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Biomedical subjects

T Aida

Publications and source records attributed to T Aida.

At least 91 records · Page 5Linked to original sources
PubMed1988

[Five cases of primary intracranial germ cell tumor treated by combination chemotherapy with cisplatin].

Five cases of non-germinoma germ cell tumor which received combination chemotherapy with cisplatin were studied to elucidate the efficacy of chemotherapy. The patients' ages ranged from 7 to 24 years old. Three of the patients were male and two were female. Locations of the tumors were suprasellar in three cases, pineal in one case and basal ganglia in the other. Three of the 5 tumors were histologically verified as yolk sac tumors, embryonal carcinoma and HCG_producing germinoma. Two were histologically unverified HCG-producing tumors. Following the reception of PVB therapy (cisplatin, vincristine and bleomycin) by all the patients, three of the HCG-producing tumors showed complete remission and two of AFP producing tumors demonstrated partial remission, and progressive healing process, respectively. Renal dysfunction in two case, leukopenia in two cases and lung fibrosis in one cae were noted as side effects. Two cases were treated only with cisplatin because ling fibrosis due to administration of bleomycin was intractable and harmful. Also the time when irradiation. It seemed better to administer chemotherapeutic agents prior to or during irradiation on account of the fact that, after radiotherapy, there is reduced blood flow in the tumor region. Also, CDDP acts as a radiosensitizer. Therefore, individual administration of cisplatin during irradiation was recommended for the initial chemotherapy against the case of non-germinoma germ cell tumors, in which an intractable side effect might be expected.

Adolescent↗
PubMed1988

[Mechanisms of cellular resistance to chloroethylnitrosourea in cell lines derived from human brain tumors].

The cytotoxic and cytogenetic effects 1-(4-amino-2-methyl 1-5-pyrimidinyl) methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) and 1, 3-bis (2-chloroethyl)-1-nitrosourea (BCNU) treatments on five cell lines derived from human malignant glioma were studied. Compared to sensitive cell line SF-126, SF-188 cells were 3- to 6.9 fold more resistant to the cytotoxic effect and 8 to 14 fold more resistant to the induction of sister chromatid exchanges (SCEs). Cytotoxic effects and induction of SCEs were intermediate for SF-268, SF-210 and SF-295 cell lines compared with SF-126 and SF-188. There was a good correlation between susceptibility to the cytotoxic effects and formation of DNA interstrand crosslinks for cells treated with ACNU and BCNU. The effects of cis-diamminedichloroplatinum (II) (cis-Pt) and nitrogen mustard (HN2) in these cells were also studied. Cis-Pt was equally cytotoxic and induced the same number of SCEs and DNA interstrand cross-links in all five cel lines. In contrast to the results obtained by treatment with chloroethylnitrosoureas (CENUs), SF-126 cells treated with HN2 were more resistant to the cytotoxic effects, the induction of SCEs, and the induction of DNA interstrand cross-links than were SF-188 cells. The repair of O6-methylguanine after treatment of these cell lines with (3H) methylnitrosourea were quantitated. SF-126 cells showed no detectable repair of O6-methylguanine, SF-268, SF-210 and SF-295 cells had intermediate levels of repair, and SF-188 had very high level of repair. These results suggest that cellular resistance to CENUs dose not result in cross-resistance to HN2 or cis-Pt, and that one of mechanisms of cellular resistance to CENUs is increased repair of O6-alkylguanine derivatives in DNA, which prevents DNA interstrand cross-links and then reduces both cytotoxic effects and the induction of SCEs in cell resistant to CENUs.

Brain Neoplasms↗
PubMed1987

Effect of caffeine on cytotoxicity and sister chromatid exchange induction in sensitive and resistant rat brain tumor cells treated with 1,3-bis(2-chloroethyl)-1-nitrosourea.

Treatment of 9L and 9L-2 cells, which are, respectively, sensitive and resistant to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), with various concentrations of BCNU followed by treatment with 1 mM caffeine potentiated BCNU cytotoxicity by 10-fold with dose modification factors of 1.5 to 1.7. The synergistic effect of caffeine on cellular toxicity diminished when caffeine was added 6 to 24 h after treatment of BCNU. The number of sister chromatid exchanges (SCEs) induced by treatment with BCNU in both cell lines showed a good correlation with cytotoxicity; the number of SCEs induced in 9L cells is 6-fold higher than the number induced in 9L-2 cells. Caffeine potentiated BCNU induction of SCEs in both 9L or 9L-2 cells by the same amount. Caffeine potentiation of BCNU-induced SCEs was also time dependent and was eliminated by a delay of 6 h between BCNU treatment and addition of caffeine. Caffeine had no effect on the formation and removal of DNA cross-links in either 9L or 9L-2 cells after BCNU treatment as determined with the alkaline elution assay. Eighteen to 24 h after BCNU treatment there was an accumulation of 9L cells in late-S-G2-M phase of the cell cycle which diminished with time. Caffeine treatment potentiated the BCNU-induced accumulation of cells in late-S-G2-M phase of the cell cycle. Our results suggest that caffeine potentiates BCNU cytotoxicity and induction of SCEs by a mechanism that is independent of repair of alkylation products, but that may depend on alterations of cellular replication in BCNU-treated cells.

