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PubMed1986

Selective distribution of fibronectin to a tumor-cell line.

Distribution of plasma fibronectin in Yoshida sarcoma-bearing rats was studied. Fibronectin from human plasma labelled with 125I was administered intravenously to the tumor bearing-rats. The ratios of specific radioactivity (cpm/g) of the tumor to that of blood or liver increased in the time course after the administration. Consequently, 48 h later, the tumor/blood and the tumor/liver ratios were estimated to be 4.6 and 2.8, respectively. In contrast, the liver/blood ratio did not increase during the experimental period. Similar results were also obtained by the administration of fibronectin from rat plasma. Whole-body autoradiography also suggested such a selective distribution. However, 125I-labelled albumin was not localized in the tumor.

Animals↗

PubMed1987

Effect of nicotinamide on hepatic microsomal drug metabolising system in tumour-bearing rats and mice.

Administration of nicotinamide to Wistar rats (100 mg/kg body wt.) bearing Yoshida sarcoma (ascites) tumour as well as to Swiss and CBA mice (250 mg/kg body wt.) bearing the transplantable fibrosarcoma and the spontaneously induced mammary carcinoma, respectively, was shown to bring about a reversal of the decreased activity of NADPH-cytochrome c reductase in host livers of the tumour-bearing animals. Nicotinamide injection was also shown to bring about a significant increase in the levels of host hepatic cytochromes P-450 and b5 and in the activities of aminopyrine demethylase and UDP-glucuronosyl transferase which were shown to be low in the tumour-bearing rats. Treatment with nicotinamide was shown to be equally effective in reversing the inhibited activities of hepatic drug metabolising enzymes observed in healthy adult rats injected with serum from the tumour-bearing rats. Administration of nicotinamide to adult male rats brought about an increased incorporation of [14C]leucine in hepatic microsomal proteins which was insensitive to inhibition by actinomycin D at a dose of 1 mg/kg body wt. but could be inhibited by the antibiotic at a lower dose of 0.1 mg/kg body wt. as well as by cycloheximide.

Animals↗

PubMed1979

The concomitant effect of unsaturated fatty acid supplemented to medium on cellular growth and membrane fluidity of cultured cells.

The membrane fluidity of cultured Yoshida sarcoma cells was determined under the culture condition in which various amounts of saturated and unsaturated fatty acids were supplemented to a serum-free medium containing defatted bovine serum albumin. The greater amount of unsaturated fatty acids was supplemented to the medium, the more active membrane fluidity and cellular growth were enhanced, while the supplementation of a saturated fatty acid had no such effect.

Animals↗

PubMed1985

Selective drug-induced reduction of blood flow in tumor transplants.

The effect of a calcium antagonist and a physiologic amine on tumor and muscle perfusion was investigated with the aim of improving the preconditions for external hyperthermia treatment of cancer. Nisoldipine (0.04-4.0 mg/kg) and 5-hydroxy tryptamine (5-HT) (0.2-8.0 mg/kg) were administered i.p. in Sprague-Dawley rats bearing Walker 256 carcinoma, Yoshida sarcoma, or a homologous tumor transplant derived from a spontaneous leiomyosarcoma of the uterus. At the maximum dosage used, nisoldipine injection caused a decrease of the regional washout rate of Xenon-133 of 63 +/- 8% (SEM) in the Walker carcinoma and an increase of 80 +/- 41% in the muscle of the hind leg. 5-HT (8 mg/kg) caused a drop of 79 +/- 29% in the Walker carcinoma and only a slight fall of the washout rate in muscle of 14 +/- 4.8%. Tumor-to-muscle uptake ratios of 11C-butanol fell from 5.63 +/- 1.98 to 3.32 +/- 1.21, and from 5.3 +/- 0.56 to 2.98 +/- 0.30, after injection of 0.2 mg/kg nisoldipine and 4 mg/kg 5-HT, respectively. Similar reaction patterns and percentage changes were observed in different tumor lines at constant doses of 0.2 mg/kg nisoldipine and 4 mg/kg 5-HT. Both drugs representing two different rationales of vasomotor action were able to reduce blood flow specifically in transplanted tumors; nisoldipine increased muscle blood flow and decreased arterial blood pressure, whereas 5-HT acted without substantial systemic effects.

Animals↗

PubMed1996

Biogenesis of hepatic acute-phase response to trauma.

