Detail of "459-86-9"

Reference

Some effects of inhibitors of polyamine synthesis on experimental prostatic cancer

Some effects of inhibitors of polyamine synthesis on experimental prostatic cancer. Dunzendorfer, U.; Releyea, N.; Whitmore, W. F., Jr.; Fogh, J.; Balis, M. E. (Urol. Lab., Sloan Kettering Inst. Cancer Res., New York, NY, USA). Arzneim.-Forsch., 34(1), 36-9 (English) 1984. CODEN: ARZNAD. ISSN: 0004-4172. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Difluoromethylornithine (DFMO) [70052-12-9] and methylglyoxal-bis(guanylhydrazone) (MGBG) [459-86-9], inhibitors of ornithine decarboxylase (ODC) [9024-60-6] and S-adenosylmethionine decarboxylase (AMDC) [9036-20-8], resp., were tested in 2 exptl. prostatic cancer models. DFMO decreased tumor size in both the rapidly growing R-3327 rat prostatic adenocarcinoma and the human DU-145 adenocarcinoma in nude mice. MGBG induced a decrease in tumor size but was highly toxic. Flutamide [13311-84-7] or 9-b-D-arabinofuranosyladenine (Ara-A) [5536-17-4] proved ineffective in decreasing tumor growth of the human DU-145 or the R-3327-G strain, resp. However, these 2 drugs increased the efficacy of DFMO against the DU-145 tumor but not against the R-3327 tumor. The DU-145 tumor had a high level of ODC which was reduced by DFMO.

Decreased cytotoxicity of aziridinylbenzoquinone caused by polyamine depletion in 9L rat brain tumor cells in vitro

Decreased cytotoxicity of aziridinylbenzoquinone caused by polyamine depletion in 9L rat brain tumor cells in vitro. Alhonen-Hongisto, Leena; Deen, Dennis F.; Marton, Laurence J. (Sch. Med., Univ. California, San Francisco, CA 94143, USA). Cancer Res., 44(1), 39-42 (English) 1984. CODEN: CNREA8. ISSN: 0008-5472. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Depletion of intracellular putrescine [110-60-1] and spermidine [124-20-9] levels by treatment with 1 mM a-difluoromethylornithine [70052-12-9], for 72 h decreased the cytotoxicity of aziridinylbenzoquinone (AZQ) [57998-68-2] towards 9L rat brain tumor cells in culture. Dose modification factors were 1.9 and 1.8 at 10 and 1% survival levels, resp. Decreased cytotoxicity could be almost completely prevented by addn. of putrescine to polyamine-depleted cells 24 h before AZQ treatment. Although AZQ alone was cytotoxic against 9L cells, metabolic activation by the S-9 rat liver microsomal fraction increased greatly the obsd. cytotoxicity. However, even with microsomal activation, pretreatment of cells with 1 mM a-difluoromethylornithine for 48 h decrease/AZQ cytotoxicity; dose modification factors were 2.4 and 2.2 at 10 and 1% survival levels, resp. Addn. of putrescine to polyamine-depleted cells 24 h before AZQ treatment prevented the decrease in cytotoxicity. Pretreatment of 9L cells for 48 h with 40 mM methylglyoxal bis(guanylhydrazone) [459-86-9] caused a decrease in the cytotoxicity of AZQ administered without microsomal activation. The dose modification factor was 1.6 at both 10 and 1% survival levels.