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Aberrations in cells

Populations of soil mites were reduced in the Chernobyl area, but no population showed a catastrophic drop in numbers. By 1987, soil microfauna — even in the most heavily contaminated plots — were comparable to controls. Flies (Drosophila spp.) from various distances from the accident site and bred in the laboratory had higher incidences of dominant lethal mutations (14.7%, estimated dose of 0.8 mGy/h) at sites nearest the accident than controls (4.3%). Fish populations seemed unaffected in July/August 1987, and no grossly deformed individuals were found. However, 34+ i 37( s levels were elevated in young fishes. The most heavily contaminated teleost in May 1987 was the carp (Carassius carassius). But carp showed no evidence of mutagenesis, as judged by incidence of chromosomal aberrations in cells from the corneal epithelium of carp as far as 60 km from Chernobyl (Sokolov et al. 1990). [Pg.1684]

Fish populations seemed unaffected in July-August 1987, and no grossly deformed ini-viduals were found however, and Cs levels were elevated in young fish. The most heavily contaminated teleost in May 1987 was the carp Carassius carassius). But carp showed no evidence of mutagenesis, as judged by incidence of chromosomal aberrations in cells from the comeal epithelium of carp as far as 60 km from Chernobyl. [Pg.700]

Fig. 3. The effect of adding 2 mM 3AB at various times after 1.5 Gy of X-rays on die induction of chromatid breaks in human lymphocytes labeled with 0.1 pCiAnl pH]dThd for 6 hr 24 hr after mitogen stimulation. The vertical bars indicate standard error of the mean. At each time point the number of induced aberrations was calculated by subtracting the number of background breaks and the number of [%QdThd-induced chromatid breaks from the total number of aberrations observed. For comparison, the number of X-ray-induced aberrations in cells not exposed to pHJdThd is indicated by the dashed horizontal line. Reprinted with permission from Wiencke etal. (10). Fig. 3. The effect of adding 2 mM 3AB at various times after 1.5 Gy of X-rays on die induction of chromatid breaks in human lymphocytes labeled with 0.1 pCiAnl pH]dThd for 6 hr 24 hr after mitogen stimulation. The vertical bars indicate standard error of the mean. At each time point the number of induced aberrations was calculated by subtracting the number of background breaks and the number of [%QdThd-induced chromatid breaks from the total number of aberrations observed. For comparison, the number of X-ray-induced aberrations in cells not exposed to pHJdThd is indicated by the dashed horizontal line. Reprinted with permission from Wiencke etal. (10).
The work was carried out on the primary culture of embryonic tissues — the mouse and human fibroblasts [16, 17], We analyzed chromosomal aberrations in cells at the stages of anaphase or telophases (ana-telophases), after treatment culture by phosphemid in a concentration of 1 x 10 W. [Pg.235]

A number of studies have shown that vitamins moderate the induction of chromosomal aberrations by radiation. Vitamins C and E given orally to mice either 2 h before, immediately after, or 2 h after 1 Gy (100 rad) of y-ray TBI significantly reduce the frequencies of micronuclei and chromosomal aberrations in BM cells. Vitamin E is the more effective (95). Administration of vitamins C and E within 5 min of irradiation is as effective as pretreatment. Protection by vitamin C has also been shown in humans. Whereas chronic treatment of rats using vitamin C (100 or 300 mg/(kg/d)) for six months prior to TBI protects against chromosomal aberrations, vitamin E is not radioprotective in this setting (96). [Pg.491]

The lymphocytes from 31 patients exposed to various organophosphate pesticides were examined for chromosomal aberrations (Van Bao et al. 1974). Five of the patients were exposed to methyl parathion only. Blood samples were taken 3-6 days after exposure and again at 30 and 180 days. A significant (p<0.05) increase was noted in the frequency of stable chromosomal aberrations in acutely intoxicated persons (although such cells are eventually lost from the cell population). Two of the methyl parathion-exposed persons had taken large doses orally in suicide attempts. The study limitations include small sample size, absence of a control group, lack of quantification of exposure levels, and possible... [Pg.81]

