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J L Redpath

Publications and source records attributed to J L Redpath.

At least 37 records · Page 2Linked to original sources
PubMed1988

A comparison of the radiation sensitivities of non-tumorigenic and tumorigenic human hybrid cell lines.

The radiation sensitivities of two related non-tumorigenic and two related tumorigenic human hybrid cell lines (HeLa x skin fibroblast) have been studied. The data show that the transformation from the non-tumorigenic to the tumorigenic state, which is accompanied by the loss of skin fibroblast chromosomes 11 and 14, is not associated with any major changes in radiation sensitivity. The data do indicate, however, a trend toward a steeper and longer initial slope to the cell survival curve for the tumorigenic cell lines, along with a subsequent reduced ability to accumulate sublethal radiation injury at low doses. Both nontumorigenic and tumorigenic cell lines have the capability of repairing sublethal injury.

Cell Line↗
PubMed1988

Suppression of the radiation-induced expression of a tumor-associated antigen in human cell hybrids by the protease inhibitor antipain.

The effect of the protease inhibitor antipain (1.25 micrograms/ml) on the radiation-induced expression of a tumor-associated antigen in human cell hybrids has been investigated. A variety of treatment protocols have been studied where antipain was present before, during and at various times post-irradiation. It was found that antipain suppressed the radiation-induced expression of the tumor-associated antigen in all treatment protocols. The most effective suppression was obtained in those protocols where the protease inhibitor was present for the first 4 h post-irradiation. A possible explanation for this observation is that antipain may inhibit an error-prone DNA repair process. However, it is clear that this is not the only mechanism whereby the inhibitor can exert its effect since suppression was obtained even when antipain was added 10 days post-irradiation, a time when any DNA repair processes would be expected to be over.

Antigens, Neoplasm↗
PubMed1988

Further studies on the radiation-induced expression of a tumor-specific antigen in human cell hybrids.

The neoplastic transformation of human cell hybrids (HeLa x skin fibroblasts) is accompanied by the expression of a cell surface protein for which monoclonal antibodies have been raised. The gamma-radiation-induced neoplastic transformation of these cells has been studied where the expression of this cell surface protein, as detected by immunoperoxidase staining, has been used as an end point. The yield of foci of positively staining cells has been shown to increase with increasing time postirradiation at which the assay is done and decrease with increasing density of viable cells plated postirradiation. The time of plating postirradiation is also an important parameter with transformation frequencies increasing over the first 6 h of postirradiation holding at confluence, followed by a gradual decrease.

Antigens, Neoplasm↗
PubMed1987

Neoplastic transformation of human hybrid cells by gamma radiation: a quantitative assay.

Human skin fibroblasts are extremely refractory to neoplastic transformation by ionizing radiation [C. Borek, Nature 283, 776-778 (1980); M. Namba, H. Nishitani, and T. Kimoto, J. Exp. Med. 48, 303-311 (1978)] and are therefore unsuitable for quantitative studies of dose-effect relationships. We show here that a nontumorigenic human hybrid cell line (HeLa X skin fibroblast) can be neoplastically transformed by treatment with gamma radiation. Furthermore, a dose-response relationship has been established. We propose that this human hybrid cell line may be a useful system for mechanistic studies of transformation from the preneoplastic to the neoplastic state by ionizing radiation and other agents.

Cell Line↗
PubMed1986

Repair of potentially lethal radiation damage in confluent and non-confluent cultures of human hybrid cells.

The repair of potentially lethal damage (PLDR) in a gamma-irradiated human hybrid cell line (skin fibroblast X HeLa) and its tumourigenic segregant has been studied as a function of cell density at the time of irradiation and during the postirradiation repair period. The data show that PLDR occurs in both non-confluent and confluent cultures of both cell lines. Furthermore, there is evidence that the extent of PLDR is dependent on cell density and that cell-cell contact may be an important factor in this regard.

Cell Communication↗
PubMed1986

UV-type damage associated with ionizing radiation: a review.

