predict brain tumor behavior and may soon guide tumor classification, diagnosis, and tumor-specific treatment strategies. Free oxygen radicals (FOR) are thought to take part in oncogenesis and cellular differentiation. This article explored the state of FORs and antioxidant system in patients with cerebral tumor. The serum concentrations of malondialdehyde (MDA), catalase, and glutathione peroxidase (GSH-Px) enzyme activities were measured in the serum of 35 patients with cerebral tumors (21 glioma, 14 meningioma) and 11 controls. MDA measurement was done with fluorometric method and catalase and GSH-Px enzyme activities were done with photometric method. Mean serum MDA levels, catalase, and GSH-Px enzyme activities were significantly higher for both glial and meningiomal tumor cases when compared to controls (p < .05). There is no significant difference between glioma and meningioma groups in terms of the aforementioned parameters (p > .05). In conclusion, lipid peroxidation and antioxidant enzymes as assessed by MDA, catalase, and GSH-Px were increased in patients with brain tumors, for this respect there is no difference between gliomas and meningiomas.
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PMID:Lipid peroxidation in patients with brain tumor. 1686 Nov 59

Different cell types response differently to toxic insult. In a previous study, it was demonstrated that the C6 glioma cell is more sensitive to Cd induced oxidative stress than the HepG2 cells. To explain the difference between the two cell lines in their response to oxidative stress, it was hypothesized that the activity of glutathione metabolizing enzymes may be different. The objective of this study is to determine the activities of glutathione peroxidase (GPx) and glutathione reductase (GR) in the two cell lines and to explain how these differences may affect the susceptibility of the two cells to oxidative stress. In the HepG2 cells, the activity of GPx was 2.24+/-0.18 micromol/mg protein/min and that for GR was 5.63+/-0.58 micromol/mg protein/min. For the C6 glioma cells, GPx and GR activities were 1.29+/-0.14 and 1.07+/-0.11 micromol/mg protein/min, respectively. Using the kinetic equilibrium: K(eq)=([GSSG]x[NADPH]x[H(+)])/([GSH](2)x[NADP(+)]), and the GSH/GSSG previously published (HepG2: 2.6 and C6 glioma: 3.6), resting NADPH/NADP(+) for the cell lines were calculated. The results showed that NADPH/NADP(+) for HepG2 cells (17.8) is higher than that in the C6 glioma cells (10.8). These data supported the notion that the reducing power (NADPH/NADP(+)) in the HepG2 cells is higher than that in the C6 glioma cell and thus, the later would be more susceptible to oxidative stress. The results also suggested that besides GSH/GSSG, the activities of GPx and GR are important in predicting tissue redox state. Applying this hypothesis to animal tissues, the ratio of the activities of the two enzymes in mouse liver, cerebral cortex, hippocampus and cerebellum were measured. It was demonstrated that the activities of GPx and GR were different in the different tissues studied. The possible correlation between enzymatic activities and the redox state in the different tissues were discussed.
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PMID:Glutathione peroxidase and glutathione reductase activities are partially responsible for determining the susceptibility of cells to oxidative stress. 1688 53

Recently, we have shown that the non-psychoactive cannabinoid compound cannabidiol (CBD) induces apoptosis of glioma cells in vitro and tumor regression in vivo. The present study investigated a possible involvement of caspase activation and reactive oxygen species (ROS) induction in the apoptotic effect of CBD. CBD produced a gradual, time-dependent activation of caspase-3, which preceded the appearance of apoptotic death. In addiction, release of cytochrome c and caspase-9 and caspase-8 activation were detected. The exposure to CBD caused in glioma cells an early production of ROS, depletion of intracellular glutathione and increase activity of glutathione reductase and glutathione peroxidase enzymes. Under the same experimental condition, CBD did not impair primary glia. Thus, we found a different sensitivity to the anti-proliferative effect of CBD in human glioma cells and non-transformed cells that appears closely related to a selective ability of CBD in inducing ROS production and caspase activation in tumor cells.
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PMID:The non-psychoactive cannabidiol triggers caspase activation and oxidative stress in human glioma cells. 1690 7

Although its concentration is generally not known, glutathione peroxidase-1 (GPx-1) is a key enzyme in the removal of hydrogen peroxide (H2O2) in biological systems. Extrapolating from kinetic results obtained in vitro using dilute, homogenous buffered solutions, it is generally accepted that the rate of elimination of H2O2 in vivo by GPx is independent of glutathione concentration (GSH). To examine this doctrine, a mathematical analysis of a kinetic model for the removal of H2O2 by GPx was undertaken to determine how the reaction species (H2O2, GSH, and GPx-1) influence the rate of removal of H2O2. Using both the traditional kinetic rate law approximation (classical model) and the generalized kinetic expression, the results show that the rate of removal of H2O2 increases with initial GPx(r), as expected, but is a function of both GPx(r) and GSH when the initial GPx(r) is less than H2O2. This simulation is supported by the biological observations of Li et al. Using genetically altered human glioma cells in in vitro cell culture and in an in vivo tumour model, they inferred that the rate of removal of H2O2 was a direct function of GPx activity x GSH (effective GPx activity). The predicted cellular average GPx(r) and H2O2 for their study are approximately GPx(r) < or =1 microm and H2O2 approximately 5 microm based on available rate constants and an estimation of GSH. It was also found that results from the accepted kinetic rate law approximation significantly deviated from those obtained from the more generalized model in many cases that may be of physiological importance.
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PMID:The rate of cellular hydrogen peroxide removal shows dependency on GSH: mathematical insight into in vivo H2O2 and GPx concentrations. 1788 26

Oxidative stress is implicated in a variety of disorders including neurodegenerative diseases, and H(2)O(2) is important in the generation of reactive oxygen and oxidative stress. In this study, we have examined the rate of extracellular H(2)O(2) elimination and relevant enzyme activities in cultured astrocytes and C6 glioma cells and have analyzed the results based on a mathematical model. As compared with other types of cultured cells, astrocytes showed higher activity of glutathione peroxidase (GPx) but lower activities for GSH recycling. C6 cells showed relatively low GPx activity, and treatment of C6 cells with dibutyryl-cAMP, which induces astrocytic differentiation, increased catalase activity and H(2)O(2) permeation rate but exerted little effect on other enzyme activities. A mathematical model [N. Makino, K. Sasaki, N. Hashida, Y. Sakakura, A metabolic model describing the H(2)O(2) elimination by mammalian cells including H(2)O(2) permeation through cytoplasmic and peroxisomal membranes: comparison with experimental data, Biochim. Biophys. Acta 1673 (2004) 149-159.], which includes relevant enzymes and H(2)O(2) permeation through membranes, was found to be fitted well to the H(2)O(2) concentration dependences of removal reaction with the permeation rate constants as variable parameters. As compared with PC12 cells as a culture model for neuron, H(2)O(2) removal activity of astrocytes was considerably higher at physiological H(2)O(2) concentrations. The details of the mathematical model are presented in Appendix.
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PMID:Kinetics of hydrogen peroxide elimination by astrocytes and C6 glioma cells analysis based on a mathematical model. 1840 82


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