Reduced glutathione and S-acetylglutathione as selective apoptosis-inducing agents in cancer therapy

Donnerstag, B.; Ohlenschläger, G; Cinatl, Jindrich; Amrani, Michael; Hofmann, Dieter; Flindt, Sven; Treusch, Gernot; Träger, Lothar

doi:10.1016/s0304-3835(96)04461-8

Cited by 19 publications

(12 citation statements)

References 29 publications

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“…The intracellular thiol level is accepted to be important in determining the extent of cellular damage induced by stress shock. The intracellular GSH concentration may determine the sensitivity of cells to damage produced by the anticancer drug (Donnerstag et al 1996). WR-2721 and GSH are thiol compounds that protect against the cytoand genotoxic effects of cyclophosphamide in bone marrow cells with increasing thiol content in the cells (Blasiak et al 2002).…”

Section: Discussionmentioning

confidence: 99%

Citrus extract modulates genotoxicity induced by cyclophosphamide in mice bone marrow cells

Hosseinimehr

Karami

2005

Journal of Pharmacy and Pharmacology

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The protective effect of citrus extract was investigated by using the micronucleus assay for anticlastogenic activity in mouse bone marrow cells; liver glutathione (GSH) content was determined against toxicity induced by cyclophosphamide. Mice were orally (gavage) pretreated with solutions of citrus peel extract (Citrus aurantium var. amara) prepared at three different doses (100, 200 and 400 mg kg(-1;) body weight) for 7 consecutive days. Then mice were injected intraperitoneally on the seventh day with cyclophosphamide (50 mg kg(-1)) and after 24 h killed for the evaluation of micronucleated polychromatic erythrocytes (MnPCEs) in bone marrow cells. Non-protein thiol levels in liver were estimated in mice injected with citrus extract with or without cyclophosphamide treatment. Administration of citrus extract before cyclophosphamide treatment significantly reduced the frequency of MnPCEs in mice bone marrow compared with the group treated with cyclophosphamide alone (P<0.0001-0.05). Citrus extract at a dose of 400 mg kg(-1) reduced MnPCEs 2.8 fold against genotoxicity induced by cyclophosphamide. Administration of cyclophosphamide depleted the GSH level in liver. Citrus extract showed excellent scavenging effects on 1,1-diphenyl-2-picryl hydrazyl radical (DPPH) at a concentration of 1.6 mg mL(-1). Application of citrus extract 1 h before cyclophosphamide treatment allowed GSH content to reach the normal level. It appeared that citrus extract, particularly flavonoids constituents with antioxidative activity, may return the GSH level to normal in stress conditions and reduces genotoxicity induced by cyclophosphamide in bone marrow cells.

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Section: Discussionmentioning

confidence: 99%

Citrus extract modulates genotoxicity induced by cyclophosphamide in mice bone marrow cells

Hosseinimehr

Karami

2005

Journal of Pharmacy and Pharmacology

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“…In addition, KMU-193 induced fragmentation of DNA, a strong index of apoptosis ( Figure 2B). It has been reported that only a few chemicals are known to have the property for selective/ preferential elimination of cancer cells without affecting the untransformed cells (Donnerstag et al, 1996;Ahmad et al, 1997). To examine whether KMU-193 triggers cancerspecific apoptosis, two types of untransformed cells were treated with KMU-193 at the indicated concentrations for 36 h. As shown in Figure 2C, the exposure of KMU-193 to the two untransformed cells led little changes of cellular viability, however treatment of A549 cells with KMU-193 resulted in markedly increased accumulation of the sub-G1 phase in a dose-dependent manner.…”

Section: Kmu-193 Induces Morphological Change and Apoptosis Of A549 Cmentioning

confidence: 99%

Treatment with a Small Synthetic Compound, KMU-193, induces Apoptosis in A549 Human Lung Carcinoma Cells through p53 Up-Regulation

Choi

Shin²,

Lee³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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“…Han Dw et al Acta Pharmacologica Sinica npg cells without affecting the normal cells [6,7,12,13] . EGCG has been shown to have suppressive effects on various cancer cells by inducing cell cycle arrest and inhibiting prolifera tion [14,15] , whereas less attention has been paid to its cytoprotective effects on normal cells.…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin-3-gallate regulates cell growth, cell cycle and phosphorylated nuclear factor-κB in human dermal fibroblasts

et al. 2011

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Aim: To investigate the effects of (-)epigallocatechin-3-gallate (EGCG), the main polyphenol in green tea, on cell growth, cell cycle and phosphorylated nuclear factor-κB (pNF-κB) expression in neonatal human dermal fibroblasts (nHDFs). Methods: The proliferation and cell-cycle of nHDFs were determined using WST-8 cell growth assay and flow cytometry, respectively. The apoptosis was examined using DNA ladder and Annexin V-FITC assays. The expression levels of pNF-κB and cell cycle-related genes and proteins in nHDFs were measured using cDNA microarray analyses and Western blot. The cellular uptake of EGCG was examined using fluorescence (FITC)-labeled EGCG (FITC-EGCG) in combination with confocal microscopy. Results: The effect of EGCG on the growth of nHDFs depended on the concentration tested. At a low concentration (200 μmol/L), EGCG resulted in a slight decrease in the proportion of cells in the S and G 2 /M phases of cell cycle with a concomitant increase in the proportion of cells in G 0 /G 1 phase. At the higher doses (400 and 800 μmol/L), apoptosis was induced. The regulation of EGCG on the expression of pNF-κB was also concentration-dependent, whereas it did not affect the unphosphorylated NF-κB expression. cDNA microarray analysis showed that cell cycle-related genes were down-regulated by EGCG (200 μmol/L). The expression of cyclins A/B and cyclin-dependent kinase 1 was reversibly regulated by EGCG (200 μmol/L). FITC-EGCG was found to be internalized into the cytoplasm and translocated into the nucleus of nHDFs. Conclusion: EGCG, through uptake into cytoplasm, reversibly regulated the cell growth and expression of cell cycle-related proteins and genes in normal fibroblasts.

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Reduced glutathione and S-acetylglutathione as selective apoptosis-inducing agents in cancer therapy

Cited by 19 publications

References 29 publications

Citrus extract modulates genotoxicity induced by cyclophosphamide in mice bone marrow cells

Citrus extract modulates genotoxicity induced by cyclophosphamide in mice bone marrow cells

Treatment with a Small Synthetic Compound, KMU-193, induces Apoptosis in A549 Human Lung Carcinoma Cells through p53 Up-Regulation

Epigallocatechin-3-gallate regulates cell growth, cell cycle and phosphorylated nuclear factor-κB in human dermal fibroblasts

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