Animals↗
PubMed1987

Cellular resistance to chloroethylnitrosoureas, nitrogen mustard, and cis-diamminedichloroplatinum(II) in human glial-derived cell lines.

We investigated the cytotoxic and cytogenetic effects of 3-(4-amino-2-methyl-5-pyrimidinyl)methyl-1-(2-chloroethyl)-1-nitrosourea and 1,3-bis(2-chloroethyl)-1-nitrosourea on five cell lines established from human glioma biopsy specimens. Compared to the sensitive cell line SF-126, SF-188 cells are 3- to 6.5-fold more resistant to the cytotoxic effects and 8- to 14-fold more resistant to the induction of sister chromatid exchanges. Cytotoxic effects and induction of sister chromatid exchanges are intermediate for SF-210 and SF-295 cell lines compared with SF-126 and SF-188. There is a good correlation between susceptibility to the cytotoxic effects and formation of DNA interstrand cross-links for cells treated with 3-(4-amino-2-methyl-5-pyrimidinyl)methyl-1-(2-chloroethyl)-1-nitrosourea . We quantitated the extent of repair of O6-methylguanine after treatment of these cell lines with [3H]methylnitrosourea. SF-126 cells showed no detectable repair of O6-methylguanine, SF-210 and SF-295 had intermediate levels of repair, and SF-188 had very high levels of repair. We conclude that the cellular capacity to repair O6-chloroethylguanine adducts in DNA, which is reflected in the methyl repair process, is an important factor in determining cytotoxic response, and that increased repair of O6-chloroethylguanine decreases cytotoxicity and causes fewer sister chromatid exchanges and DNA interstrand cross-links to form in cells treated with chloroethylnitrosoureas. We studied the effects of cis-diamminedichloroplatinum(II) and nitrogen mustard in these cell lines. cis-Diamminedichloroplatinum(II) was equally cytotoxic and induced the same number of sister chromatid exchanges and DNA interstrand cross-links in all five cell lines. In contrast to the results obtained by treatment with chloroethylnitrosoureas, SF-126 cells treated with nitrogen mustard are 7.6-fold more resistant to the cytotoxic effects, 2-fold more resistant to the induction of sister chromatid exchanges, and 3-fold more resistant to the induction of DNA interstrand cross-links than are SF-188 cells. The results of this investigation with five human glial-derived cell lines clearly indicate that the molecular mechanisms of cellular resistance to alkylating chemotherapeutic agents are highly specific. Cellular resistance to chloroethylnitrosoureas does not result in cross-resistance to nitrogen mustard or cis-diamminedichloroplatinum(II).

Carmustine↗
PubMed1987

Inhibition of O6-alkylguanine-DNA-alkyltransferase activity potentiates cytotoxicity and induction of SCEs in human glioma cells resistant to 1,3-bis(2-chloroethyl)-1-nitrosourea.

SF-188 is a human glioma-derived cell line resistant to the cytotoxic effects of and the induction of sister chromatid exchanges (SCEs) by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU). Pretreatment of SF-188 cells with N-methyl-N-nitrosourea (MNU) for 1 h increased the cytotoxicity of a 1-h treatment with BCNU 2- to 10-fold and doubled the number of SCEs; the magnitude of these effects was dependent on the dose of both agents. Treatment of SF-188 cells with MNU resulted in a dose-dependent inhibition of O6-alkylguanine-DNA-alkyltransferase (O6-AT) activity. Low doses of MNU, which did not significantly inhibit O6-AT, did not potentiate SCE induction. Higher doses of MNU inhibited O6-AT and potentiated cytotoxicity and the induction of SCEs. These results are consistent with the hypothesis that in resistant cells treated with BCNU, O6-AT repairs O6-chloroethylguanine before it can form a DNA interstrand cross-link. Inhibition of this enzyme allows for the formation of BCNU-induced DNA interstrand cross-links resulting in increases in cytotoxicity and induction of SCEs. The correlation between cytotoxicity and the induction of SCEs suggests that measurement of SCEs may be useful for determining the cellular response of normal and tumor cells to in vivo treatment with combinations of chemotherapeutic agents.