The bioorganic pathway(s) of hepatic acute-phase response in rat to single and compounded traumata triggered either by chemical or physical injury has been re-evaluated for the purpose of advancing a better understanding of mechanisms of hepatic regeneration. These insights would be useful in cases of liver cirrhosis and end-stage liver diseases and may allow avenues of surgical management other than liver transplantation. Mechanisms of acute-phase response in rat to a single inflammatory stimulus, e.g. intoxication with phalloidin, alpha-amanitin, subcutaneous administration of carageenan, subcutaneous implantation of Yoshida sarcoma or i.p. administration of Zajdela ascites are discussed and compared with (a) acute-phase response to intoxication by various factors leading to the development of liver cirrhosis, and (b) acute-phase response of nascent hepatocytes where hepatic regenerative activities were induced by chemical intoxication or surgical partial hepatectomy. Interestingly, hepatic acute-phase response was not limited only to these injuries outlined above but also to psychological conditions.

Acute-Phase Proteins↗

PubMed1992

Inhibition of collagenase by aranciamycin and aranciamycin derivatives.

Aranciamycin (1), an anthracycline antibiotic, was found to be an inhibitor of Clostridium histolyticum collagenase, with an IC50 = 3.7 x 10(-7) M. Elastase and trypsin were not inhibited at concentrations less than or equal to 10(-5) M. A number of aranciamycin derivatives 2-13 were prepared and tested for collagenase inhibition. While loss of activity was found for derivatives modified in the sugar ring or rings B and D of the aglycone, increased potency was found when the tertiary alcohol at C-9 was esterified. All compounds 1-13 were found to inhibit DNA synthesis of Yoshida sarcoma tumor cells.

Animals↗

PubMed1999

Manipulation of the ubiquitin-proteasome pathway in cachexia: pentoxifylline suppresses the activation of 20S and 26S proteasomes in muscles from tumor-bearing rats.

The development of pharmacological approaches for preventing the loss of muscle proteins would be extremely valuable for cachectic patients. For example, severe wasting in cancer patients correlates with a reduced efficacy of chemotherapy and radiotherapy. Pentoxifylline (PTX) is a very inexpensive xanthine derivative, which is widely used in humans as a haemorheological agent, and inhibits tumor necrosis factor transcription. We have shown here that a daily administration of PTX prevents muscle atrophy and suppresses increased protein breakdown in Yoshida sarcoma-bearing rats by inhibiting the activation of a nonlysosomal, Ca(2+)-independent proteolytic pathway. PTX blocked the ubiquitin pathway, apparently by suppressing the enhanced expression of ubiquitin, the 14-kDa ubiquitin conjugating enzyme E2, and the C2 20S proteasome subunit in muscle from cancer rats. The 19S complex and 11S regulator associate with the 20S proteasome and regulate its peptidase activities. The mRNA levels for the ATPase subunit MSS1 of the 19S complex increased in cancer cachexia, in contrast with mRNAs of other regulatory subunits. This adaptation was suppressed by PTX, suggesting that the drug inhibited the activation of the 26S proteasome. This is the first demonstration of a pharmacological manipulation of the ubiquitin-proteasome pathway in cachexia with a drug which is well tolerated in humans. Overall, the data suggest that PTX can prevent muscle wasting in situations where tumor necrosis factor production rises, including cancer, sepsis, AIDS and trauma.

Adenosine Triphosphatases↗

PubMed1970

Intrathecal chemotherapy. Selection of cytostatic agents.

Selection of cytostatic agents for intrathecal administration is the subject of this paper.Both the toxic side effects-destruction of blood-brain barrier and change of body weight-and the cytostatic effects on intracranially transplanted Yoshida ascites sarcoma were investigated of intrathecal administration of various cytostatic agents. As a result, it may be concluded that Methotrexate and Endoxan and lower dose of mitomycin C are suitable drugs for intrathecal chemotherapy.Based on these findings, clinical cases of malignant brain tumours were treated with intrathecal chemotherapy.Grateful acknowledgement is made to Professor Dennosuke Jinnai for his constant interest and guidance in this investigation.

Animals↗

PubMed2001

Identification of cathepsin L as a differentially expressed message associated with skeletal muscle wasting.

