Chromosome aberrations, from

Chromosomal aberrations, from ozone exposure, 8, 342, 363-64 Chromotrophic acid procedure, to measure oxidant concentration, 185 Cigarette-smoking... 

Fig. 1. (left) Dicentric frequency of normal ( ) and Down Syndrome (- -) lymphocytes after X-ray with 150 rads in the presence of 3 mM SAB. Whole blood was treated with 3 mM SAB for 30 min prior to X-irradiation. After X-ray the cells were incubated in the presence of SmM SAB for an additional 0, 1, 3, or 6 hr before PHA stimulation. At the end of the incubation period, the cells were washed twice with culture medium and then returned to RPMI1640 medium containing 2% PHA. Six hr after PHA stimulation 1 mM bromodeoxyuridine was added to each culture. Forty-eight hr after the addition of PHA, 2 ng of colcemid was added to the cultures to induce mitotic arrest, and 2 hr later the lyinphocytes were harvested. The lymphocytes were stained using the fluorescence plus Geimsa method. One hundred metaphases from first division cells were analyzed for chromosome aberrations from each culture. 

Ethylene oxide has been shown to produce mutagenic and cytogenic effects in a variety of test systems (226). An increased frequency of chromosomal aberrations in peripheral lymphocytes of monkey exposed to ethylene oxide for 104 weeks has been reported (240). In mice, it is an effective inducer of chromosome breaks leading to dominant-lethal mutations. In addition, ethylene oxide has been shown to induce heritable effects in the heritable translocation test conducted in mice exposed to ethylene oxide by inhalation (241,242). In this study, male mice were exposed to ethylene oxide ranging from 165 to 300 ppm for 6 h per day 5 or 7 days/week for 8.5 weeks. Ethylene oxide has also been shown to bind to proteins (243) as well as to DNA (244). Several studies on ethylene oxide-exposed workers have demonstrated an increased incidence of chromosomal aberrations and sister chromatid exchanges the relevance of such effects to human health evaluation is currendy uncertain. 

In a case-control study of pesticide factory workers in Brazil exposed to methyl parathion and formulating solvents, the incidence of chromosomal aberrations in lymphocytes was investigated (De Cassia Stocco et al. 1982). Though dichlorodiphenyltrichloroethane (DDT) was coformulated with methyl parathion, blood DDT levels in the methyl parathion-examined workers and "nonexposed" workers were not significantly different. These workers were presumably exposed to methyl parathion via both inhalation and dermal routes however, a dose level was not reported. The exposed workers showed blood cholinesterase depressions between 50 and 75%. However, the baseline blood cholinesterase levels in nonexposed workers were not reported. No increases in the percentage of lymphocytes with chromosome breaks were found in 15 of these workers who were exposed to methyl parathion from 1 week to up to 7 years as compared with controls. The controls consisted of 13 men who had not been occupationally exposed to any chemical and were of comparable age and socioeconomic level. This study is limited because of concomitant exposure to formulating solvents, the recent history of exposure for the workers was not reported, the selection of the control group was not described adequately, and the sample size was limited. 

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... 

Both AML and ALL are presumed to arise from clonal expansion of a single arrested cell. As these cells expand, they acquire one and often more chromosomal aberration, including translocations, inversions, deletions, point mutations, and... 

Effect. Chromosomal aberrations have been reported in lymphocytes following exposure to 241Am (Bauchinger et al. 1997 Kelly and Dagle 1974). Additionally, high radiation doses from internally deposited americium can cause bone marrow changes and altered blood values (Filipy et al. 1995 Priest et al. 1995). However, none of these effects are specific to americium. 

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]. 

Eleven male volunteers aged 20-30 years ingested lead acetate for 49 days. PbB levels were kept at approximately 40 pg/dL. The frequency of chromosome aberrations was assayed after lymphocyte culture for 72 hours and found to be no different from that of 10 controls. The lymphocytes from lead-exposed subjects did show a higher mitotic activity (Bulsma and DeFrance 1976). 

Genotoxic Effects. Evaluation of the genotoxicity of lead in humans has focused on evaluations of lymphocytes from occupationally or environmentally exposed persons (Table 2-10) and in vitro studies of structural chromosomal aberrations and sister chromatid exchange in cultures of lymphocytes taken from healthy individuals (Table 2-11). Results of studies with human lymphocyte cultures exposed in vitro to lead acetate were nearly equally divided between positive (Beek and Obe 1974 Niebuhr and Wulf 1984) and negative (Beek and Obe 1975 Deknudt and Deminatti 1978 Gasiorek and Bauchinger 1981 Schmid etal. 1972). 

The nucleus of all eucariotic cells contains the carrier of the genetic information in the chromosomes. It is possible to visualize the chromosomes and analyze their number and pattern during a special period of cell division (the metaphase). Alterations from their normal shapes are observed as structural chromosome aberrations. These are chromosome type aberrations (terminal and interstitial deletions, dicentrics and rings), chromatid aberrations (gaps, breaks and exchanges) and sister chromatid exchanges. Spontanous frequencies of such chromosome... 

Investigations with Animals. A further support of the hypothesis described above can be found in investigations carried out with animals Leonard et al. (1979) found in an area with high natural radioactivity in France a small but significant increase of chromosome aberrations in the lymphocytes of rabbits. The rabbits were kept in a hut for 12 months, and received up to 0.7 Gy/year from gamma rays together with more than 6 Gy alpha doses from radon and daugthers. Further experiments with rabbits at radon exposure under controlled conditions have shown that the chromosome... 

Deng Zhi-cheng and Li Yuan-huy, The Main Cause of Chromosome Aberration Increase in Blood Lymphocytes of Uranium Miners, Private Communication from Department of Radiation Medicine, North China, Institute of Radiation Protection China (1983) ... 

Purrott, R.J., A.A. Edwards, D.C. Lloyd, and J.W. Stather, The Induction of Chromosome Aberrations in Human Lymphocytes by in Vitro Irradiation With Alpha-Particles From Pu 239, Internat. J. Radiation Biology 38 277-284 (1980). 

Human cells exposed to various nickel compounds have an increased frequency of chromosomal aberrations, although sister chromatid exchange frequency is unaffected. Cells from nickel refinery workers exposed to nickel monosulfide (0.2 mg Ni/m3) or nickel subsulfide (0.5 mg Ni/m3) showed a significant increase in the incidence of chromosomal aberrations (Boysen et al. 1980 WHO 1991 USPHS 1993). No correlation was evident between nickel exposure level and the frequency of aberrations (USPHS 1993). 

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). 

Sperm chromosomes, 0.23, 0.45, 0.91, or 1.82 Gy, single acute exposure Thyroid, single acute exposure Chromosomal aberrations increased linearly from 6.1% at 0.23 Gy to 62% at 1.82 Gy 14... 

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