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PubMed2001

Treatment of VX2 carcinoma implanted in the liver with arterial and intraperitoneal administration of oily anticancer agents.

PURPOSE: Long-term survival and cure cannot be achieved in patients with unresectable, advanced abdominal cancer, because no chemotherapeutic treatment has definite antitumor activity for malignant solid tumor and its dissemination. In this study, arterial and intraperitoneal administration of oily anticancer agents, which have properties that permit targeted chemotherapy for VX2 carcinoma implanted in the liver, was attempted to achieve long-term survival. MATERIALS AND METHODS: Rabbits bearing VX2 tumors in the liver measuring 1-2 cm in diameter received an arterial injection of 0.2 ml of nitrogen mustard N-Oxide (HN2-O) dissolved in Lipiodol (7.5 mg/ml), a newly developed oily anticancer agent, for the tumor and an intraperitoneal injection of a cocktail of oily anticancer agents for the prevention of intraperitoneal dissemination. RESULTS: Twelve out of thirteen rabbits survived and VX2 cancer was not observed in these 12 rabbits. The controls received a sham operation, an intraperitoneal injection of the cocktail of oily anticancer agents alone, or an arterial injection of HN2-O/Lipiodol alone. In these control groups, 27 out of 29 rabbits died of cancer. To examine the dose form for arterial injection, 14 rabbits received an arterial injection of the simple mixture of HN2-O dissolved in physiological saline and Lipiodol, with an additional intraperitoneal injection of the cocktail. Eight of these 14 rabbits died of enlargement of the hepatic tumor and peritoneal dissemination. CONCLUSION: Long-term survival and cure was achieved in almost all rabbits bearing VX2 tumor in the liver by simultaneous arterial and intraperitoneal injection of oily anticancer agents.

Animals↗

PubMed1989

Effects of nitrogen mustard-N-oxide on ionic activities of inner ear fluid and ionic permeabilities of the cochlear partition in the guinea pig.

The effect of nitrogen mustard-N-oxide (NMO) on the endocochlear potential (EP) was investigated from the aspect of the ion concentrations and permeabilities in the cochlea. Compared with the untreated animals, in NMO-treated animals 20 to 30 hours after administration, the EP was decreased (30.8 +/- 3.5 mV in NMO versus 82.4 +/- 1.6 mV in control), the K+ concentration in perilymph of the scala tympani was increased (8.2 +/- 1.0 mM versus 5.3 +/- 0.7 mM), the K+ concentration in endolymph was decreased (128.5 +/- 10.6 mM versus 157.9 +/- 7.9 mM), and the Na+ concentration in endolymph was increased (9.6 +/- 3.6 mM versus 2.5 +/- 0.4 mM). The permeability coefficient for Na+ of the cochlear partition in the NMO-treated animals significantly decreased, while that for Cl- significantly increased. The negative EP, which presumably exists in the normal state, diminished further (-2.7 mV versus -27.8 mV), and the calculated electrogenic potential of the EP was depressed remarkably (33.5 mV versus 110.2 mV). The results suggest that the effects of NMO involved changes in ion permeabilities of the partition and the inhibition of electrogenic transport processes in the cochlea.

Animals↗

PubMed1991

[Study of the mechanism of supporting cells repairing the organ of Corti in terms of cell kinetics--nuclear DNA synthesis of supporting cell of the organ of Corti in the cochlea damaged by nitromin administration].

