Effects of Exposure of Animals to Oxygen Atmosphere at Low Pressure on Lipid Peroxidation and Antioxidant Defense.

Relatively short-term (2.5 or 5 h) exposure of Wistar rats to oxygen atmosphere at moderate pressure (1.10-1.15 atm) resulted in an increase in LPO level and reduction of antioxidant activity in the blood serum. An increase in malondialdehyde concentration 1 day after termination of the exposure was followed by a decrease in the inhibiting activity of free radical oxidation of liposomal phospholipids induced by Fe(II) ions (100 µm). Malondialdehyde concentration increased by 1.29 times already after 2.5-h exposure and did not changed when the duration of the exposure to oxygen atmosphere was prolonged to 5 h. These data confirm the necessity of using substances potentiating antioxidant defense of the body during exposure to normobaric oxygenation.

Cytogenetic adaptive response in cultured human lymphocytes: dependence on the time of exposure to adapting and challenging doses of gamma-rays.

Human lymphocytes from 16 healthy donors were exposed in vitro to an adapting dose of gamma-rays (0.05 Gy) at G0, or G1, or G1/S stage of the cell cycle and subsequently to a challenging dose of gamma-rays at G1, or G1/S, or S (1 Gy), or G2 (0.5 Gy) stage. Frequencies and distributions of the induced chromosome aberrations were analyzed in first-division metaphases. The data averaged over the donors revealed the protective action of the adapting exposure under the irradiation schemes with the challenging dose delivered at S or G2 stage. The majority of aberrations induced at these stages belonged to the chromatid type, and their yield was significantly higher in G2-exposed cells than in S-exposed cells. However, the relative reduction of the challenging dose effect (about 34%) in the adapted cells did not depend on the magnitude of this effect, and its value remained the same (within the experimental error) if aberrations were subdivided into chromosome and chromatid types or grouped as total deletions and total fragments. The adaptive response was not revealed under the schemes with the challenging dose delivered at G1 or G1/S stage. Analysis of the individual results showed that, in one and the same donor, the adaptive response could be observed under one irradiation scheme and not observed under other schemes, the most effective schemes being those with the challenging dose delivered at G2 stage. Four donors, however, did not show the adaptive response even under such schemes. Data on aberration distributions suggested that different repair processes, rather than a unique one, may underlie the adaptive response.

The effects of radiation and alkylating agents on chromatin degradation in normal and tumour lymphoid cells.

The dynamic of chromatin degradation was studied in thymocytes and LS/BL tumour cells. In permeabilised LS/BL cells, the rate of DNA degradation induced by endogenous calcium and magnesium-dependent endonuclease was approx. 25 times slower than in thymocytes. In LS/BL cells irradiation does not induce chromatin degradation. The alkylating agent TS 160 induced chromatin degradation in both LS/BL lymphosarcoma cells and thymocytes.

A comparison of chromatin degradation in irradiated normal and tumorous lymphoid cells.

Irradiation of mice with doses of 2 and 4 Gy induced extensive chromatin degradation in the thymocytes within 6 hours accompanied by an increase in polydeoxynucleotide (PDN) content (36 and 42 times, respectively). Fifteen hours after irradiation the PDN level was considerably lower, however, still being 4.7 and 14 times the control values after doses of 2 and 4 Gy. The PDN content in control LS/BL lymphosarcoma cells was similar as that in the thymocytes of non-irradiated mice. Unlike in the thymocytes, irradiation of lymphosarcoma cells did induce no statistically significant increase in the PDN level 6 and 15 hours after the irradiation, respectively. It has been reported previously (Matyásová et al. 1973) that chromatin of LS/BL cells degraded similarly as that in the irradiated thymocytes. The results of the present experiments thus provide additional evidence for changes of LS/BL cell properties due to long term cultivation. These cells, however, are still able to react by chromatin fragmentation to nitrogen mustard treatment.

The radiosensitivity of lymphosarcoma cells as determined by the liver colony method.

The liver colony method is based on the observation that intravenous injection of an appropriate number of LS/BL cells into isologous non-irradiated hosts leads to the formation of colonies of proliferating cells in the livers of these animals. The relationship between the number of cells injected and the number of colonies appearing in the livers was determined. This technique was used to measure the radiation sensitivity of LS/BL cells and it yielded a Do of 1.05 Gy. The results show that LS/BL cells have a similar radiation sensitivity as other mammalian cells. The liver colony assay used to determine the radiation sensitivity of the lymphosarcoma LS/BL cells can also be used whenever the number of viable tumour cells in a suspension is to be estimated.

Viscosimetric analysis of the occurrence and repair of DNA single-strand breaks in irradiated animal tissues.

The yields of immediate DNA single-strand breaks in normal tumour tissues of irradiated animals were measured by a viscosimetric method of determination of high-polymer single-strand DNA molecular weight in alkaline nuclear lysates. It has been shown that in irradiated thymus, bone marrow leukocytes, Ehrlich ascitic carcinoma and Zaidel hepatoma cells (first group by tissues) in vivo the yields of DNA single-strand breaks were characterized by 80 to 130 eV per break. In in vivo irradiated liver, lymph node, spleen, and sarcoma 180 cells (second group of tissues) the yields of DNA single-strand breaks have been characterized by 30 to 40 eV per break. DNA single-strand breaks of the first group of tissues have rejoined 1 hour after the irradiation in vivo; DNA single-strand breaks of the second group have not done so.