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Biomedical subjects

E Kano

Publications and source records attributed to E Kano.

70 records · Page 4Linked to original sources
PubMed1976

Modifying effects of inactivated bovine serum on the acute toxicity of methylmercuric chloride in cells cultured in vitro.

Dynamics of the killing of Ehrlich's murine ascites tumor cells by methylmercuric chloride, MMC, were investigated. Thresholds in the killing action of MMC were observed in the MMC treatment concentration, but not in the MMC treatment time. Inactivated bovine serum protected the E-cells from killing by MMC in vitro. The apparent MMC toxicity was reduced as the serum concentration increased, but remaining partially at high concentrations. Thus the serum increases the threshold for MMC toxicity. It was confirmed that the mode of action, observed as the kinetics of the acute lethality by suspicious substances, could be examined promptly on the mammalian cell level by the present experimental system.

Animals↗
PubMed1969

Cell killing by actinomycin D in relation to the growth cycle of chinese hamster cells.

Using Chinese hamster cells in culture, we have measured the effectiveness of actinomycin D to suppress division as a function of the position, or age, of a cell in its growth cycle. Cells were first exposed to millimolar concentrations of hydroxyurea in order to produce a synchronized population just before the onset of DNA synthesis. Thereafter, the survival response after 30 min exposures to actinomycin D was measured. Cells become resistant as they enter the S phase and then sensitive again in the latter part of S. When they reach G(2) (or G(2)-mitosis) they are maximally resistant; at 1.0 microg/ml, for example, the survival in G(2) is 30-fold greater than it is in G(1). These results, plus measurements reported earlier on the interaction of damage in S cells due to actinomycin D and X-irradiation, suggest that the age-response pattern of the toxic effects of this drug probably reflects both the functional capacity of DNA-actinomycin complexes and the ability of this antibiotic to penetrate chromatin and bind to DNA.

Animals↗
PubMedDate not supplied

In vitro effect of hyperthermia on chemoenhancement and uptake of cisplatin in human pharyngeal carcinoma KB cells.

The purpose of this study was to assess the efficacy of hyperthermia (42 or 44 degrees C) as a modifier of cis-diamminedichloroplatinum (II) (CDDP) cytotoxicity and platinum incorporation in human pharyngeal carcinoma KB cells. To maximize the interactive effect, we examined the time sequence of high (above 43 degrees C) or low (below 43 degrees C) hyperthermia and CDDP. Within the dose range of CDDP studied, there was a marked synergism between the effects of heating at 44 degrees C and subsequent CDDP exposure for 5 h. Pretreatment at 44 degrees C for 30 min or at 42 degrees C for 4 h enhanced CDDP cytotoxicity more than posttreatment at 44 degrees C for 30 min or at 42 degrees C for 4 h. However, the chemoenhancement ratio of pretreatment at 44 degrees C for 30 min was higher then that of pretreatment at 42 degrees C for 4 h, although the thermal isotoxic dose decreased the cell count to 60% under both conditions. There was a significant increase in CDDP uptake after hyperthermia at 44 degrees C. These results indicate that high hyperthermia effectively enhances subsequent CDDP cytotoxicity in human pharyngeal carcinoma KB cells.

Antineoplastic Agents↗
PubMedDate not supplied

Effects of cis-diamminedichloroplatinum (CDDP) and cis-diammine (1,1-cyclobutanedicarboxylate) platinum (CBDCA) on thermotolerance development and thermosensitivity of the thermotolerant cells.

The interactive effects of combined treatment with heat and CDDP (0.5 micrograms/ml) or CBDCA (10 micrograms/ml) were examined on the surviving fractions of V-79 cells. Both CDDP and CBDCA treatment induced a slight enhancement in thermosensitivity of thermotolerant cells. The development of thermotolerance during step-up heating was partially inhibited by simultaneous treatment with CDDP or CBDCA throughout the heating process. Simultaneous heat treatment at 42 degrees C with either drug showed marked interactive effect and inhibited the thermotolerance developed during 42 degrees C heating.

Animals↗
PubMedDate not supplied

Role of heat-shock proteins in the induction of thermotolerance in Chinese hamster V79 cells by heat and chemical agents.

To examine the involvement of heat shock proteins in the induction of thermotolerance in Chinese hamster V79 cells, thermotolerance was induced by heating of the cells at 42 degrees C for 4 h or at 44 degrees C for 20 min, or by treatment of the cells with 50 microM sodium arsenite for 3 h or 20 micrograms/ml puromycin for 4 h. Under unstressed conditions V79 cells synthesized constitutively three major heat-shock proteins, hsp70, hsp85 and hsp105. On exposure to conditions under which thermotolerance was induced, the synthesis of constitutive hsp70, hsp85 and hsp105 increased, but the inducible form of hsp70 was not synthesized, indicating that this inducible form was not necessary for the induction of thermotolerance. Although the amounts of heat-shock proteins synthesized in the cells that acquired thermotolerance were not always more than those synthesized constitutively in unstressed cells, the stressed cells synthesized heat-shock proteins (especially hsp70) preferentially over other proteins. As the level of hsp70 in the thermotolerant cells was almost the same as that in unstressed cells, the specific accumulation of hsp70 seemed not to be required for the acquisition of thermotolerance. From these findings it seemed likely that, for the induction of thermotolerance in V79 cells, hsp70 preferentially synthesized during or after the stress has an important function. Or the synthesis of heat shock proteins may not be important, and constitutively synthesized heat-shock proteins acquire a specific function during or after the stress.

