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PubMed1981

Metabolic fate on 1-hexylcarbamoyl-5-fluorouracil and 5-fluorouracil in mice bearing ascites sarcoma 180.

Patterns of metabolism and disposition in plasma of tumor-bearing mice after oral administration of [6(-14)C]1-hexylcarbamoyl-5-fluorouracil ([6(-14)C]HCFU) resembled those in plasma of normal mice, but elimination of [6(-14)C]HCFU and 5-fluorouracil (FUra) was slower in tumor-bearing mice. The level of 1-(5-hydroxyhexylcarbamoyl)-5-fluorouracil (HHCFU) was lower in tumor-bearing mice. Also detected in plasma were [6(-14)C]HCFU, HHCFU, 1-(3-carboxypropylcarbamoyl)-5-fluorouracil, FUra, 5,6-dihydro-5-fluorouracil, and alpha-fluoro-beta-alanine. FUra originating from [6(-14)C]HCFU was retained over 6 hours, whereas intact FUra after [6(-14)C]FUra administration disappeared within 2 hours. The pattern of metabolism in ascitic fluid was similar to that in plasma after [6(-14)C]HCFU and [6(-14)C]FUra administration, but FUra was retained for a longer period in ascitic fluid. In sarcoma 180 cells, the maximum concentration of total radioactivity was observed 1 or 2 hours after [6(-14)C]FUra or [6(-14)C]HCFU administration, respectively, and the level of intact HCFU was very low. The principal metabolites were nucleotides that were maintained for a long period after administration of both compounds. The pattern of other metabolites after [6(-14)C]HCFU administration was also similar to that after [6(-14)C]FUra administration.

Administration, Oral↗
PubMed1989

[Influence of laurocapram on ultrastructures of mouse skin and sarcoma 180 membrane].

Laurocapram (Lau), 1-dodecyl-hexahydro-2 H-azepin-2-one, (azone) is a new percutaneous penetration enhancer. However, the mechanism of its action for absorption promoter of other agents is still unknown. In this paper the effect of Lau on ultrastructures of skin surface and tumor cell membrane were studies. Lau (2%) suspension was applied to abdominal skin of ICR/JCL, C 57 BL mice or one side of abdominal skin of nude mouse with drug and other side with the vehicle solvent once daily for 2-3 d. The skin was excised at 4 h after the final medication for examination under scanning electron microscope (SEM). The results showed the numerous small infolding lines which divided the skin surface into small areas with vesiculation and peeled the epidermal surface to form a few minor holes. The cuticles of the hair shaft dropped off and became thinner. Numerous desquamated cells around the orifice of the hair were fractured, detached and widened. Sarcoma 180 cells were incubated with Lau 25 micrograms/ml at 37 degrees C for 4 h. The microvilli of some cells dropped off and the size of villi became thinner and shorter. The top of some villi of the cells appeared occasionally thick to make the profile as a bat. The surface of numerous naked cells became rugged and rough and showed many black minor holes in the area of denuded cell membrane or dropped microvilli. More than 100 holes in the exposed surface of the naked cell were seen. It seemed that the Lau drilled holes on the biomembrane and enlarged the orifice of hair follicles and thus enhanced the transdermal absorption.

Animals↗
PubMed1980

[In vivo cell cycle synchronization of the murine sarcoma 180 by continuous colcemid infusion (author's transl)].

In recent years, partial synchronization in vivo of normal tissues or solid tumors has been achieved by some investigators. A study of synchronization in vivo is valuable for not only analysis of the cell cycle kinetics, but also chemotherapy. Most of the chemotherapeutic agents and radiation show a specific reaction to a specific phase of cell cycle. This concept supports the value of chemotherapy using synchronization of tumor cells. In other words, the chemotherapeutic effect is enhanced by killing greater numbers of tumor cells which are gathered in a specific phase after synchronization. At the same time toxic effects are reduced by allowing normal tissue escaping from the effective phase. Colcemid is one of the most useful metaphase arrest agents. Colcemid blocks cells at metaphase by disrupting the mitotic spindle, and has been found to be less toxic than colchicine. Colcemid, when used in optimum dosage and duration of exposure, will accumulate tumor cells in metaphase with less toxic effects on normal tissues. Synchronization of the accumulated cells will be achieved after colcemid release. The purpose of this study is to examine the effects of colcemid on the cell cycle and to maximize synchrony after release of colcemid in sarcoma 180 tumor bearing mice. A mitotic linear accumulation was obtained by continuous colcemid infusion at 5.82 microgram/hr. Low dose colcemid infusion (0.582 and 1.455 microgram/hr) for 14 hours did not accumulated mitotic cells, but doses more than 5.82 microgram/hr of colcemid blocked it completely, accumulating 25.5% of cells after a 20 hours infusion. Therefore, mitotic accumulate by using colcemid is thought to be dose and time dependent within the limited range. However, the rates of mitotic accumulation were underestimated probably because of the increment of pyknoses and inhibition of DNA synthesis by high dose and long exposure of colcemid. A four hours colcemid infusion at 5.82 microgram/hr accumulated 11% of tumor cells without severe damage on cell cycle timing. The cells accumulated in mitotic phase recovered 3-4 hours after release of colcemid, and partial tumor synchronization was achieved in the following next one cycle. The rate of synchronization was thought to be about 30%, which was compatible with that of synchronization in vivo. Therefore, colcemid infusion at optimal dosage and duration of exposure can synchronize tumor cells reasonably. It is possible that therapeutic potential will be elevated if G1 or S phase specific drugs are used as killing agents after synchronization with colcemid. Moreover, higher synchrony will be obtained after several intermittent infusions of colcemid.

Animals↗
PubMed1997

Proteolytic activities of mouse sarcoma 180 cells that are inhibited by Bowman-Birk and Kunitz protease inhibitors.

In this study, using zymogram analysis two proteolytic activities were identified in the mouse sarcoma 180 (S-180) cells that were activated by trypsin treatment and inhibited by both BBI and ACTI. These enzymes, with molecular weights of 46 kDa (dominant band) and 62 kDa (minor band), were mainly localized in the cytosol, and had optimal activity at pH 7 and 8 respectively. Their inhibition by DFP, BBI and ACTI but not EDTA and TPCK indicated they were trypsin-like serine proteases and may be the intracellular target-enzymes of protease inhibitors. The level of the precursor of the 62 kDa protease was significantly increased in the S-180 solid and soft tumors, whereas the level of the 46 kDa precursor was almost undetectable, implying that a physiological role may be played by these serine proteases during tumor invasion.

Animals↗
PubMed1983

Alteration in natural resistance of sarcoma 180 tumor to Bouvardin (NSC 259968) following hyperthermia.

Sarcoma-180 (S-180) tumor cells grown in Swiss mice displayed natural resistance to Bouvardin (NSC 259968) when administered alone in a single dose or in multiple doses. Hyperthermia treatment (43 degrees C for 1 hr) alone did not show any tumor growth reduction. However, the drug combined with hyperthermia markedly reduced tumor growth suggesting that hyperthermia alters the natural resistance of S-180 cells to Bouvardin.

Animals↗