The induction of UV-type damage by ionizing radiation in repair deficient strains of E. coli is reviewed. Both photoreactivable and non-photoreactivable types of damage can be observed. The induction of UV-type damage is largely independent of the presence of free-radical reactive agents (e.g. oxygen and thiols), but is dependent upon the energy of the photon--or electron--beam used, the radiation geometry and the optical absorbance of the extracellular medium. On the basis of calculations and experimental evidence, it is clear that one mechanism whereby such damage arises is through the generation of Cerenkov emission. However, small yields of UV-type damage can be produced using X-rays whose energy is below the threshold for production of Cerenkov emission. In this instance, the damage induction mechanism is thought to involve a direct excitation process.

Absorption↗
PubMed1986

Mutation induction in Escherichia coli WP2 uvrA by Cerenkov emission associated with 137Cs gamma irradiation.

Evidence is presented for the mutation of the tryptophan-requiring bacterial strain Escherichia coli WP2 uvrA from auxotrophy to prototrophy, and from streptomycin sensitivity to resistance, by Cerenkov emission associated with 137Cs gamma irradiation. Furthermore, the data strongly suggest a more than additive interaction between the gamma-induced damage and that induced by Cerenkov emission for both mutations scored. An additional observation is that mutant yields (expressed as mutants/10(7) survivors) show a dependence on the number of viable cells plated for both uv (254 nm) and Cerenkov-induced mutations, but not for those induced by gamma irradiation. This demonstrates another similarity between uv- and Cerenkov-induced damage.

Cesium Radioisotopes↗
PubMed1985

Repopulation in irradiated pig skin: late versus early effects.

In the first 16 weeks after irradiation, two distinct waves of reaction can be observed in pig skin, the first wave (3-9 weeks) represents the expression of damage to the epithelium while the second is indicative of primary damage to the dermis, mediated through vascular injury. Following beta-irradiation with a strontium-90 applicator, a severe epithelial reaction was seen with little subsequent dermal effects. X-rays (250 kV), on the other hand, produced a minimal epithelial response at doses which led to the development of dermal necrosis after 10-16 weeks. Comparison of single doses with two equal doses separated by 28 days produced a D2-D1 value of 14.0 Gy at the doses which produced moist desquamation in 50% of fields (ED50) after strontium-90 irradiation. After X-irradiation, comparison of ED50 doses for the later dermal reaction suggested a D2-D1 value of 4.2 Gy. These values of D2-D1 for epithelial and dermal reactions in pig skin were compared with earlier data from this laboratory for similar split-dose experiments with a one-day interval. Such a comparison allowed for the estimation of the component of recovery in the present 28-day interval experiments due to repopulation. This component was found to be 6.5 Gy for the early epithelial damage, but was zero for the later dermal damage.

Animals↗
PubMed1985

Radiobiological studies of human hybrid cells (skin fibroblasts X HeLa) and their tumourigenic segregants.

Data are presented on the survival characteristics following gamma-irradiation of a human hybrid cell line (skin fibroblasts X HeLa), and its tumourigenic segregant, which indicate that transition from the non-tumourigenic to the tumourigenic state is associated with a decrease in the ability to accumulate and repair sublethal damage. Previous studies have demonstrated that this transition to the tumourigenic state is also associated with loss of specific chromosomes (one copy each of chromosomes 11 and 14). It is suggested that this loss of chromosomes may account for the change in radiosensitivity.

Cell Survival↗
PubMed1984

Implications of tissue target-cell survival-curve shape for values of split-dose recovery doses: late versus early effects.

Recent data from this laboratory on split-dose recovery for early and late effects in pig skin are consistent with the linear-quadratic model for cell survival, and with relative cell survival-curve shapes for early- and late-effect target cells where the early-effect cells have an initially steeper and straighter survival-curve than the late-effect cells.

Animals↗
PubMed1984

Induction of lethal damage in E. coli by Cerenkov emission associated with high-energy X-rays: the effect of bromouracil substitution.

5.1. The damages induced in E. coli AB2487 recA by Cerenkov emission and ionizing radiation contribute in an additive fashion to the overall lethality, and do not interact in a synergistic fashion. 5.2. BU substitution enhances the lethal action of high energy X-irradiation on E. coli AB2487 recA by a mechanism involving enhanced radiosensitivity and enhanced photosensitivity.

Bromouracil↗