Animals↗
PubMedDate not supplied

Characteristic synthesis and redistribution of 70 kd heat shock protein in thermotolerant Chinese hamster V79 cells.

Upon exposure to heat shock the increased rate of hsp70 synthesis decreased more rapidly in thermotolerant V79 cells than in the non-thermotolerant cells. However, the levels of hsp70 in the thermotolerant cells at 12 h after a heat shock were almost the same as those in the non-thermotolerant cells. On the other hand, the migration of hsp70 from cytoplasm to nucleoli after a heat shock was very rapid in both thermotolerant and non-thermotolerant cells, but hsp70 in the nucleoli disappeared faster in the thermotolerant cells than in the non-thermotolerant cells, and this coincided with the faster decline of hsp70 synthesis in the thermotolerant cells. For the characteristic distribution of hsp70, protein synthesis was not required. Furthermore, the induction and expression of thermotolerance by the cells were little affected by the inhibition of protein synthesis. Thus, the synthesis of hsp70 itself seemed not to be essential for the induction and expression of thermotolerance of the cells, although hsp70 may be essential for thermoresistance of cells. The rapid decrease of hsp70 synthesis and the rapid disappearance of hsp70 from the nucleoli after a heat shock may be essential for the expression of thermotolerance of the cells.

Animals↗
PubMedDate not supplied

In vitro effects of hyperthermia combined with cisplatin or peplomycin on the human maxillary carcinoma cell line IMC-2.

We examined the interactive effects of hyperthermia combined with cisplatin (CDDP) (0.5 micrograms/ml) or peplomycin (PEP) (1.0 microgram/ml) on surviving fractions of human maxillary carcinoma IMC-2 cells. Either CDDP or PEP enhanced the 44 degree C thermosensitivity of thermotolerant cells after heating at 42 degrees C for 2 hours. The development of thermotolerance at 42 degrees C with either of the two drugs for 2 hours was not inhibited by CDDP, but it was partially inhibited by PEP. Moreover, for PEP throughout the entire period of 42-44 degrees C step-up heating, the 44 degree C thermosensitivity of thermotolerant cells after heating at 42 degrees C with PEP for 2 hours was enhanced similarly to that at 44 degrees C with PEP. Heating at 42 degrees C combined with either of the two drugs showed a marked interactive effect.

Antineoplastic Agents↗
PubMedDate not supplied

Combined effects of hyperthermia and CPT-11 on DNA strand breaks in mouse mammary carcinoma FM3A cells.

The interaction between hyperthermia and a DNA topoisomerase I inhibitor, 7-ethyl-10-(4-(1-piperidyl)-1-piperidyl)-carbonyloxy- camptothecin (CPT-11), was studied in the mouse mammary carcinoma FM3A cells. When the cells were treated with CPT-11 at a concentration of 5 micrograms/ml and 44 degrees C hyperthermia for 60 min, an enhancement of formation of single stand breaks (ssb) of DNA was observed. However, a decrease of ssb was observed when hyperthermia was combined with CPT-11 at 50 micrograms/ml. For inhibition of DNA synthesis additive effects were observed for treatment with CPT-11 at 5 micrograms/ml combined with hyperthermia. On the other hand, protective effects were observed for the combined treatment at 50 micrograms/ml. These results indicate that the hyperthermic modification of the effect of CPT-11 on the induction of DNA damage was diverse at low or high concentrations.

Animals↗
PubMedDate not supplied

Effect of heat-drug sequences on thermoenhancement and uptake of cis-DDP in human pharyngeal carcinoma.

To discover the point of maximum interactive effect, we examined the time sequence of high (above (42.5 degrees C) or low (below 42.5 degrees C) -hyperthermia and cis-diammine dichloroplatinum (II) (CDDP). Simultaneous or post-hyperthermic CDDP (0.5 micrograms/ml) treatment at 43 degrees C resulted in a slight synergistic effect, with thermoenhancement ratios (TER) of 1.42 or 1.38, respectively, and there was a significant increase CDDP uptake after both combinations compared with pre-hyperthermic CDDP treatment. However, at 42 degrees C, the maximal interaction (TER = 8.57) was obtained when KB cells were simultaneously heated with CDDP, there was also a significant increase of CDDP uptake by simultaneous procedures compared with pre or post-hyperthermic CDDP treatment. These results indicate that simultaneous or post-hyperthermic CDDP treatment for high-hyperthermia and simultaneous CDDP treatment for low-hyperthermia are the most effective means of CDDP thermochemotherapy with hyperthermia.

Antineoplastic Agents↗