Elsevier

Biochemical Pharmacology

Volume 51, Issue 1, 12 January 1996, Pages 87-90
Biochemical Pharmacology

Short communication
Glutathione and glutathione S-transferase in benign and malignant prostate cell lines and prostate tissues

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Abstract

Metastatic prostate adenocarcinoma is unresponsive to alkylator chemotherapy with virtually no prolonged remissions. Glutathione (GSH) and glutathione S-transferase (GST) have been reported to play a role in tumor resistance to alkylator therapy; however, there are no baseline studies that have investigated and compared GSH and GST in human prostate cell lines and tissues. Thus, we determined the GSH content and GST activity in benign prostate, in primary and metastatic prostate adenocarcinoma tissues, in immortal adenocarcinoma cell lines, and in primary cell cultures derived from both benign prostate and primary prostatic carcinoma tissue. The GSH content was higher in the immortal cell lines than in the fresh tissues and primary cultures. Conversely, the GST activity was significantly higher in the tissues and primary cultures than in the cell lines. The GSH content and GST activity of the primary cultured prostatic cells were similar to those of the prostate tissues. The differences between the immortal prostate cancer cell lines and prostate tissue are of sufficient magnitude to suggest that in vitro results with cell lines may not extrapolate to prostate cancer in vivo. The GSH content and GST activity in a prostate specific antigen-secreting human prostate tumor xenograft, LuCaP23, maintained in nude mice were similar to those of human prostate tissue and primary cultures. Both the xenograft and primary cultures from patients with prostate cancer may be more appropriate models than established cell lines for investigating techniques to increase the effectiveness of alkylators in prostate cancer.

Keywords

prostate cancer
glutathione
glutathione S-transferase

Abbreviations

GSH
glutathione
BSO
buthionine sulfoximine
GST
glutathione S-transferase
PSA
prostate specific antigen
BPH
benign prostatic hypertrophy

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This project was supported by a VA MERIT Award and an Antonio Principi Memorial Cancer Fund Award to R.L.F. The LuCaP model was derived at the University of Washington, in part through the support of the Richard M. Lucas Foundation.