Disease relevance of Zilascorb

• 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 [1].
• Role of hydrogen peroxide (H2O2) in the induction of antitumor activity against chemically-induced rat hepatocellular carcinoma by sodium 5,6-benzylidene-L-ascorbate (SBA) was investigated [2].
• Ascorbic acid derivatives which produced radicals (sodium 5,6-benzylidene-L-ascorbate (SBA), sodium-L-ascorbate, D-isoascorbic acid) dose-dependently reduced the viable cell number of human squamous carcinoma (HSC-2, HSC-4, NA), human salivary gland tumor (HSG) and human promyelocytic leukemia (HL-60) cell lines [3].

High impact information on Zilascorb

• The expression of HIV-antigen on U1 cells induced by TPA or TNF-alpha was found to be prevented by sodium 5,6-benzylidene-L-ascorbate (SBA) in a concentration-dependent manner [4].
• Mitochondrial control of cell death induction by sodium 5,6-benzylidene-L-ascorbate [5].
• Treatment of HL-60 cells with sodium 5,6-benzylidene-L-ascorbate (SBA) or sodium ascorbate induced apoptotic cell death characterized by chromatin condensation, nuclear fragmentation, loss of microvilli, and production of numerous vacuoles and apoptotic bodies [6].
• Sodium 5,6-benzylidene-L-ascorbate, intravenous administration of which induces degeneration of human inoperable tumors and rat hepatocellular carcinoma in vivo, induces apoptotic or non-apoptotic cell death, depending on the types of target cells [7].
• Induction of non-apoptotic cell death by sodium 5,6-benzylidene-L-ascorbate in a human salivary gland tumor cell line [8].

Chemical compound and disease context of Zilascorb

• 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 [9].

Biological context of Zilascorb

• Induction of DNA fragmentation in human myelogenous leukemic cell lines by sodium 5,6-benzylidene-L-ascorbate and its related compounds [10].
• During apoptosis of HL-60 cells induced by either sodium ascorbate, sodium 5,6-benzylidene-L-ascorbate (SBA) or dopamine, the consumption of nonpolar and polar amino acids (neutral or acidic) generally declined, except for Cys, Met and Arg, whereas the production of Gly and Glu was slightly increased [11].

Anatomical context of Zilascorb

• Sodium L-ascorbate, L-ascorbic acid, D-isoascorbic acid, sodium 6-beta-O-galactosyl-L-ascorbate and sodium 5,6-benzylidene-L-ascorbate, at the concentration of 1-10 mM, induced apoptotic cell death characterized by cell shrinkage, nuclear fragmentation and internucleosomal DNA cleavage in human promyelocytic leukemic HL-60 cells [12].

Associations of Zilascorb with other chemical compounds

• In vitro modulating effect of the reversible protein synthesis inhibitor zilascorb (2H) on cis-diamminedichloroplatinum (II)-induced cytotoxicity [13].
• The effect of twenty amino acids on the radical intensity of four antioxidants (sodium L-ascorbate, sodium 5,6-benzylidene-L-ascorbate, gallic acid, caffeic acid) was investigated, using ESR spectroscopy [14].

Gene context of Zilascorb

• The effect of various physiological fluids on the radical intensity of sodium ascorbate and sodium 5,6-benzylidene-L-ascorbate (SBA) was investigated using ESR spectroscopy [15].
• We investigated whether sodium 5,6-benzylidene-L-ascorbate (SBA) induces apoptotic cell death in a human salivary gland tumor cell line HSG, using two different cytochemical methods [8].

Analytical, diagnostic and therapeutic context of Zilascorb

• The stability of sodium 5,6-benzylidene-L-ascorbate (SBA), consisting of two diastereomers, was investigated by high-performance liquid chromatography [16].

References