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Biomedical subjects

N Rucker

Publications and source records attributed to N Rucker.

33 records · Page 2Linked to original sources
PubMed1986

Expression of potentially lethal damage in Chinese hamster cells exposed to hematoporphyrin derivative photodynamic therapy.

Experiments were performed to determine whether the expression and/or repair of potentially lethal damage could be observed in mammalian cells exposed to hemataporphyrin derivative (HPD) photodynamic therapy (PDT). Photodynamic therapy was combined with posttreatment protocols known to inhibit the repair of potentially lethal damage in cells treated with X-rays, ultraviolet radiation, or alkylating agents. Potentiation of lethal damage from photodynamic therapy was induced by hypothermia (4 degrees C) following short (1 h) or extended (16 h) HPD incubation conditions. Caffeine potentiated the lethal effects of PDT only when cells were incubated with HPD for extended time periods. However, 3-aminobenzamide had no effect on the cytotoxic actions of PDT following either short or extended HPD incubations. Recovery from potentially lethal damage expressed by posttreatment hypothermia was complete within 1 h, while recovery from potentially lethal damage expressed by posttreatment caffeine required time periods of up to 24 h. The lack of effect of 3-aminobenzamide on expression of potentially lethal damage following photodynamic therapy may be related to direct inhibition of adenosine diphosphoribose transferase by photodynamic therapy. These results indicate that the expression and repair of potentially lethal damage can be observed in cells treated with PDT and will vary as a function of porphyrin incubation conditions.

Animals↗
PubMed1985

In vitro and in vivo light dose rate effects related to hematoporphyrin derivative photodynamic therapy.

In vitro and in vivo experiments were performed to evaluate the parameter of light dose rate as it relates to the efficiency of hematoporphyrin derivative (HPD)-induced photosensitization. Exponentially growing Chinese hamster ovary cells were incubated with HPD (25 micrograms/ml) and were then exposed to red light (630 nm) delivered at different dose rates. A total of five dose rates (0.5, 5.0, 15, 23, and 60 milliwatts/sq cm) were examined following a 1-hr HPD incubation, two dose rates (1 and 20 milliwatts/sq cm) were examined after a 12-hr HPD incubation, and three dose rates (0.4, 4, and 40 milliwatts/sq cm) were examined following a 16-hr incubation and a 30-min serum wash protocol. The effect of light dose rate was determined from cell survival curves obtained by standard clonogenic colony formation assays. Similar levels of cellular toxicity were obtained when cells from each HPD incubation group were treated with equal doses of red light delivered at different dose rates. For in vivo experiments, albino mice were given injections of HPD (7.5 mg/kg) and 24 h later the right hind leg of each mouse was treated with localized red light (630 nm). A total dose of 270 J/sq cm was delivered to the right hind leg at dose rates of 5, 25, or 125 milliwatts/sq cm. The resulting acute skin damage induced by HPD photosensitization was scored over a 30-day period, and skin response curves for the three dose rates were obtained. Comparable levels of damage were induced in each of the three experimental groups. The results obtained from both in vitro and in vivo studies indicate that the photosensitizing efficiency of HPD photodynamic therapy is not affected by nonthermal variations in clinically relevant dose rates of delivered light.

Animals↗
PubMed1983

Comparison of mutagenicity and induction of sister chromatid exchange in Chinese hamster cells exposed to hematoporphyrin derivative photoradiation, ionizing radiation, or ultraviolet radiation.

Cell culture studies have been performed to compare the mutagenic potential and the induction of sister chromatid exchanges for hematoporphyrin derivative photoradiation, ionizing radiation, and UV radiation. The mutation frequency in Chinese hamster ovary cells at the hypoxanthine-guanine phosphoribosyltransferase locus was measured using resistance to 6-thioguanine. Phenotypic expression time prior to mutation selection was also examined. Treatment with either X-rays or UV was effective in producing mutants resistant to 6-thioguanine, but treatment with hematoporphyrin derivative photoradiation (at comparable toxicity levels) did not induce any mutagenic activity above background levels. The hematoporphyrin derivative incubation and photosensitization conditions used in this study did induce sister chromatid exchanges at frequencies comparable to those induced by X-rays but at lower frequencies than for UV treatments.

