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Biomedical subjects

L Hieber

Publications and source records attributed to L Hieber.

28 records · Page 2Linked to original sources
PubMed1987

Heavy ion effects on cellular DNA: strand break induction and repair in cultured diploid lens epithelial cells.

The relative biological effectiveness (RBE) for the induction of DNA strand breaks and the efficiency of repair of these breaks in cultured diploid bovine lens epithelial cells was measured, using accelerated heavy ions in the linear energy transfer (LET)-range up to 16,200 keV/micron. At LET values above 800 keV/micron, the number of DNA strand breaks induced per particle increases both with the atomic number of the projectile and with its kinetic energy. About 90 per cent or more of the strand breaks induced by ions with an LET of less than 10,000 keV/micron are repaired within 24 h. Repair kinetics show a dependence on the particle fluence (irradiation dose). At higher particle fluences a higher proportion of non-rejoined breaks is found, even after prolonged periods of incubation. At any LET value, repair is much slower after heavy-ion exposure than after X-irradiation. This is especially true for low energetic particles with a very high local density of energy deposition within the particle track. At the highest LET value (16,200 keV/micron), no significant repair is observed.

Animals↗
PubMed1987

Absence of a dose-rate effect in the transformation of C3H 10T1/2 cells by alpha-particles.

The findings of Hill et al. (1984) on the greatly enhanced transformation frequencies at very low dose rates of fission neutrons induced us to perform an analogous study with alpha-particles at comparable dose rates. Transformation frequencies were determined with gamma-rays at high dose rate (0.5 Gy/min), and with alpha-particles at high (0.2 Gy/min) and at low dose rates (0.83-2.5 mGy/min) in the C3H 10T1/2 cell system. alpha-particles were substantially more effective than gamma-rays, both for cell inactivation and for neoplastic transformation at high and low dose rates. The relative biological effectiveness (RBE) for cell inactivation and for neoplastic transformation was of similar magnitude, and ranged from about 3 at an alpha-particle dose of 2 Gy to values of the order of 10 at 0.25 Gy. In contrast to the experiments of Hill et al. (1984) with fission neutrons, no increased transformation frequencies were observed when the alpha-particle dose was protracted over several hours.

Alpha Particles↗
PubMed1986

The mammalian genetic stress response.

A number of carcinogenic and cocarcinogenic agents induce new gene products in mammalian cells including primary human skin fibroblasts. These have been defined by cDNA cloning techniques, by protein resolutions in 2D PAGE and by the detection of new enzymatic functions. The uniform and transient genetic reaction is tentatively called the genetic stress response.

Animals↗
PubMed1984

HZE effects on mammalian cells.

In track segment experiments cell survival and chromosome aberrations of mammalian cells have been measured for various heavy ion beams between helium and uranium in the energy range between 0.5 and 960 MeV/u, corresponding to a velocity range of 0.03 to 0.87 C, and an LET spectrum from 10 to 15 000 keV/micrometers. At low LET, the cross section (sigma) for cell killing increases with increasing LET and shows a common curve for all ions regardless of the atomic number. This indicates that in this region the track structure of the different ions is of only a minor influence, and it is rather the total energy transfer, which is important for cell killing. At higher LET values, deviations from a common sigma-LET curve can be observed which indicate a saturation effect. The saturation of the lighter ions occurs at lower LET values than for the heavier ions. These findings are also confirmed by the chromosome data, where the efficiency for the induction of chromosomal aberrations for high LET particles depends on the track structure and is nearly independent of LET. In the heavier beams (Z > or = 10) individual particles cause multiple chromosome breaks in mitotic cells.

Animals↗
PubMed1984

Cell cycle dependent G2 delay and killing of L929 cells after exposure to 241Am alpha particles.

