Cellular glutathione as a protective agent against 4-hydroperoxycyclophosphamide cytotoxicity in K-562 cells

@article{Peters2008CellularGA,
  title={Cellular glutathione as a protective agent against 4-hydroperoxycyclophosphamide cytotoxicity in K-562 cells},
  author={Richard H. Peters and K. Ballard and John E. Oatis and David J. Jollow and Robert K. Stuart},
  journal={Cancer Chemotherapy and Pharmacology},
  year={2008},
  volume={26},
  pages={397-402}
}
SummaryExposure of cells of the K-562 erythroleukemia cell line to 4-hydroperoxycyclophosphamide (4-HC), an analog of activated cyclophosphamide, causes a concentration-dependent inhibition of in vitro colony formation by these cells. For investigation of the role of glutathione (GSH) in the metabolism of 4-HC, GSH levels of K-562 cells were modulated by exposing the cells to buthionine sulfoximine (BSO), a specific inhibitor of GSH synthesis, and/or to GSH ethyl esters. Both the mono- and… 
1 Citations

References

SHOWING 1-10 OF 36 REFERENCES
Glutathione depletion as a determinant of sensitivity of human leukemia cells to cyclophosphamide.
The role of glutathione (GSH) as a determinant of cellular sensitivity to the cytotoxic and DNA-damaging effects of cyclophosphamide (CP) was studied in a dual culture system of rat hepatocytes and
Effect of glutathione depletion by L-buthionine sulfoximine on the cytotoxicity of cyclophosphamide in single and fractionated doses to EMT6/SF mouse tumors and bone marrow.
TLDR
A possible role for BSO as a clinical chemosensitizer, which could be combined with fractionated doses of CYC and may be effective on small cancerous lesions is suggested.
Role of glutathione in the metabolism-dependent toxicity and chemotherapy of cyclophosphamide.
TLDR
Acrolein in vivo preferentially reacts with glutathione, and sulfhydryl-containing compounds may protect against acrolein toxicity and at the same time not interfere with the chemotherapeutic activity of CP.
Protective role of thiols in cyclophosphamide-induced urotoxicity and depression of hepatic drug metabolism.
TLDR
Administration of N-acetylcysteine or sodium-2-mercaptoethane sulfonate with cyclophosphamide, while not protecting against leukopenia, protected against the enzymatic inactivation and urotoxicity.
Pharmacokinetics and metabolism of sodium 2-mercaptoethanesulfonate in the rat.
TLDR
The formation of the pharmacologically active thiol form from dimesna is associated with the consumption of equimolar concentrations of reduced glutathione.
Synthesis and preliminary antitumor evaluation of 4-(SR)-sulfido-cyclophosphamides
TLDR
A preliminary evaluation of the curative effect after a single IV injection of 4-(S-ethane)-and 4-ethanol)-sulfidocyclophosphamide in rats bearing Yoshida ascites sarcoma or in nu/nu mice bearing human breast carcinoma xenografts suggested that these sulfido derivatives possess the same oncostatic efficacy as activated cycloph phosphamide itself.
Glutathione monoethyl ester: preparation, uptake by tissues, and conversion to glutathione.
Inhibition of the protective effect of cyclophosphamide by pre-treatment with buthionine sulfoximine.
Combinations of 4-hydroperoxycyclophosphamide (4-HC) and cisplatin for bone marrow purging in autologous marrow transplantation: an update.
TLDR
At concentrations resulting in equivalent toxicity to marrow CFU-GM, cisplatin seemed to be more toxic to murine spleen blast colony forming cells (CFC-BC) than 4-HC, and the drugs in combination appeared to have at least additive toxicities against CFC- BC.
Studies on the in vivo formation of acrolein: 3-hydroxy-propylmercapturic acid as an index of cyclophosphamide (NSC-26271) activation.
  • R. Alarcon
  • Biology, Chemistry
    Cancer treatment reports
  • 1976
3-Hydroxypropylmercapturic acid (MCA) has been quantitatively determined in the urine of rats given cyclophosphamide (CP), related antineoplastic agents, allyl alcohol, or acrolein, with a simple
...
...