Carmustine↗
PubMed1987

[Anticancer drug induced sister chromatid exchange and correlation to cell survival in human brain tumor cells].

Sister chromatid exchanges (SCEs) induced by four anticancer drugs, 3-(4-amino-2-methyl-5-pyrimidyl) methyl-1-(2-chloroethyl)-1-nitrosourea (ACNU), 1-3-bis (2-chloroethyl)-1-nitrosourea (BCNU), nitrogen mustard (HN2), cis-diamminedichloroplatinum (II) (cis-Pt) were examined on five cell lines derived from human malignant glioma biopsy specimens, and compared to results obtained with colony-forming efficiency (CFE) assay. Treatment of the five cell lines with these four drugs produced concentration-dependent increases in SCEs. Treatment with ACNU induced the most SCEs in SF-126 cells decreasing in SF-268 cells followed by SF-210 cells, SF-295 cells, and the least SCEs in SF-188 cells. The results of the SCE assay with BCNU in these cell lines were similar with ones with ACNU. In contrast to results obtained with nitrosoureas, the most SCEs were induced in SF-188 cells and the least were induced in SF-126 cells by the treatment of HN2. The frequency of SCEs induced with cis-Pt was almost similar in the five cell lines. The number of SCEs induced by the treatment of ACNU, BCNU, HN2 and cis-Pt in five cells lines showed a good correlation with cytotoxicity measured by CFE assays, and induction of SCEs occurred at much lower concentrations of these anticancer drugs than those required to induced cell kill. These results suggest that measurement of induced SCEs in human brain tumor cells treated with some anticancer drugs provide a more sensitive indicator of drug action than CFE assay and that SCE assays may be a useful method of the in vitro sensitivity test to some anticancer drugs.

Antineoplastic Agents↗
PubMed1987

Effects of polyprenoic acid on thermal injury.

This study was designed to determine the effect of polyprenoic acid on wound healing in rats after thermal injury and to compare the effect with healing in vitamin A deficient controls and in retinol-fed vitamin A deficient rats. Both polyprenoic acid and retinol visibly accelerated wound healing after thermal injury. Both enhanced the induction of platelets in the peripheral blood but neutrophils were not affected by polyprenoic acid. Histologically, in the hypo-vitamin A rat, polyprenoic acid administration increased both capillary formation and also the production of fibroblasts and collagen deposition in the wound by comparison with control vitamin A deficient animals; similar effects were produced by retinol feeding. These results indicate that both polyprenoic acid and retinol can facilitate wound healing. 3H-thymidine incorporation into dermal tissues showed that in polyprenoid-fed rats capillaries multiplied 1.3 times, epithelial cells 2.1 times, and fibroblasts 2.0 times faster than those in vitamin A-deficient animals; 3H-thymidine incorporation was greater after polyprenoid feeding than after retinol feeding. Polyprenoid thus stimulates both collagen deposition and neo-vascularization within burns, and so accelerates healing.

Animals↗
PubMed1986

Early membrane damage during ischemia in rat heart.

Effects of ischemia on cell membrane of rat heart were investigated. The endothelial surface revealed the existence of ruthenium red-positive glycocalyx at the anionic site. Membrane bound enzyme as Na-K ATPase was mostly located in the inner side and pinocytotic vesicles of endothelial cell. The clumping and dispersion in glycocalyx of endothelial cells was observed in an ischemic heart and it may prove the functional disturbance of plasma membrane. A potential and functional defect with reduced activity of Na-K ATPase occurred within 1 hr of vascular ligation. The membrane dysfunction due to these molecular changes has been proved by the membrane permeability alteration as well as the intracytoplasmic localization of horseradish peroxidase as tracer.

Animals↗
PubMed1986

Increased repair of O6-alkylguanine DNA adducts in glioma-derived human cells resistant to the cytotoxic and cytogenetic effects of 1,3-bis(2-chloroethyl)-1-nitrosourea.

We investigated the cytotoxic and cytogenetic effects of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) treatment on two cell lines derived from human glioma biopsy specimens. SF-188 cells are 3-fold more resistant to the cytotoxic effects of BCNU and 14-fold more resistant to sister chromatid exchange (SCE) induction caused by BCNU treatment than are SF-126 cells. After treatment with BCNU, 60% fewer DNA interstrand crosslinks were found in SF-188 than in SF-126 cells. The O6-methylguanine alkylation product was removed rapidly from DNA in SF-188 cells treated with [3H]methylnitrosourea, but very little repair of alkylation product occurred in SF-126 cells. These results suggest that one of the mechanisms responsible for cellular resistance to BCNU treatment is increased repair of O6-alkylguanine products in DNA, which reduces the number of crosslinks formed and thereby increases survival and reduces the number of SCEs induced in resistant cells.

