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Biomedical subjects

F T Cross

Publications and source records attributed to F T Cross.

38 records · Page 3Linked to original sources

Adaptive response of human lymphocytes for the repair of radon-induced chromosomal damage.

In human lymphocytes low doses of X-rays can decrease the number of chromatid deletions induced by subsequent high doses of sparsely ionizing X-rays. Because of the concern with the carcinogenic effects of low doses of alpha-particles from radon in homes, experiments were carried out to see if low doses of X-rays could also decrease the yield of chromosomal aberrations induced by subsequent exposure to radon. Human peripheral blood lymphocytes were irradiated with low doses of X-rays (2 cGy) at 48 h of culture, exposed to radon at 72 h of culture, and analyzed for the presence of chromatid aberrations at subsequent intervals. The frequency of chromatid aberrations induced by radon alone increased with time after exposure, indicating exaggerated differences in the stage sensitivity of cell cycle stages to high-LET radiation. Furthermore, the numbers of aberrations per cell did not follow a Poisson distribution but were over dispersed, as might be expected since high-LET radiations have a high relative biological effectiveness compared with low-LET radiations. Nevertheless, lymphocytes exposed to 2 cGy of X-rays before radon exposure contained approximately one-half the number of chromatid deletions compared with lymphocytes treated with radon alone and analyzed at the same time. Thus, the putative chromosomal repair mechanism induced by low doses of sparsely ionizing radiation is also effective in reducing chromosomal aberrations induced by radon, which hitherto had been thought to be relatively independent of repair processes.

Adaptation, Physiological↗

Metaphase chromosome aberrations as markers of radiation exposure and dose.

Chromosome aberration frequency provides the most reliable biological marker of dose to detect acute accidental radiation exposure. Significant radiation-induced changes in the frequency of chromosome aberrations can be detected at very low doses (Lloyd et al., 1992). In animal studies chromosome aberrations provide a method to relate exposure to cellular dose. Using an in vivo/in vitro approach, aberrations provided a biological marker of dose from radon progeny exposure, which was used to convert exposure, work level months (WLM) to dose in grays (Gy) delivered to rat tracheal epithelial cells. Injection of Chinese hamsters with 144Ce, which produced a low-dose rate exposure of bone marrow to low-linear energy transfer (LET) radiation, increased the cell sensitivity for the induction of chromatid exchanges by subsequent external 60Co exposure. Our paper provides information on using molecular chromosome probes to "paint" chromosomes and score chromosome damage. This approach illustrates how technical advances make it possible to understand the mechanisms involved in the formation of chromosome aberrations. These studies demonstrate the usefulness of chromosome damage as a biological marker of dose and cellular responsiveness.

Animals↗