Results of methyl parathion assays involving effects on chromosomes have also been contradictory. For sister chromatid exchange, Waters et al. (1982) reported a positive response in Chinese hamster ovary cells only in the presence of metabolic activation system, while methyl parathion tested positive without a metabolic activation system in Chinese hamster V79 cells (Chen et al. 1981), cultured normal human lymphoid cells (Chen et al. 1981 Gomez-Arroyo et al. 1987 Sobti et al. 1982), and Burkitt s l5miphoma cells (Chen et al. 1981). Chen et al. (1981) found a significant dose-related increase in sister chromatid exchange in both hamster and human cultured cells, but dose-related cell cycle delays were less pronounced in human cell lines than in V79 cells. Negative results were obtained for chromosomal aberrations in human lymphocytes without a metabolic activation system (Kumar et al. 1993). [Pg.86]

Oral administration of 11.6 mg/kg/day of endosulfan to rats for up to 30 days also failed to induce chromosomal damage in bone marrow and spermatogonial cell systems, but it is not known how soon after treatment the animals were killed. As shown in mouse studies (Usha Rani and Reddy 1986), a latency period of 60 days was required to see chromosomal aberrations in spermatogonia. However, relatively significant changes were observed for mitotic indices (Dikshith et al. 1978). [Pg.103]

Nuzzo, F., Sala, F., Biondi, D., Casati, A., Cestaro, B., and de Carli, L. (1985). Liposomes induce chromosome aberrations in human cultured cells, Exp. Cell Res., 157. 397-408. [Pg.330]

Brittain E, Noel P, Metcalfe DD Demonstration of an aberrant mast-cell population with clonal markers in a subset of patients with idiopathic anaphy- 72 laxis. Blood 2007 110 2331-2333. [Pg.66]

Chensue SW, Lukacs NW, Yang TY, et al. Aberrant in vivo T helper type 2 cell response and impaired eosinophil recruitment in CC chemokine receptor 8 knockout mice. J Exp Med 2001 193(5) 573-584. [Pg.251]

Cytogenetic research showed that the average group frequency of cells with chromosomal aberrations in lymphocytes is many times higher in personnel producing the fungicide zineb (5.53%, with fluctuations from 4.00-8.50%) than in the control group (0.95%) [A97]. [Pg.66]

Deknudt G, Gerber GB. 1979. Chromosomal aberrations in bone-marrow cells of mice given a normal or a calcium-deficient diet supplemented with various heavy metals. Mut Res 68 163-168. [Pg.508]

Bartkova, J., Lukas, J. and Bartek, J. (1997) Aberrations of the Gl- and Gl/ S-regulating genes in human cancer. Progress in Cell Cycle Research 3, 211-220. [Pg.141]

Grant WF (1994) The present status of higher plant bioassays for the detection of environmental mutagens. Mutat Res 310 175-185 Grant WF, Owens ET (2001) Chromosome aberrations in Pisum for the study of environmental mutagens. Mutat Res 488 93-118 Kalweit S, Utesch D, von der Hude W, Madle S (1999) Chemically induced micronucleus formation in V79 cells-comparison of three different test approaches. Mutat Res 439 183-190... [Pg.300]

Tributyltins and other organotins induce chromosomal aberrations in mammals, although this was not observed in tests with aquatic invertebrates (Dixon and Prosser 1986). Studies with isolated rat hepatoma cells, TBT, and PCB 126, show that TBT inhibits cytochrome P-4501A activity, and PCB 126 induces EROD activity. However, PCB-induced EROD activity was potentiated by coexposure to low noncytotoxic concentrations of TBT (Kannan et al. 1998b). Authors concluded that TBT does not interfere with Ah receptor binding and that potentiation of EROD activity and cytotoxicity as a result of coexposure to PCB 126 and TBT is significant because they coaccumulated in a variety of marine organisms. [Pg.617]

Structural chromosome aberrations, particularly chromatid gaps and increased frequency of fragment exchange, were observed in rat bone marrow cells after 14 days of exposure to 240 mg Zn/L drinking water (Kowalska-Wochna et al. 1988). Chromosomal aberrations were observed in bone marrow cells of mice fed diets equivalent to 650 mg Zn/kg BW daily, in mice exposed to zinc oxide by inhalation, and in mice maintained on a low-calcium diet (USPHS 1989). Aberrations in bone marrow of mice given 5000 mg Zn/kg diet may be associated with calcium deficiency (Leonard and Gerber 1989). Calcium is displaced by zinc in calcium-depleted conditions, leading to chromosomal breaks and interference in the repair process (USPHS 1989). [Pg.647]

Sofuni, T. and M. Ishidate, Jr. 1988. Induction of chromosomal aberrations in active oxygen-generating systems. I. Effects of paraquat in Chinese hamster cells in culture. Mutation Res. 197 127-132. [Pg.1191]


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