Survival and G2 delay of L929 mouse fibroblasts exposed to 3.4-MeV alpha particles depend on the cell age at the time of irradiation. Greatest sensitivity for both endpoints has been found at the G1/S transition: The surviving fraction of G1/S cells is reduced to 0.11 following 1 Gy of alpha particles compared to 0.31 for early G1 cells. The G2 + M transit time rises from 3 hr for control cells to 22 and 30 hr for cells irradiated with 0.3 Gy in G2 or at the G1/S boundary, respectively. Cells irradiated in early G1 do not show increased G2 + M transit times. Growth delay as calculated for the entire population increases linearly with dose by 23 hr/Gy of alpha particles.

Alpha Particles↗
PubMed1983

PCC technique reveals severe chromatin lesions and repair in G2-arrested cells after alpha irradiation.

Exponentially growing Chinese hamster V79 cells were exposed to 4 MeV alpha particles emitted by an americium-241 source. The chromatin of cells arrested in G2 by alpha irradiation is severely damaged, though all cells were still capable to condensate their chromatin after fusion with mitotic cells. In addition to the common types of aberrations (breaks, gaps, dicentrics and exchanges) cells were found possessing one or more chromosomes with long stretches of undercondensed chromatin. Repair of these lesions was indicated by site-specific unscheduled DNA synthesis and by the observation that condensation of these regions improved during G2 arrest.

Alpha Particles↗
PubMed1983

Caffeine-mediated release of alpha-radiation-induced G2 arrest increases the yield of chromosome aberrations.

Severe and partly irreversible G2 arrest caused by americium-241 alpha-particles in Chinese hamster V79 cells acted as a competing process to the yield of detectable aberrant mitoses at metaphase. With increasing dose of alpha-radiation an increasing fraction of cells was irreversibly arrested in G2 with the consequence of interphase death before the first post-irradiation mitosis. This irreversible G2 arrest (demonstrated by flow cytofluorometry and mitotic indices) could be overcome by adding caffeine 8 hours after irradiation, the time point of maximum G2 arrest (80-90 per cent of all cells). Within 3.5 hours the number of aberrant mitoses increased by this treatment from 54 to 96 per cent and from 65 to 99.9 per cent for doses of 1.75 and 4.38 Gy of alpha-particles, respectively. The aberration frequency per mitotic cell, scored as chromatid and isochromatid breaks, rings, interchanges and dicentrics increased by a factor of about 3 after releasing G2 arrested cells. The frequency distribution of aberrations per cell revealed that, after 4.38 Gy, 58 per cent of the formerly G2-arrested cells had more than five aberrations per cell compared to only 8 per cent without the interaction of caffeine.

Alpha Particles↗
PubMed1982

Comparative study of G2 delay and survival after 241 Americium-alpha and 60cobalt-gamma irradiation.

Survival and G2 dalay following exposure to either 60Cobalt-gamma-rays or 241Americium-alpha-particles were studied in eight mammalian cell lines of human and animal origin including human fibroblasts from normal individuals and from patients with Ataxia telangiectasia or Fanconi's anemia. For both endpoints the effectiveness of alpha particles was greater as compared to gamma-rays. RBE values for G2 delay (4.6-9.2) were in general comparable to RBE values derived from initial slopes of survival curves (RBE alpha) but higher compared to the ratio of mean inactivation doses (RB-DML). Ataxia cells were particularly sensitive to cell killing by gamma-irradiation (D37 = 0.57 Gy), however, showed average sensitivity to alpha-particles of high LET (D37 = 0.30 Gy). With the exception of Ataxia cells, cell killing and G2 delay seem to be related processes if individual cell cycle parameters are taken into account.

Alpha Particles↗
PubMed1981

G2-delay after irradiation with alpha-particles as studied in synchronized cultures and by the bromodeoxyuridine-33258H technique.

Division delay of mouse L-929 fibroblasts after alpha-irradiation is due to a pronounced lengthening of their G2-phase. Experiments on synchronously and asynchronously growing cultures revealed a cell cycle phase-dependent sensitivity of this effect: Cells irradiated in G2 or at the G1/S border suffered a longer G2-delay than cells irradiated at mid- or late-S. Progression through G2 was nearly normal at doses up to 0.3 Gy if cells were exposed during G1 phase.

Alpha Particles↗