Alkylation↗
PubMed1986

Temporary low oxygen conditions for the formation of nitrate reductase and nitrous oxide reductase by denitrifying Pseudomonas sp. G59.

Formation of nitrate reductase (NaR) and nitrous oxide reductase (N2OR) by a Pseudomonas sp. G59 did not occur in aerobic or anaerobic conditions, but was observed in a microaerobic incubation in which an anaerobically grown culture was agitated in a sealed vessel initially containing 20 kPa oxygen in the headspace. During the microaerobic incubation, the oxygen concentration in the headspace decreased and dissolved oxygen reached 0.1-0.2 kPa. NaR activity was detected immediately and N2OR activity after 3 h of incubation irrespective of the presence or absence of NO3- or N2O. In the presence of NO3-, NO2- was accumulated as a major product, but N2O was observed in low concentrations only after N2OR appeared. After microaerobic incubation for 3 h, N2OR formation continued even anaerobically in an atmosphere of N2O. In contrast, Escherichia coli formed NaR not only microaerobically but also anaerobically. However, NaR formation by E. coli was inhibited by sodium fluoride under anaerobic, but not under microaerobic conditions. The Pseudomonas culture did not possess fermentative activity. It is suggested that the dependence on microaerobiosis for the formation of these reductases by the Pseudomonas culture was due to an inability to produce energy anaerobically until these anaerobic respiratory enzymes were formed.

Aerobiosis↗
PubMed1986

[A case of multiple teratomas combined with embryonal carcinoma].

It is rare to find primary multiple teratomas among intracranial tumors. We report a case of multiple teratomas combined with embryonal carcinoma. A 22-year-old man was admitted to our hospital because of loss of appetite and emaciation. Neurological examination was negative except bilateral optic nerve atrophy and generalized hyperreflexia. The endocrinological study showed panhypopituitarism and partial DI. CT scan revealed irregularly enhanced abnormal masses involving suprasellar cistern and the septum pellucidum. The tumors were removed by the transcallosal approach, and the histopathological study showed mature teratoma which contained cartilage, epithelium of GI tract, ciliated epithelium, smooth muscle, fat tissue. Within the tumor of the septum pellucidum, nests of markedly pleomorphic epithelial tumor cells with necrosis, nuclear pleomorphism and mitosis were identified, embryonal carcinoma. At necropsy, no carcinomatous lesions were identified in other organs. Multiple teratomas from nonmetastatic, separate origins have been rate by reported in the literature. In our case, histologically, the mass in the suprasellar cistern was diagnosed as mature teratoma and the mass of the septum pellucidum was mature teratoma combined with embryonal carcinoma. It seemed likely that each of the tumors was developed from different origins.

Adult↗
PubMed1985

Comparison of sister-chromatid exchange induction caused by nitrosoureas that alkylate or alkylate and crosslink DNA.

We have investigated the induction of sister-chromatid exchanges (SCEs) in 9L rat brain tumor cells treated with the alkylating agent 1-ethyl-1-nitrosourea (ENU) and 3-(4-amino-2-methyl-5-pyrimidinyl)methyl-1-(2-chloroethyl)-1-nitrosourea (ACNU), an agent that both alkylates and crosslinks DNA. Induction of SCEs by ACNU was found to be 143-fold greater than for ENU. However, on an equimolar basis, the alkylation of DNA by 14C-ACNU was approximately 3.2-fold higher than for 14C-ENU. After correction for this difference was made, the induction of SCEs by ACNU was calculated to be 45-fold greater than for ENU. While DNA alkylation products formed by ACNU and ENU are similar, the chloroethyl alkylation product(s) of ACNU can form DNA-interstrand crosslinks; the ethyl alkylation product(s) of ENU cannot. Based on these findings, we propose that the increased induction of SCEs caused by ACNU is a result of the formation of DNA interstrand crosslinks.

Alkylating Agents↗
PubMed1985

Primary neuroblastoma of the nasal cavity and review of literature.

Primary neuroblastoma of the nasal cavity is very rare, and it is one of the most difficult tumor to differentiate from other small round cell tumors. The present case was proved to be olfactory neuroblastoma by histological, electron microscopical and histochemical findings. This is the first case in which biogenic amines were proven by glyoxylic acid-induced fluorescence in vitro. Discussions were made on the pathological differences with adrenal neuroblastoma.

Adult↗