Alteration of skeletal muscle protein breakdown is a hallmark of a set of pathologies, including sepsis, with negative consequences for recovery. The aim of the present study was to search for muscle markers associated with protein loss, which could help in predicting and understanding pathological wasting. With the use of differential display reverse transcription-PCR, we screened differentially expressed genes in muscle from septic rats in a long-lasting catabolic state. One clone was isolated, confirmed as being overexpressed in septic skeletal muscle and identified as encoding the lysosomal cysteine endopeptidase cathepsin L. Northern- and Western-blot analysis of cathepsin L in gastrocnemius or tibialis anterior muscles of septic rats confirmed an elevation (up to 3-fold) of both mRNA and protein levels as early as 2 days post-infection, and a further increase 6 days post-infection (up to 13-fold). At the same time, the increase in mRNAs encoding other lysosomal endopeptidases or components of the ubiquitin-proteasome pathway did not exceed 4-fold. Cathepsin L mRNA was also increased in tibialis anterior muscle of rats treated with the glucocorticoid analogue, dexamethasone, or rats bearing the Yoshida Sarcoma. The increase in cathepsin L mRNA was reduced by 40% when the tumour-bearing animals were treated with pentoxifylline, an inhibitor of tumour necrosis factor-alpha production. In conclusion, these results demonstrate a positive and direct correlation between cathepsin L mRNA and protein level and the intensity of proteolysis, and identify cathepsin L as an appropriate early marker of muscle wasting. Cathepsin L presumably participates in the pathological response leading to muscle loss, with glucocorticoids and tumour necrosis factor-alpha potentially being involved in the up-regulation of cathepsin L.

Animals↗

PubMed1998

Anticancer activity and toxicity of S-1, an oral combination of tegafur and two biochemical modulators, compared with continuous i.v. infusion of 5-fluorouracil.

S-1 is an oral combined form of 1 M tegafur [a prodrug of 5-fluorouracil (5-FU)], 0.4 M 5-chloro-2,4-dihydroxypyridine (a reversible inhibitor of dihydropyrimidine dehydrogenase) and 1 M potassium oxonate (an inhibitor of orotate phosphoribosyltransferase). S-1 has been shown to exert a potent antitumor effect with low gastrointestinal toxicity in experimental tumor models. We have therefore compared the antitumor effect of oral S-1 with that of continuous infusion of 5-FU in rats bearing transplants of human and murine tumors. Almost complete inhibition of the tumor growth was obtained on 7 day schedules in Yoshida sarcoma-bearing rats by consecutive administration of 30 mg/kg/day of oral S-1 and 40 mg/kg/day infusion of 5-FU. However, a significant difference between the incidence of toxicities of S-1 and 5-FU, including body weight loss and diarrhea, was noted. The rats given the 5-FU infusion had marked weight loss and severe diarrhea, while those given oral S-1 had neither. Although about 50% inhibition of the tumor growth was attained with 15 mg/kg/day of oral S-1 and 30 mg/kg/day infusion of 5-FU in nude rats with xenografted human colon cancer (KM12C), the rate of body weight loss in the 5-FU-treated group was distinctly higher than in the S-1-treated group. The ratio of the 5-fluoronucleotide concentrations in gastrointestinal tissue to that in the tumor was lower in the S-1-treated rats than in the 5-FU-treated rats. In conclusion, the results suggest that oral S-1 might be more effective in the treatment of cancer patients than continuous infusion of 5-FU, from the standpoint of antitumor potency and toxicity.

Administration, Oral↗

PubMed1996

Enhanced anticancer effect of vincristine with methionine infusion after methionine-depleting total parenteral nutrition in tumor-bearing rats.

Methionine-depleting total parenteral nutrition (Met(-) TPN), in which an amino acid solution devoid of L-methionine and L-cysteine is infused, is thought to reduce tumor cell growth through acting as a partial late S-G2 (i.e., late-S and G2 phases) blocker. The antitumor effect of vincristine (VCR), which acts on mitotic phase cells, was examined with methionine infusion immediately after Met(-) TPN in Yoshida sarcoma (YS)-bearing rats. Rats were given Met(-) TPN for 8 days immediately after inoculation with YS cells (days 0 to 8), which was followed by methionine-containing (Met(+)) regular TPN for 3 days (days 9-11) along with intraperitoneal administration of 0.05 mg/kg/day VCR. All rats were then fed solid food and water ad libitum until they died, with 0.1 mg/kg VCR administration on days 12 and 13. As controls, a Met(-) TPN only group, Met(+) TPN groups with and without VCR, and freely fed groups with and without VCR were studied. The progression of YS was markedly suppressed by Met(-) TPN with VCR. The median survival time in days was 25 days, significantly longer (P<0.001) (generalized Wilcoxon's tests) by 11 to 14 days than that of any of the other groups. In conclusion, VCR appears to have greater efficacy as an anticancer agent when administered together with methionine after Met(-) TPN.

Animals↗

PubMed1999

Antitumor effects due to irreversible stoppage of tumor tissue blood flow: evaluation of a novel combretastatin A-4 derivative, AC7700.

