Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sodium ascorbate induced cytotoxicity against human glioblastoma T98G cells in RPMI1640 medium supplemented with fetal bovine serum or human serum samples was studied. Several human serum samples significantly reduced the cytotoxic activity of sodium ascorbate, regardless of sex, age or the disease of the serum donor with or without heat-inactivation of the serum. ESR spectroscopy revealed that this serum effect was not simply due to the alteration of the ascorbyl radical intensity, produced from sodium ascorbate. The present study suggests that the apoptosis-inducing activity of sodium ascorbate might be significantly affected by human serum.
 ...
PMID:Effect of the type of serum in the medium on sodium ascorbate-induced cytotoxicity. 871 24

The cytotoxic activity of sodium 5,6-benzylidene-L-ascorbate (SBA) against human KG-1-C glioma and T98G glioblastoma cell lines was augmented by pretreatment of the cells with L-buthionine-[S, R]-sulfoximine (BSO), which reduced the intracellular glutathione concentrations. SBA produced shrunken cells and large DNA fragments, without the induction of nuclear and internucleosomal DNA fragmentation. The rapid elevation of intracellular free Ca2+ concentration observed after SBA treatment was further augmented by BSO pretreatment. A confocal experiment with Fluo-3 fluorescence revealed that SBA markedly elevated the free Ca2+ concentration in the nuclear region, but did not significantly affect that in the cytoplasmic region. The present study suggests that the nuclear accumulation of Ca2+ is an important initial step for cell death induction by SBA.
 ...
PMID:Ca2+ mobilization during cell death induction by sodium 5, 6-benzylidene-L-ascorbate. 891 62

ESR spectroscopy revealed that high molecular weight natural substances, such as protein-bound polysaccharide PSK, alkali-lignin and lignin sulfonate, significantly enhanced the ascorbyl radical intensity derived from sodium ascorbate or ascorbic acid in culture medium. Enhancement of the ascorbyl radical intensity was coupled with rapid degradation of ascorbate. These substances synergistically enhanced the ascorbate-induced cytotoxicity against human leukemic and glioblastoma cell lines. These data suggest the possible role of the ascorbyl radical in cytotoxicity induction.
 ...
PMID:Enhancement of radical intensity and cytotoxic activity of ascorbate by PSK and lignins. 891 16

ESR spectroscopy revealed that the radical intensity of sodium ascorbate and ascorbic acid was significantly higher under hyperthermic conditions. The enhancement of ascorbyl radical intensity was coupled with the accelerated degradation of ascorbate and cytotoxicity induction against human leukemic and glioblastoma cell lines. Sodium ascorbate produced higher ascorbyl radical intensity and more potent cytotoxicity, as compared with ascorbic acid. These data demonstrate that ascorbic acid does not inhibit, but rather stimulates the cytotoxic action of hyperthermia. The combination of hyperthermia and ascorbate treatment might produce higher antitumor activity.
 ...
PMID:Enhancement of radical intensity and cytotoxic activity of ascorbate by hyperthermia. 891 17

Cytotoxic activity of sodium ascorbate against a human glioblastoma T98G cell line was concentration-dependently inhibited by serum in the RPMI1640 medium. The inhibitory effect of sera from pancreatic or stomach cancer patients was significantly higher than that of fetal bovine serum (FBS), with or without heat-inactivation. The cytotoxic activity of sodium ascorbate almost completely disappeared in 60-80% of patient sera. ESR spectroscopy revealed that both patient sera and FBS increased the ascorbyl radical intensity, but to significantly lower extents, as compared with that attained by RPMI1640 medium. The present study suggests the importance of re-evaluating the efficacy of not only ascorbate but also other chemotherapeutic drugs under more physiological conditions.
 ...
PMID:Inhibition of cytotoxic activity of ascorbate by human cancer patient sera. 906 88

Various metal ions were investigated for their ability to modify the radical intensity and cytotoxic activity of sodium ascorbate or ascorbic acid. The addition of metal ions, such as Cu+, Cu2+, Fe2+, Zn2+, Mn2+ and Fe3+, dose-dependently enhanced the ascorbyl radical intensity whereas Na+, K+, Ca2+ and Mg2+ were totally inactive. The enhancement of ascorbyl radical intensity by metal ions was tightly coupled with the accelerated degradation of ascorbate. Addition of either serum or albumin significantly reduced the stimulation effect of Cu2+, and almost completely eliminated that of Fe3+ and Zn2+. The noncytotoxic concentration of Cu2+ significantly enhanced the cytotoxicity of ascorbate against cultured human glioblastoma T98G cell line. The present data suggest the possible role of metal ions in the regulation of the biological activity of ascorbate.
 ...
PMID:Effect of metal ions on radical intensity and cytotoxic activity of ascorbate. 913 59

