Chromosome damage

Bredinin, Neosidomycin, and SF-2140. Bredinin (62), isolated from the culture filtrates of Eupenicillium brefeldianum (1,4), inhibits the multiplication of L5178Y, HeLa S3, RK-13, mouse L-ceUs, and Chinese hamster cells. GMP can reverse the inhibition by (62), but (62) is not incorporated into the nucleic acids. The inhibition of nucleic acid synthesis and chromosomal damage in the S and G 2 phases that is caused by (62), is reversed by GMP. It blocks the conversion of IMP to XMP and XMP to GMP. In combination with GMP, (62) interferes with intracellular cAMP levels and thereby inhibits cell division. 

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). 

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

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. 

Muragenicuy, genotoxicity Rats, mice, bacterial strains, yeasts Few days Potential to cause mutations, chromosomal damage, and... 

An in-vitro test with mammalian cells (chromosomal damage or mouse lymphoma tk assay)... 

An in-vivo test in rodents (chromosomal damage in haematopoietic cells)... 

High doses of LSD may cause chromosome damage in experimental animals (Dishotsky et al. 1971). Chromosomal aberrations in humans have been related to drug abuse in general. Pharmacologically pure LSD, however, has not been demonstrated to cause a detectable increase in chromosome damage (Li and Lin 1998). 

Human hematopoietic cells/RPMI 1788, 7191 B411-4 Chromosomal damage No data Degraeve et al. 1985 Huang 1973... 

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). 

Caffeine and almost all of its metabolites cross the placenta and diffuse into virtually all fetal tissues.12 Caffeine has been shown to produce chromosomal damage in mammalian cells.3 There is an increase in fetal mortality and morbidity when pregnant rats are fed caffeine in increasing doses.4... 

Muro LA, Goyer RA. 1969. Chromosome damage in experimental lead poisoning. Arch Pathol 87 660-663. 

Riordan ML, Evans HJ. 1974. Absence of significant chromosome damage in males occupationally exposed to lead. Nature 247 50-53. 

Schwanitz G, Lenhert G. Gebhart E. 1970. [Chromosome damage after occupational exposure to lead.] Deutsch Med Wschr 95 1630-1641. (German)... 

Pohl-Ruling, J. and P. Fischer, Chromosome Aberrations in Inhabitants of Areas With ELevated Natural Radioactivity, in Radiation-Induced Chromosome Damage in Man (T. Ishihara and M.S. Sasaki, ed) pp. 527-560, A.R. Liss, Inc., New York (1982). 

U. Mukherjee, R. Nowotny, P. Palitti, Z. PolikovA, T. Sharma, and W. Schmidt, Chromosomal Damage Induced in Human Lymphocytes by Low Doses of D-T Neutrons, Mutation Research 173 267-272 (1986). 

Figure 15 illustrates that intraperitoneal injection of l44Ce citrate produced the same amount of chromosome damage as a protracted whole-body exposure to Co on a per rad to liver basis in Chinese hamsters (Brooks et al., 1972). Acute exposure to Co at high dose rates produces a nonlinear increase in damage as a function of dose (Brooks et al., 1971). 

Fig. 15. Effect of beta irradiation from Ce- Pr and gamma irradiation from Co on the production of liver chromosome damage.

Monomethylhydrazine-induced mutagenesis was not observed in Ames Salmonella/ microsome with activation (Matheson et al. 1978). In vivo tests in mice (dominant lethal, revertants in host-mediated assay), and dogs (micronuclei) were negative (reviewed in Trochimowicz 1994). However, in vitro chromosomal damage in human and rat tissue has been demonstrated, although in vivo liver DNA damage (as determined by DNA alkaline elution) was equivocal (reviewed in Trochimowicz 1994). 

Acute or subacute arsenic exposure can lead to elevated tissue residues, appetite loss, reduced growth, loss of hearing, dermatitis, blindness, degenerative changes in liver and kidney, cancer, chromosomal damage, birth defects, and death. 

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... 

In vivo test for chromosomal damage using rodent hematopoietic cells Gene Mammalian In vivo... 

It is known that more fetal wastage than generally believed and many spontaneous abortions arise as a result of the presence of dominant lethal mutations in the developing embryo, many of which appear to be due to major chromosomal damage. In addition, impairment of male fertility may also be a consequence of exposure to mutagens. 

The in vitro cytogenetic assay is a short-term mutagenicity test for detecting chromosomal damage in cultured mammalian cells. 

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