The relation between tumor tissue blood flow (tBF) reduction and antitumor effects was investigated. Changes in tBF of normal tissues (liver, kidney cortex, bone marrow and brain cortex) and tumors (Yoshida sarcoma subline, LY80 and Sato lung carcinoma, SLC) due to i.v. administration of AC7700 (1, 3, 10 mg/kg), one of the combretastatin A-4 derivatives, were measured with the hydrogen clearance method. The change in blood flow in tumor microfoci was also observed directly using a rat transparent chamber. Chemotherapy against the solid tumors (LY80, SLC) was performed by administering AC7700 7 times at intervals of 3 days and the effect on the tumor growth, the histological effect, the effect on lymph node metastasis and the survival rate were investigated. Tumor tBF showed a dose-dependent response to AC7700. Although tumor tBF decreased markedly at a dose of 1 mg/kg, it tended to recover partly within several hours. At 10 mg/kg, however, tumor tBF completely stopped within approximately 30 min and never recovered in many regions. The irreversible stoppage of tumor tBF was observed in large s.c. tumors and in microfoci as well. On the other hand, in normal tissues, tBF changes due to AC7700 were not uniform. In the liver, although tBF decreased by approximately 50% at 10 mg/kg AC7700, it recovered within 8 h. In the brain, although the mean maximum reduction was 35%, the blood flow recovered to the original level within 24 h. The blood flow in the kidney cortex did not change at all. In the bone marrow, tBF decreased by approximately 80%. Generally, the blood flow reduction in normal tissues tended to be reversible. The effect on tumor growth and the histological effect were also dependent on the dose of AC7700. The tumor growth was markedly inhibited by 10 mg/ kg AC7700 and extensive necrosis was induced. Lymph node metastases were significantly inhibited and survival was prolonged significantly. In the control group, all 8 SLC tumor-bearing rats died of cancer, the presence of which was verified by gross and microscopic evaluation, within 45 days after tumor implantation. On the other hand, in the treated group, 2 of 8 rats recovered completely and survived. No obvious side effects such as body weight loss, anemia or diarrhea were observed at the dose used in this experiment. From these results, we conclude that strong antitumor effects are obtained by stopping tumor tBF irreversibly and by shutting off the nutritional supply into tumor tissue. AC7700 has been demonstrated to be a promising anticancer compound which has such an action.

Animals↗

PubMed2000

Tumor-selective blood flow decrease induced by an angiotensin converting enzyme inhibitor, temocapril hydrochloride.

To enhance chemotherapeutic efficacy against cancer, it is important to deliver anticancer drugs preferentially to cancer cells and to retain the drugs there for a prolonged time. The in vivo prolongation of the exposure time of anticancer drugs in tumors can be accomplished by decreasing tumor tissue blood flow (tBF) after anticancer drug administration. The present study demonstrated that temocapril hydrochloride, an angiotensin converting enzyme inhibitor, decreases tumor tBF markedly in LY80 tumor, a subline of Yoshida sarcoma in the rat, without affecting the blood flow in liver, kidney, bone marrow, and brain. In tumor areas with flow of above 20 ml/min/100 g, the tBF decreased by approximately 50% due to temocapril. In tumor areas with tBF of about 20 ml/min/100 g, it became less than 3 ml/min/100 g with temocapril and did not recover during the 2 h experiment. These findings were obtained not only in large tumors, but also in microfoci growing within a transparent chamber. Furthermore, even when temocapril was administered under the condition of increased tumor tBF by administering angiotensin II, tumor tBF decreased immediately. Using this technique, it should be possible to trap anticancer drugs selectively in tumor tissue for an extended period of time.

Angiotensin II↗

PubMed1980

Cooperation of murine F T and parental B lymphocytes in rejection of a xenogeneic tumour: adaptive differentiation of B lymphocytes?

The primary humoral immune response to rat Yoshida ascites sarcoma (YAS) grown in mice was used to study thymus-dependent (T) and bone marrow-derived (B) lymphocyte cooperation. It was shown that B6D2F1 T lymphocytes that do not cooperate with parental B lymphocytes enabled parental B lymphocytes from B6 leads to B6D2F1 radiation chimaeras to reject the tumour. However, when the bone marrow cells from B6 leads to B6D2F1 chimaeras were used to reconstitute parental B6 mice, these B6 leads to B6D2F1 leads to B6 mice lost their tolerance to D2 transplantation antigens, and their B lymphocytes were not able to cooperate with B6D2F1 T lymphocytes. In our search for the reasons for the failure of F1 T cells to be effective in parental and P leads to F1 leads to P TIR mice, rejection of F1 T cells was excluded because : (i) immune reactivity in TIR mice was found to be either absent or minimal; (ii) parental TIR mice did not produce any detectable cytotoxic antibodies after an intravenous injection of F1 splenic T cells; and (iii) YAS rejection was not induced at very high doses of F1 T cells. However, in a cell transfer system we were able to demonstrate that injection of spleen cells from parental TIR mice could thwart the successful cooperation of transferred F1 T cells with host B cells. Collectively, these data suggest that the changes of the collaborative potential of parental B cells as achieved in the F1 environment could be ascribed to 'adaptive' differentiation of B lymphocytes. It appears that the differentiation process that has rendered nonsyngeneic chimaeric cells able to cooperate was independent of the exogenous antigen.