3H-thymidine autoradiography in vivo was carried out on normal mature mice, whose organs of Corti were securely damaged by Nitrogen Mustard-N-oxide (nitromin). The cell kinetics of supporting cells of the organ of Corti were examined and relation between these changes and mechanisms of supporting cells to maintain the organ of Corti was discussed in this paper. A few grains in various kinds of supporting cells in S stage, which were not found in control mice without nitromin injection, were discovered. Those were detected in Hensen's cell, Deiters' cell, Claudius' cells, and inner phalangeal cell. Mitosis was seen in one Claudius' cell in addition. Therefore some supporting cells seem to be able to synthesize DNA and proliferate in the acutely damaged organ of Corti even in mature cochlea and those in G0 stage begin to go around cell cycle as occasion demands. Although labelled supporting cells decreased over time, the portion of supporting cell is likely to change in proportion as the extension of damage in the organ of Corti. If this new dynamic change of cell kinetics in the acutely damaged organ of Corti means the reaction to repair the organ of Corti, the supporting cells seem to have a reasonable role to maintain the organ of Corti including repairment of reticular lamina.

Animals↗

PubMed1992

Hypobaric hypoxia: a method for testing bioreductive drugs in vivo.

Hypobaric hypoxia has been used to induce tumor hypoxia for in vivo comparison of the anti-tumor effects of the bioreductive agents SR 4233 (3-amino-1,2,4-benzotriazine-1,4-dioxide), RSU 1069 (1(2-nitro-1-imidazolyl)-3-aziridino-2-propanol), and Nitromin (methylbis(2-chloroethyl)amine N-oxide). BDF mice bearing the T50/80 mammary carcinoma were treated with these agents over a range of doses under normobaric (oxic) and hypobaric (hypoxic) conditions. The time taken for the tumor to double treatment volume (volume doubling time) was used as a measure of anti-tumor effect. Volume doubling time was plotted against log dose and dose response curves were fitted. A dose enhancement ratio (the ratio of drug doses required to give an equivalent anti-tumor effect under oxic and hypoxic conditions) was determined. The dose enhancement ratios for SR 4233 and RSU 1069 were 8.8 and 8.5, respectively, showing that these agents had an equivalent and substantial enhancement of their cytotoxicity when combined with hypobaric hypoxia. For Nitromin, no significant dose response effect was obtained under oxic conditions precluding the calculation of the dose enhancement ratio. SR 4233 was found to have increased systemic toxicity when combined with hypobaric hypoxia, suggesting that it is more readily activated than the other drugs tested. This in vivo test system will allow determination of the dose enhancement ratio for novel bioreductive agents and facilitate their comparison.

Animals↗

PubMed1993

Mechanism of lack of development of negative endocochlear potential in guinea pigs with hair cell loss.

The endocochlear potential (EP), and the concentration of K+, Na+ and Cl- were measured simultaneously in endolymph of guinea pigs. The EP was 85.6 +/- 0.8 mV in normal guinea pigs, 90.7 +/- 0.8 mV in the kanamycin-treated animals, and 91.6 +/- 1.2 mV in those treated with nitrogen mustard-N-oxide (NMNO). Thirty minutes after the onset of anoxia, the EP (negative EP) was -29.3 +/- 1.0 mV in the normal group, -0.2 +/- 1.0 mV in the kanamycin-treated group, and -1.9 +/- 1.3 mV in the NMNO-treated group. The permeability coefficients of K+ (Pk), Na+ (Pna) and Cl- (Pcl) across the endolymph-perilymph barrier during the period of 20-30 min after the onset of anoxia in the normal group were (341.6 +/- 38.2) x 10(-9) cm3 sec-1, (53.0 +/- 8.1) x 10(-9) cm3 sec-1 and (111.8 +/- 27.2) x 10(-9) cm3 sec-1, respectively. Pk was decreased in the kanamycin- and NMNO-treated groups. Pna did not differ between the normal and treated groups. Pcl was increased in the kanamycin- and NMNO-treated groups. The K+:Na+:Cl- permeability ratio was 1:0.16:0.32 in the normal group, 1:1.12:11.6 in the kanamycin-treated group, and 1:0.44:5.60 in the NMNO-treated group. The results indicate that the lack of development of a negative EP in the kanamycin- and NMNO-treated guinea pigs was attributable to the increased Pcl and the decreased Pk across the endolymph-perilymph barrier, probably the organ of Corti, during anoxia.

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