Dose threshold for residual γH2AX, 53BP1, pATM and p-p53 (Ser-15) foci in X-ray irradiated human fibroblasts.

Background: Enumeration of residual DNA repair foci 24 hours or more after exposure to ionizing radiation (IR) is often used to assess the efficiency of DNA double-strand break repair. However, the relationship between the number of residual foci in irradiated cells and the radiation dose is still poorly understood. The aim of this work was to investigate the dose responses for residual DNA repair foci in normal human fibroblasts after X-ray exposure in the absorbed dose range from 0.

Early and Late Effects of Low-Dose X-ray Exposure in Human Fibroblasts: DNA Repair Foci, Proliferation, Autophagy, and Senescence.

The effects of low-dose radiation exposure remain a controversial topic in radiation biology. This study compares early (0.5, 4, 24, 48, and 72 h) and late (5, 10, and 15 cell passages) post-irradiation changes in γH2AX, 53BP1, pATM, and p-p53 (Ser-15) foci, proliferation, autophagy, and senescence in primary fibroblasts exposed to 100 and 2000 mGy X-ray radiation.

Changes in the Number of Residual γH2AX Foci in Ki-67-Positive and Ki-67-Negative Human Fibroblasts Irradiated with X-Rays in Doses of 2-10 Gy.

We studied changes in the number of residual γH2AX foci in cultured human fibroblasts with different expression of the cell proliferation marker protein Ki-67 24, 48, and 72 h after exposure to X-ray radiation in doses of 2-10 Gy. It was shown that, regardless of the expression of Ki-67, the number of residual γH2AX foci in irradiated cells linearly depends on the absorbed dose of X-ray radiation. However, the quantitative yield of residual γH2AX foci per unit of the absorbed dose in Ki-67 cells 24 and 48 h after irradiation was higher than in Ki-67 cells by 1.

Residual Foci of DNA Damage Response Proteins in Relation to Cellular Senescence and Autophagy in X-Ray Irradiated Fibroblasts.

DNA repair (DNA damage) foci observed 24 h and later after irradiation are called "residual" in the literature. They are believed to be the repair sites for complex, potentially lethal DNA double strand breaks. However, the features of their post-radiation dose-dependent quantitative changes and their role in the processes of cell death and senescence are still insufficiently studied.

DNA Damage in Splenocytes of Mice Exposed to Secondary Radiation Created by 650 MeV Protons Bombarding a Concrete Shielding Barrier.

The proportion of splenocytes with a high level of DNA double-strand breaks was determined in mice exposed to primary and secondary radiation created by bombarding of a concrete barrier (thickness 20, 40, and 80 cm) by 650 MeV protons. The proportion of splenocytes with a high level of DNA double-strand breaks was assessed by flow cytometric analysis of γH2AX and TUNEL cells. It is shown that concrete barrier can significantly reduce primary proton radiation; the severity of negative biological effects in mice irradiated in the center of the proton beam decreased with increasing the thickness of this barrier.