In order to test whether ascorbyl radical can directly induce apoptotic cell death, it was produced by the reaction of sodium L-ascorbate with L-ascorbate oxidase. Sodium L-ascorbate induced cytotoxicity against both human glioblastoma and promyelocytic leukemic cell lines. The addition of ascorbate oxidase significantly enhanced both degradation and radical generation of ascorbate, but completely eliminated its cytotoxic activity against both of these cells. These data demonstrate that the ascorbyl radical is not the sole determinant of apoptosis induction.
 ...
PMID:Effect of ascorbate oxidase on radical intensity and cytotoxic activity of ascorbate. 913 65

We investigated the effect of deferoxamine mesylate (DFO), an iron chelator, to test whether ascorbate-induced cytotoxicity is due to iron-catalyzed oxidation. Exposing human promyelocytic leukemic HL-60 cells to either sodium ascorbate or ascorbic acid for 1 h resulted in the progressive production of apoptotic cells characterized by cell shrinkage, as well as nuclear and internucleosomal DNA fragmentation. The addition of micromolar to millimolar concentrations of DFO during the 1-h exposure did not inhibit, but rather enhanced the ascorbate-induced apoptosis in both regular and serum-free RPMI1640 medium. However, a higher concentration of serum significantly inhibited the ascorbate-induced cytotoxicity. In contrast, the cytotoxic activity of ascorbate against T98G human glioblastoma cells was enhanced or reduced by micromolar and millimolar concentrations of DFO, respectively. Ascorbate significantly increased the oxidation potential in the culture medium, and the pro-oxidant action of ascorbate was further augmented by the presence of the cells. DFO did not significantly affect the ascorbyl radical intensity and only slightly reduced the ascorbate-elevated oxidation potential. These data demonstrated that ascorbate can induce cytotoxicity even in iron-deficient medium.
 ...
PMID:Effect on an iron-chelator on ascorbate-induced cytotoxicity. 919 88

Millimolar concentrations of ascorbic acid or sodium ascorbate induced cytotoxicity against human glioblastoma T98G cells. Addition of hot water and sodium hydroxide extracts of the bark of Acer nikoense Maxim. synergistically enhanced the cytotoxic activity of ascorbate. Human peripheral blood lymphocytes and polymorphonuclear cells were relatively resistant to ascorbate, the Acer nikoense Maxim. extract, or a combination of them. The extracts stimulated the degradation of ascorbates via ascorbyl radical production, in parallel with their ability to stimulate the cytotoxic activity of ascorbate. The results suggest the medicinal efficacy of the Acer nikoense Maxim. extracts.
 ...
PMID:Enhancement of cytotoxic activity of ascorbate by Acer nikoense Maxim. Extracts. 949 49

Sodium-L-ascorbate, L-ascorbic acid, D-isoascorbic acid, sodium 5,6-benzylidene-L-ascorbate and sodium-6-beta-O-galactosyl-L-ascorbate, which produce ascorbyl radicals during the oxidative degradation, also induced cytotoxicity against cultured human renal carcinoma (TC-1) and glioblastoma multiform tumor (T98G) cell lines. On the other hand, L-ascorbic acid 2-phosphate magnesium and L-ascorbic acid 2-sulfate dipotassium salt, which do not produce the ascorbyl radical, were inactive. This suggests the possible role of the ascorbyl radical for cell death induction. T98G cells were more resistant to ascorbate analogs than TC-1 and HL-60 cells, possibly due to higher intracellular glutathione concentrations. Ascorbate treatment induced rapid elevation of both intracellular concentration of cAMP and Ca2+ in HL-60 cells, but not in TC-1 and T98G cells. However, the elevation of cAMP by theophyline and N,2-dibutyryl adenosine 3,5 cyclic monophosphate (dibutyryl cAMP) resulted in a decrease in the viable cell number. This suggests the possible role of cAMP for ascorbate-induced cell death.
 ...
PMID:Induction of cell death by ascorbic acid derivatives in human renal carcinoma and glioblastoma cell lines. 1065 1


1 2 3 4 Next >>