A cell survival model with saturable repair after irradiation

Summary A cell survival model with saturable repair has been developed. The model is based on the assumption that after irradiation the cell can be in one of the following three states: In state A the viable cells have no lesions, in state C cells carry lethal lesions and in state B cells exhibit potentially lethal lesions which can be repaired by a saturable enzymatic repair system or which are converted to lethal lesions. The model incorporates five parameters. The applicability of the model has been demonstrated by fitting 11 experimental data sets obtained with different cell lines, different kinds of radiation and variable repair times simulated by liquid holding recovery or inhibition of repair processes by different agents. The model and the results obtained are discussed in relation to published results.Dedicated to Prof. K.G. Zimmer on his 75th birthday     

Effect of humoral factors of the spleen after irradiation]

It is stated that therapeutic effect of humoral factors isolated from the cattle spleen is associated with its influence on alpha 2-macroglobulin (alpha 2-MG) performing a protective function. The results obtained permit recommending the isolated preparations to increase total resistivity of the organism under irradiation.     

Recovery course in mouse spleen and bone marrow after continuous irradiation.

The paper deals with the recovery process of some parameters in the spleen and bone marrow till day 60 after continuous irradiation with a daily dose of 476.5 mGy (50 R), 957 mGy (100 R) and 4785 mGy (500 R) up to the total accumulated dose of 9570 mGy (1000 R). The recovery process in the spleen and bone marrow are relatively significant and completed till day 28 or 60 respectively after irradiation.     

The rate of repair of a radiation lesion of the central nervous system during protracted and fractionated irradiation

In experiments with fractionated and prolonged irradiation of guinea pigs and dogs it was shown that the recovery of CNS from acute radiation affection may be approximated, for different animal species, by an exponential function at a rate of 0.02 h-1 and a half-life period of approximately 30 h.     

The kinetics of repair in mouse lung after fractionated irradiation

The kinetics of repair of sublethal damage in mouse lung was studied after fractionated doses of 137Cs gamma-rays. A wide range of doses per fraction (1.7-12 Gy) was given with interfraction intervals ranging from 0.5 to 24 h. The data were analysed by a direct method of analysis using the incomplete repair model. The half-time of repair (T1/2) was 0.76 h for the pneumonitis phase of damage (up to 8 months) and 0.65 h for the later phase of damage up to 12 months. The rate of repair was dependent on fraction size for both phases of lung damage and was faster after large dose fractions than after small fractions. The T1/2 was 0.6 h (95 per cent c.1. 0.53, 0.69) for doses per fraction greater than 5 Gy and 0.83 h (95 per cent c.1 0.76, 0.92) for doses per fraction of 2 Gy. Repair was nearly complete by 6 h, at least for the pneumonitis phase of damage. To the extent that extrapolation of these data to humans may be valid, these results imply that treatments with multiple fractions per day that involve the lung will not be limited by the necessity for interfraction intervals much longer than 6 h.     

Splenic hemopoiesis of the platypus (Ornithorhynchus anatinus): evidence of primary hemopoiesis in the spleen of a primitive mammal

The generation of blood cells has been observed in the spleen and in the bone marrow of the platypus. Hemopoiesis was found to be far more active in the spleen than in the bone marrow judging by the number of proliferating hemopoietic elements within a unit area of tissue from each organ. Granulocytes, erythroblasts, and megakaryocytes, with the related immature forms for each cell line, were noted in the spleen. In contrast, there were very few examples of immature forms of these cell lines and a complete absence of mature megakaryocytes in the bone marrow. These findings suggest that the spleen is the primary hemopoietic organ in the platypus. Since the platypus is one of two species representing the most primitive existing mammals, it seems likely that the spleen may be the primary hemopoietic organ in mammalian evolution.     

Repair processes of hemopoiesis after applying cyclophosphamide. I. Morphological changes in the bone marrow, spleen and thymus

Processes of hemopoiesis repair were monitored in rats till the day 30 after applying cyclophosphamide in doses of 100 and 200 mg X kg-1. Profound decrease of the hemopoietic activity in the bone marrow, spleen, and thymus was observed till the day 3. The reported changes were reversible, since the myelopoiesis was recovered till the day 10 in the bone marrow and the erythropoiesis in the spleen till the day 20. Significantly slower progress in repair process was observed in the lymphoid tissue; here the recovery was not completed till the day 30.     

Changes of lipofuscin-like pigments in erythrocytes and spleen after whole-body gamma irradiation of rats

Whole-body gamma irradiation of rats induced the formation of lipofuscin-like pigments in erythrocytes. Erythrocytes that were damaged by oxidation were scavenged in the spleen, and lipofuscin-like pigments were transferred from erythrocytes to the spleen during this process. The time course of lipofuscin-like pigments in erythrocytes and spleen indicates that the pigments were not induced by the action of free radicals produced by ionizing radiation but rather were a sequela of postirradiation metabolic changes.     

Postreplication repair in mammalian cells after ultraviolet irradiation: a model.

A model is presented for bypass of ultraviolet-induced damage in DNA during replication. The overall process is initiated by the introduction of a single-strand break into parental DNA near the point of arrest of synthesis, followed by a transient crossing-over step similar to that envisaged in genetic recombination. The mechanism proposed provides an alternative explanation to existing models and is entirely consistent with available data on postreplication repair in mammalian cells. In addition the model explains the low level of recombination repair observed in mammalian cells.