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Chromosome damage, effects

Benzyl chloride caused genetic mutations and chromosome-damaging effects in a wide variety of in vitro assays it was not mutagenic in vivo in the mouse micronucleus assay. ... [Pg.81]

Abel, G. 1987. Chromosome-damaging effect of beta-asarone on human lymphocytes. Planta Med. 53(3) 251-253. [Pg.10]

Hirono, I., H. Mori, and C.C.J. Culvenor. 1976. Carcinogenic activity of coltsfoot, Tussilago farfara L. Gann 67(1) 125-129. Kraus, C., G. Abel, and O. Schimmer. 1985. Studies on the chromosome damaging effect of some pyrrolizidine alkaloids in human lymphocytes in vitro. Planta Med. 51(2) 89-91. [Pg.888]

Donaldson K, Golyasnya N, Davis JMG. Long and short amosite asbestos samples comparison of their chromosome-damaging effects to cells in culture with the results of other in vitro and in vivo assays of toxicity. In Davis JMG, Jaurand MC, eds. Cellular and Molecular Effects of Minerals and Synthetic Dusts and Fibres. Berlin, Springer-Verlag, 1994 221-226. [Pg.426]

Total frequencies of environmental illness are difficult to measure. When causes can be identified, however, scientists observe that frequencies of occurrence of a particular illness vary directly with the severity and extent of exposure. Particularly frequent in the workplace are skin lesions from many different causes and pulmonary diseases related to the inhalation of various dusts, such as coal dust (black lung), cotton dust (brown lung), asbestos fibers (asbestosis), and silica dust (silicosis). Environmental agents can also cause biological effects without overt clinical illness (for example, chromosome damage from irradiation). [Pg.47]

F. Reproductive toxins Chemicals which affect the reproductive capabilities including chromosomal damage (mutations) and effects on fetuses (teratogenesis) ... [Pg.182]

Extensive research is currently underway to use biological markers (biomarkers) in exposure and risk assessment. Biomarkers include the reaction products of chemicals or their metabolic products with biological macromolecules, especially with DNA. They also involve indicators of effect, such as chromosomal damage, and indicators of individual genetic susceptibility. [Pg.325]

Fig. 15. Effect of beta irradiation from Ce- Pr and gamma irradiation from Co on the production of liver chromosome damage. Fig. 15. Effect of beta irradiation from Ce- Pr and gamma irradiation from Co on the production of liver chromosome damage.
Air concentrations of 28.5 mg/m3 for 4 h daily on days 9-12 of gestation caused fetotoxic effects and chromosomal damage to liver cells by day 18 effects included reduced survival, impaired growth, retarded limb ossification, and bone abnormalities. At 2.9 mg/m3, a 9.9% decrease in fetal weight was recorded at 0.26 mg/m3, a 3.1% decrease was measured Oral dosages of 400-600 mg/kg BW on days 7-16 of gestation produces fetal malformations (cleft palate), delayed skeletal ossification, and fetal weight reduction 200-600 mg/kg BW daily for 10 days (DMA) produced fetal and maternal toxicity... [Pg.1526]

The in vivo micronucleus test is used for the detection of damage to chromosomes as well as the mitotic apparatus in bone marrow or peripheral blood cells of rodents. The assay system has been well standardized.14-17 The basic features of the test system are (1) the effect of the test chemical is observed in anucleated polychromatic erythrocytes (PCEs) (2) PCEs have a relatively short lifespan, so that any micronuclei they contain must have been generated as a result of recently induced chromosome damage (3) micronuclei are readily identifiable and their distribution is well defined and (4) the frequency of induced micronuclei in PCEs is dependent on sampling times. [Pg.307]

Other adverse effects LSD is not teratogenic, but it can increase spontaneous abortions due to uterotonic effects. Use during pregnancy is unnecessary and clearly contraindicated. LSD appears to have weak, if any, mutagenic effects (Cohen and Shiloh 1977-78). Claims of chromosomal damage have showed conflicting results, and have not been supported in humans. [Pg.355]

Although only limited data are available, the weight of evidence indicates that 1,2-diphenylhydrazine is genotoxic in animals. In particular, positive results were obtained in all assays with mammalian systems Overall, the available evidence suggests that 1,2- diphenylhydrazine may cause chromosomal damage or other genotoxic effects in humans. [Pg.36]

Cytogenetic studies have been conducted using bone marrow cells of rats following inhalation exposure to 1,4-dichlorobenzene (Anderson and Richardson 1976). Three series of exposures were carried out (1) one exposure at 299 or 682 ppm for 2 hours (2) exposures at 75 or 500 ppm, 5 hours per day for 5 days and (3) exposures to 75 or 500 ppm, 5 hours per day, 5 days per week for 3 months. Bone marrow cells from both femurs were examined for chromosome or chromatid gaps, chromatid breaks, fragments, or other complex abnormalities. In all three experiments, exposure to 1,4-dichlorobenzene failed to induce any effects indicative of chromosomal damage. Other genotoxicity studies are discussed in Section 2.5. [Pg.58]

Hamsters and rats were exposed to an average concentration of 817 and 820 ppm, respectively, for 4 days. In both animal species, there were distinct signs of toxicity 4 of 10 hamsters died during the exposure. Chromosome analysis of bone marrow cells after the exposure indicated no damaging effects. [Pg.100]

The p53 protein is essential for the induction of apoptosis as a response to chromosomal damage (e.g., y-irradiation). It acts by blocking DNA replication of damaged cells. Cells deficient in p53 replicate in spite of the DNA damage to accumulate further mutations, thereby producing effects similar to overexpression of Bcl-2 to favor the accumulation of further mutations and reduce the efficiency of drugs for chemotherapy (E2). [Pg.75]

After metabolic activation, it depoly-merizes DNA and causes chromosomal damage and also nucleic acid synthesis inhibition. It is found to be effective in Hodgkin s disease and carcinoma of lungs. [Pg.378]

Reproductive Toxicology (mammalian) The study of the effects of chemicals on the adult reproductive and neuroendocrine systems, the embryo, foetus, neonate and prepubertal mammal. Reproductive Toxins Tire tenn refers to a specific target organ characterization of effect. These are chemicals which affect the reproductive capabilities including chromosomal damage (mutations) and effects on fetuses (teratogenesis). Signs and symptoms include birth defects sterility. Examples are lead and DBCP. [Pg.256]

Its genotoxic properties have received little attention. DNA damage has been observed in treated mammalian cells, but it is not mutagenic in bacteria and does not cause chromosomal damage in cultured mammalian cells or dominant lethal effects in mice. [Pg.355]


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Chromosomal damage

Damage effect

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