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At least 1,081 records · Page 60Linked to original sources
PubMed1979

Rescue of marker phenotypes: effects of BUdR sensitization, hypoxia and high LET.

The survival curve of colony-forming ability of Chinese hamster wg3h cells has been compared with the dose-response curve for the expression of an active thymidine kinase (TK) gene from these cells. The TK+ phenotype was measured by hybrid colony formation after fusion of wg3h (TK+) cells with Chinese hamster A23 (TK-) cells. The TK+ survival data fitted a multi-target curve up to 3 krad of 137 Cs irradiation, when a highly resistant fraction of hybrid colonies was seen at about 1 per cent survival. The Do of TK+ survival for the multi-target region was 3.1-4.0 times greater, than that of wg3h survival, even when the Do for cell survival varied between 136 and 545 rad by 14 MeV neutrons and hypoxia respectively. This parallel modification of cell and TK+ sensitivities suggests that the lesions causing cell inactivation are of the same type as those that cause marker inactivation. Using 14 MeV neutron data the approximate target size for TK inactivation was calculated to be 0.54-0.91 per cent of the DNA content of the cell (or about one-fifth to one-tenth of a chromosome). The data support the idea that marker inactivation results primarily from damage occurring outside the marker gene. BUdR labelling of wg3h cells before irradiation caused slight toxicity (30 per cent reduction in plating efficiency) and a twofold increase in cell sensitivity. However, the sensitivity of the TK+ phenotype increases by only 30 per cent. The increased cell sensitivity thus appeared to result from synergism between increased sensitivity of DNA to strand breakage and metabolic toxicity, the latter being largely overcome by fusion with normal cells.

Animals↗
PubMed1988

Modulation of radiation-induced chromosome aberrations by DMSO, an OH radical scavenger. 1: Dose-response studies in human lymphocytes exposed to 220 kV X-rays.

Human G0 lymphocytes were exposed to 220 kV X-radiation in the presence or absence of DMSO, an efficient selective scavenger of OH radicals. Our studies demonstrate that DMSO affects a concentration-dependent modulation of induced asymmetrical aberrations in human lymphocytes exposed to approximately 3.0 Gy, with maximum protectible fractions of approximately 70 percent at DMSO concentrations of greater than or equal to 1 M. The dose dependency for dicentrics in lymphocytes acutely exposed to X-ray doses of 0.51 to 4.98 Gy in the absence of DMSO is adequately described by the linear-quadratic dose-response function Y = alpha D + beta D2. Data from duplicate cultures exposed in the presence of 1 M DMSO produce an excellent fit to the regression function modified as follows: Y(+ DMSO) = alpha(delta D) + beta(delta D)2 where the 'dose modifying' factor delta = 0.501. We interpret these findings as providing evidence that OH radical-mediated lesions in DNA account for approximately 50 percent of the dose dependency for dicentrics resulting from either one-track or two-track events, following exposures of non-cycling cells to moderate-to-high doses of low LET radiation. These data may be used in additional calculations to derive an estimate of approximately 6 x 10(8) s-1 for the rate of reaction of OH radicals with DNA targets involved in aberration formation.

Chromosome Aberrations↗
PubMed1992

Antimutagenic effects of radioprotector WR-2721 against fission-spectrum neurons and 60Co gamma-rays in mice.

The antimutagenic effects of the radiation protective agent, S-2-(3-aminopropylamino)ethylphosphorothioic acid (WR-2721), were studied against fission-spectrum-neutron- and 60Co-gamma-ray-induced mutagenesis in mice. Mutagenesis at the hypoxanthine-guanine phosphoribosyl transferase (hprt) locus was measured 56 days following whole-body irradiation with JANUS neutrons (single doses, 50-150 cGy) or 60Co photons (single doses, 250-750 cGy). Splenic T lymphocytes from B6CF1 mice were grown in round-bottomed 96-microwell culture plates with or without the selective agent 6-thioguanine (6-TG). The mutant frequency, as a result of exposure to neutrons or 60Co photons, increased 100-fold with dose. Doses of 150 cGy neutrons and 750 cGy 60Co photons were equally mutagenic. When animals were injected with WR-2721 at a dose of 400 mg/kg body weight, i.p., 30 min before whole-body irradiation with JANUS neutrons or 60Co photons, mutant frequencies were significantly reduced at all radiation doses (i.e. protection factors of 1.4 and 2.4, respectively). Thus, the aminothiols are effective antimutagens. A novel clinical application of these compounds could be in their use to protect against radiation- and/or chemotherapy-induced genotoxic damage to normal cells.

Amifostine↗