Animals↗
PubMed1982

Tissue distribution of 3H-hematoporphyrin derivative in athymic "nude" mice heterotransplanted with human retinoblastoma.

Quantitative uptake levels of tritium-labeled hematoporphyrin derivative (3H-HpD) have been obtained for normal and malignant tissue of athymic "nude" mice heterotransplanted intraocularly with human retinoblastoma. It was determined that eyes with tumor accumulated higher levels of 3H-HpD than those in control eyes. In addition, an improved therapeutic retention ratio of the drug (eyes with tumor compared with control eyes) was obtained at extended time intervals after administration.

Animals↗
PubMed1980

Variability in DNA distributions of human neuroblastomas after cyclophosphamide.

Major changes in DNA distributions of two human neuroblastoma cell lines growing in vitro and in athymic nude mice occurred after treatment with cyclophosphamide. Pulse treatment of LA-N-1 cells in vitro with liver S-9-activated cyclophosphamide (10 micrograms/ml) caused approximately 50% cytotoxicity; flow microfluorometric analysis of surviving cells demonstrated an increased proportion of G2 + M cells and a decreased proportion of G1 cells, particularly at 48 hrs. Even though LA-N-1 tumors in nude mice did not regress after one dose of cyclophosphamide (250 mg/kg), the percent of G2 + M cells increased and the percent of G1 cells decreased 4-6 days after treatment; the percent of cells in S increased at 2 and again at 8 days. SK-N-MC cells were affected differently by cyclophosphamide. Pulse treatment of these cells in vitro with liver S-9-activated cyclophosphamide caused greater than 85% cytotoxicity and nearly complete elimination of cells in G2 + M at 24 and 48 hrs. Likewise, SK-N-MC tumors in nude mice regressed greater than 50% after cyclophosphamide, and the proportion of G2 + M cells decreased markedly 2-6 days after therapy. We conclude that cyclophosphamide can have different cytotoxic and cytokinetic effects on neuroblastomas. In addition, marked cytokinetic effects may occur even though changes in tumor size are minimal or not detectable.

Animals↗
PubMed1975

Correlation between balance of specific chromosomes and expression of malignancy in hamster cells.

Four 1-theta-D-arabinofuranosylcytosine (ara-C)-and one dimethylnitrosamine-transformed Syrian hamster cell lines were established. All produced tumors when inoculated into newborn hamsters. Specific chromosome changes were found in these lines consistent with changes observed recently by other investigators. Clones that had either high or low malignant potential were derived from two fibrosarcomas produced by one of the ara-C-transformed cell lines. The expression of malignancy in these clones was associated with an excess of 57 chromosomes over 73 chromosomes.

Animals↗
PubMed1975

Malignant transformation of mouse cells by cigarette smoke condensate.

A low-nicotine cigarette smoke condensate, 12 fractions of the condensate, and a reconstituted sample were tested for their ability to induce transformation in the mouse cell line 3H/10T-1/2 CL-8. This cell line is noted for its remarkable low spontaneous rate of transformation. Both the crude condensate and the reconstituted sample as well as two specific fractions induced transformation in the mouse cells. These transformed cells produced fibrosarcomas when injected s.c. into antithymocyte serum-treated syngeneic mice.

Animals↗
PubMedDate not supplied

In vitro and in vivo preclinical chemotherapy studies of human neuroblastoma.

Two human neuroblastoma cell lines, LA-N-1 and SK-N-MC growing in vitro and as subcutaneous tumors in athymic nude mice, were evaluated for their sensitivity to cyclophosphamide, doxorubicin (Adriamycin), and vincristine. In vitro, cyclophosphamide, following liver S-9 metabolic activation, and vincristine were significantly more cytotoxic to SK-N-MC than to LA-N-1 cells; doxorubicin was equally cytotoxic to both cell types. Treatment of nude mice bearing LA-N-1 and SK-N-MC tumors with cyclophosphamide and vincristine produced significant reduction (> 50%) in SK-N-MC tumor weights but not in LA-N-1 tumor weights. Doxorubicin failed to produce significant reduction in the weight of either the LA-N-1 or the SK-N-MC tumor. These sensitivities were generally similar to the clinical response of the tumors to these same agents. Such an in vitro and in vivo system using these and other neuroblastoma cell lines may provide a preclinical model for evaluating the activity of chemotherapeutic agents against human neuroblastoma.

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