As the measurement of chromosomal translocations increases in popularity for quantifying prior radiation exposure, information on the possible decline of these "stable" aberrations over time is urgently needed. We report here information about the persistence of radiation-induced chromosome aberrations in vivo over the life span of a rodent. Female C57BL/6 mice were given a single whole-body acute exposure of 0, 1, 2, 3 or 4 Gy (137)Cs gamma rays at 8 weeks of age. Chromosome aberrations were analyzed from peripheral blood samples at various intervals between 1 day and 21 months after exposure. Aberrations were detected by painting chromosomes 2 and 8. Translocations decreased dramatically during the first 3 months after irradiation, beyond which time the frequencies remained relatively constant out to 1 year, when the effects of aging and clonal expansion became significant. Both reciprocal and nonreciprocal translocations increased with age in the unexposed control animals and were involved in clones. As expected of unstable aberrations, dicentrics decreased rapidly after exposure and reached baseline levels within 3 months. These results indicate that the persistence of translocations induced by ionizing radiation is complicated by aging and clonal expansion and that these factors must be considered when quantifying translocations at long times after exposure. These results have implications for biological dosimetry in human populations.
Cadmium (Cd) is an essential material used in the battery, metal-coating, and alloy industries. In addition to these industrial uses, it is also a component of cigarette smoke. Therefore, exposure to cadmium is widespread and presents a considerable health concern. Cadmium is known to be a carcinogen; however, the possible mechanism of carcinogenesis with regards to the activation and inactivation of cancer-related genes has not yet been fully elucidated. In this study, amplification, expression, and point mutation of cancer-related genes associated with Cd-induced cell transformation in BALB/c-3T3 cells were studied. Six proto-oncogenes (K-ras, c-myc, c-fos, c-jun, c-sis, and erbB), as well as the p53 tumor suppressor, were investigated for gene amplification using differential polymerase chain reaction (PCR), while the expression of the proteins produced by these genes was evaluated by Western blot analysis. Point mutations in K-ras and p53 were studied by PCR restriction fragment length polymorphism analysis and DNA sequencing. There were no point mutations observed in codons 12, 13, and 61 of K-ras or in exons 4-10 of p53 and no observed differences in the levels of any of the proteins studied. Among 10 Cd-induced transformed cell lines, significant gene amplification was found for c-myc and c-jun in 50% and 80% of the cell lines, respectively. Chromosome painting was performed to confirm that this amplification was not simply due to additional copies of the chromosomes carrying these oncogenes. In addition, reverse-transcription PCR (RT-PCR) was performed to confirm increased expression of c-myc and c-jun. These results suggest that cell transformation induced by Cd may be attributed, at least in part, to gene amplification of c-myc and c-jun and that some of the Cd-transformed cells may possess neoplastic potential resulting from genomic instability.
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