In parallel to delayed reproductive death and delayed micronuclei in surviving V79 cells that have been reported, the frequency of apoptosis and dicentrics was investigated in the same cell line, 1-2 weeks after X-ray doses between 1 and 12 Gy. Apoptosis was assessed by morphological criteria after staining with Giemsa and using the Apoptag method in parallel. The frequency of apoptosis peaked 48 h after irradiation at about 35% as a function of dose and then decreased to about 10% on day 3. It remained 10 times higher than in unirradiated cells until day 14. The frequency of dicentric chromosomes 24 h after irradiation increased according to a linear-quadratic function, up to about 110% after 12 Gy, decreased 3 days later to about 10% and remained about 5-fold higher than in control cells. The dose-response relationship was similar for all the various end-points of expression of radiation induced genomic instability, showing a steep increase of the frequency with dose up to 3-4 Gy and with no further increase at higher radiation doses.

Evidence has accumulated that radiation induces a transmissible persistent destabilization of the genome, which may result in effects arising in the progeny of irradiated but surviving cells. An enhanced death rate among the progeny of cells surviving irradiation persists for many generations in the form of a reduced plating efficiency. Such delayed reproductive death is correlated with an increased occurrence of micronuclei. Since it has been suggested that radiation-induced chromosomal instability might depend on the radiation quality, we investigated the effects of alpha particles of different LET by looking at the frequency of delayed micronuclei in Chinese hamster V79 cells after cytochalasin-induced block of cell division. A dose-dependent increase in the frequency of micronuclei was found in cells assayed 1 week postirradiation or later. Also, there was a persistent increase in the frequency of dicentrics in surviving irradiated cells. Moreover, we found an increased micronucleus frequency in all of the 30 clones isolated from individual cells which had been irradiated with doses equivalent to either one, two or three alpha-particle traversals per cell nucleus. We conclude that the target for genomic instability in Chinese hamster cells must be larger than the cell nucleus.

V79 Chinese hamster cells were irradiated with doses of 1-12 Gy 300 kV X-rays. Their colony-forming ability and the frequency of micronuclei in binucleate cells after treatment with cytochalasin B was determined at various times after irradiation. The frequency of micronuclei determined within the first 24 h after irradiation increased with doses up to 4 Gy and decreased as the dose increased further. Up to 4 Gy there was a close correlation between surviving fraction and the fraction of cells without micronuclei although the surviving fraction was 2-3 times lower than the fraction of cells without micronuclei. Six, 10 or 13 days after irradiation with either 9 or 12 Gy the plating efficiency and the frequency of micronuclei after cytokinesis block with cytochalasin B was determined in the irradiated, but surviving, cells. The delayed plating efficiency of irradiated cells was significantly decreased. The proportion of binucleated cells was in the normal range at 6-13 days after irradiation, indicating that the proliferative activity of irradiated but surviving cells was not depressed at that time. The micronucleus frequency, however, was significantly increased at all times after irradiation. There was little heterogeneity of plating efficiency and micronucleus frequency among 12 clones which had been isolated for irradiated cultures, 3 weeks after 12 Gy.

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Background and aim: Carcinoembryonic antigen (CEA) carcinoembryonic antigen is one of the tumor markers that is expressed in many colorectal, stomach, pancreatic, lung and chest cancers. The exact mechanism for releasing this antigen from the cell surface to the cancer patients is still unknown. Carcinoma-embryonic antigen proteins are bound to a cell membrane through a glycosyl-phosphate tidal inositol (GPI-anchor) linkage. There is evidence that specific phospholipase enzymes interfere with the breakdown of GPI binding and the removal of CEA from the cell surface. Considering these evidence and data, we investigated the probable role of glycosyl phosphatidyl inositol phospholipase (GPI-PLD) D in hydrolysis and the release of carcinoma amniobiline antigens. Materials and methods: In this study, we demonstrated the expression of GPI-PLD in some cell lines of adenocarcinoma of colorectal using RT-PCR. The level of carcinogenic amniotic antinase released by one of the cancer cell lines (LS-180), which freely releases large amounts of carcinoma ambrionic antigen in the culture medium, was detected in the presence and absence of specific inhibitors and activators of this enzyme.