Animals↗

PubMed1993

Antitumor effect of a mycotoxin: rubratoxin B.

The antitumor effect of rubratoxin B, a mycotoxin, has been studied. Yoshida ascites sarcoma cells, in vitro in contact for 30 min with the drug and injected immediately afterwards into young rats by the intraperitoneal route, produced the survival of 80% of the animals and the doubling of the median survival time of the rats developing neoplasia. In vivo administration of the drug by the intraperitoneal route 24 h after implantation of tumor cells determined the prolongation of median survival time; supplied by other routes both against T8 sarcoma of Guérin and Yoshida ascites sarcoma it was ineffective. The differences between in vitro and in vivo results can be explained by a rapid neutralization of the drug on behalf of the organism's enzymes or by being bound to proteins and peritoneal cells unlike tumor cells.

Animals↗

PubMed1982

Effect of 1,3,3,5,5-pentaziridino-1-thia-2,4,6-triaza-3,5-diphosphorine-1-oxide, a new antitumor agent with inorganic ring, on various experimental tumors.

1,3,3,5,5-Pentaziridino-1-thia-2,4,6-triaza-3,5-diphosphorine-1-oxide (SOAz), a new antitumor agent, was evaluated for antitumor activity against various mouse- and rat-tumor systems. The optimal treatment regimens of SOAz (i.p.) gave 262% and 134% increase in life span (ILS) in mice with P388 leukemia and L1210 leukemia implanted intraperitoneally, respectively, and 239% ILS in rats with Yoshida sarcoma of which 86% survived for 60 d after intraperitoneal tumor implantation. The compound showed a definite activity against Lewis lung carcinoma implanted intravenously. The compound also exhibited 80-100% inhibition of tumor local growth in all of four experimental tumor systems used in the present study. In contrast to cyclophosphamide, SOAz was active against B16 melanoma and Meth A, and demonstrated high activity against a subline of L1210 leukemia resistant to cyclophosphamide.

Animals↗

PubMed1975

Combined cancer chemotherapy with cyclophoshamide and an inducer of microsomal drug-metabolizing enzymes (cytochrome P-450) in tumor-bearing rats.

The fifty percent alive period in Yoshida sarcoma-bearing and AH66F-bearing rats was prolonged by an administration in a single dose of 100 mg cyclophosphamide/kg body weight in a group pretreated with phenobarbital as compared with that pretreated with saline. However, there was little difference in fifty percent alive period between AH109A (insensitive to cyclophosphamide)-bearing rats and controls even when they were pretreated with phenobarbital. In chemotherapy with anti-cancer drugs, inductive or inhibitory effects of the drugs on microsomal drug-metabolizing enzymes should be taken into consideration.

Animals↗

PubMed1981

Effects of inducer of liver drug-metabolizing enzyme on blood level of active metabolites of cyclophosphamide in rats and in cancer patients.

It was already reported that a masked compound, cyclophosphamide (Endoxan, EX) undergoes the first step metabolism by a drug-metabolizing enzyme in liver microsomes, cytochrome P-450. By pretreatment with phenobarbital as an inducer of P-450, the maximum blood level of active metabolites of EX (normustard-like substances) in normal rats was 2.3 times higher than that in non-treated rats, in conformity with the increase in amount of liver P-450 and in alkylating activity of EX. In YS (Yoshida sarcoma)-bearing rats, the value of liver P-450 went down day by day to 1/2 on the 4th day after inoculation, but it remained normal when animals were pretreated with phenobarbital. In parallel with this, the blood level of normustard-like substances after EX administration was normal or showed a tendency toward increase. In 11 clinical cases pretreated with phenobarbital, the blood level of normustard-like substances 1 to 3 hr after EX administration, at the time when it reaches the peak was 1.5 times higher on an average than that in cases without pretreatment.

Adult↗