![]() The least studied markers of radiation exposure are the dumbbell-shaped nuclei. As a result, after anaphase, nucleoplasmic bridges are newly formed. The end sections of such broken chromosomes are recognized by the DNA repair system as double-strand breaks and are cross-linked to form dicentric chromosomes. ![]() The resulting nucleoplasmic bridges break during cytokinesis with the formation of “tailed” nuclei. It can be said that a cell exposed to ionizing irradiation undergoes a “breakage–fusion–bridge” cycle during repeated mitotic divisions. The formation of “tails” is closely related to the formation of nucleoplasmic bridges. “Tailed” nuclei were found in the cells of different fish species, as well as in humans, after exposure to ionizing radiation. In this connection, it is possible to observe nucleoplasmic bridges while studying cells in the cytochalasin block, where further division of the cytoplasm does not occur. Usually, it undergoes a rupture during cytokinesis, resulting in the formation of so-called “tailed” nuclei. During the formation of two new nuclei of daughter cells in the telophase, the formed nucleoplasmic bridge is also covered with a nuclear envelope. Such bridges arise when the centromere of the dicentric chromosomes diverges to the opposite poles of the cell during anaphase. In addition to micronuclei, another types of nuclei pathology, generally accepted in radiobiology as markers of DNA damage, are nucleoplasmic bridges. At the same time, several variants of micronucleus “fate” are possible: degradation of the micronucleus, its removal from the cell, apoptosis of the whole cell, or cooperation of the micronucleus with the basic cell nucleus. Fragments or whole chromosomes eventually become covered with a nuclear envelope and morphologically look similar to the cell nuclei, not exceeding one-third of its diameter. ![]() Micronuclei may contain either an acentric region of the chromosome or an entire chromosome that has not been distributed to one of the opposite poles during anaphase of mitosis. They appear as fragments of the cell nucleus, which carry an incomplete part of the genome. Micronuclei are the most studied form of nuclei pathology. In this case, the mechanism of their occurrence caused by ionizing radiation is associated with the formation of double-strand breaks of DNA and as a consequence ring and dicentric chromosomes. Such anomalies arise after pathological mitotic divisions and are clearly distinguishable in a light microscope. Among these anomalies, micronuclei, nucleoplasmic bridges, and “tailed” nuclei are distinguished. ![]() Ionizing radiation effects on cell populations as a genotoxic agent could lead to the appearance of cells with morphologically anomalous nuclei. More than that, most of the chromosomal aberrations are converted into dumbbell-shaped nuclei in vitro in the culture of lymphocytes in the cytochalasin block. Comparison of the frequencies of occurrence of dicentric and ring chromosomes with frequencies of occurrence of nuclear anomalies allows us to conclude that these nuclear anomalies are formed as a result of chromosomal aberrations arising in lymphocytes under the action of ionizing radiation. At the same time, frequencies of occurrence of chromosomal aberrations (dicentric and ring chromosomes) in the culture of lymphocytes exposed to the same radiation doses were studied. Dose-dependent curves of the occurrence of lymphocytes containing “tailed” nuclei, nucleoplasmic bridges, or dumbbell-shaped nuclei after irradiation have been constructed. To stop the cell cycle of cultured lymphocytes after the first mitotic division, a cytokinesis block was performed using cytochalasin B. In this article, we present the results of the study of the frequency of occurrence of three types of nuclear anomalies (“tailed” nuclei, nucleoplasmic bridges, and dumbbell-shaped nuclei) in vitro in human lymphocytes cultured with cytochalasin B when exposed to X-rays at doses of 0.0, 0.1, 0.2, 0.4, 0.5, 0.7, 1.0, 1.5, and 2.0 Gy. Nuclear anomalies of different types appear in cells in response to the action of ionizing radiation after the passage of the first mitotic division.
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