scispace - formally typeset
Search or ask a question
Topic

Sister chromatid exchange

About: Sister chromatid exchange is a research topic. Over the lifetime, 3187 publications have been published within this topic receiving 90029 citations. The topic is also known as: replication-born DSB repair by SCE & GO:1990414.


Papers
More filters
Journal ArticleDOI
TL;DR: This chapter summarizes the most relevant methodologies available for evaluation of cytogenetic damage induced in vivo in mammalian germ cells for chromosome damage in rodent germ cells.
Abstract: This chapter summarizes the most relevant methodologies available for evaluation of cytogenetic damage induced in vivo in mammalian germ cells. Protocols are provided for the following endpoints: numerical and structural chromosome aberrations in secondary oocytes or first-cleavage zygotes, reciprocal translocations in primary spermatocytes, chromosome counting in secondary spermatocytes, numerical and structural chromosome aberrations, and sister chromatid exchanges (SCE) in spermatogonia, micronuclei in early spermatids, aneuploidy in mature sperm. The significance of each methodology is discussed. The contribution of novel molecular cytogenetic approaches to the detection of chromosome damage in rodent germ cells is also considered.

40 citations

Journal ArticleDOI
TL;DR: In a UV-sensitive mutant (43-3B) which has an increased spontaneous frequency of SCEs, it is found that this increase is due to incorporated BrdUrd.
Abstract: We have utilized monoclonal antibody against BrdUrd to detect sister-chromatid exchanges in CHO cells. This technique allows detection of SCEs at very low levels of BrdUrd incorporation. At incorporation level of 5.0%, a frequency of about 2 SCEs/cell/cycle was found. In a UV-sensitive mutant (43-3B) which has an increased spontaneous frequency of SCEs, it is found that this increase is due to incorporated BrdUrd. In MMS- and MMC-treated cells, an influence of BrdUrd on the frequencies of induced SCEs was found only when high concentrations of mutagens were employed.

39 citations

Journal ArticleDOI
TL;DR: Hepatic microsomes from rats pretreated with PCB were found to metabolize the food mutagen 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine (PhIP) to one of which was identified as the N-hydroxy derivative, N-OH-PhIP, which seems to be a proximate mutagenic metabolite of PhIP.
Abstract: Hepatic microsomes from rats pretreated with PCB were found to metabolize the food mutagen 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine (PhIP) to two major metabolites, one of which was identified as the N-hydroxy derivative, 2-hydroxy-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine (N-OH-PhIP). This identification was based on mass spectral (MS), UV and HPLC data by comparison with N-OH-PhIP prepared by chemical synthesis, as well as the specific activity of the compound in the Ames Salmonella test. Synthetic N-OH-PhIP was prepared by catalytic reduction of the nitro derivative of PhIP, which was synthesized from PhIP by diazotization and reaction with sodium nitrite. N-OH-PhIP was mutagenic to Salmonella typhimurium TA98 without metabolic activation and had a specific mutagenic activity of 2700 revertants/nmol. N-OH-PhIP thus seems to be a proximate mutagenic metabolite of PhIP. Other direct acting mutagens were not detected in the microsomal incubation mixture after HPLC separation. N-OH-PhIP also induced sister chromatid exchange (SCE) in Chinese hamster ovary cells (CHO cells) without metabolic activation. The specific activity of N-OH-PhIP in this assay was approximately 3 times higher than the activity of PhIP with microsomal activation.

39 citations

Journal ArticleDOI
TL;DR: The data support the involvement of C8-deoxyguanosine adducts in mutation and SCE induction, and indicate that the structure of the group adducted to DNA may be an important factor in determining the magnitude of these biological responses.
Abstract: Chinese hamster ovary cells were exposed to N-hydroxy-2-aminofluorene, N-hydroxy-N'-acetylbenzidine and 1-nitrosopyrene, and the resulting DNA adducts, sister-chromatid exchanges (SCEs) and mutations at the hypoxanthine-guanine phosphoribosyl transferase locus were quantified. Each agent produced a major DNA adduct substituted through the C8 of deoxyguanosine. When the data from all three agents were combined, both mutation and SCE induction correlated strongly with the concentration of DNA adducts. However, significant differences were found in the relationships between adduct formation and the biological responses produced by the individual agents. While N-hydroxy-N'-acetylbenzidine induced the most mutations per adduct, N-hydroxy-2-aminofluorene caused the greatest number of SCEs per adduct. The data support the involvement of C8-deoxyguanosine adducts in mutation and SCE induction, and indicate that the structure of the group adducted to DNA may be an important factor in determining the magnitude of these biological responses. These findings also suggest that SCE and mutation induction are independent expressions of DNA damage.

39 citations

Journal ArticleDOI
TL;DR: Differences in behaviour between the 5-bromodeoxyuridine-substituted template strands in Bloom's syndrome and normal human fibroblasts have been investigated in order to elucidate the mechanism responsible for the elevated baseline sister-chromatid exchange (SCE) frequency in BS.
Abstract: Differences in behaviour between the 5-bromodeoxyuridine (BrdU)-substituted template strands in Bloom's syndrome (BS) and normal human fibroblasts have been investigated in order to elucidate the mechanism responsible for the elevated baseline sister-chromatid exchange (SCE) frequency in BS. Alkaline sucrose gradient analysis of the normal and BrdU-substituted DNA strands showed the former to be of higher mol. wt. and of mature size while the latter were of lower molecular size, resulting from breaks introduced during the repair of the BrdU with no differences discernible between BS and normal cells. The rates of removal of BrdU were similar in BS and normal cells, which indicates that the increased SCE level in BS is not due to different rates of repair of the BrdU. The maturation of newly synthesized DNA on a normal template is delayed in BS cells compared with normal cells although it is complete at 18 h, the time it is acting as a template for DNA synthesis. In the presence of a BrdU-substituted template the maturation although further delayed is complete in normal cells by 12 h but in BS cells is not complete even by 30 h, when the newly synthesized strand, due to cell cycle delay produced by the incorporation of BrdU, becomes a template in the next round of DNA synthesis. It is suggested that a similar delay in maturation probably occurs when a new strand containing BrdU is synthesized on a normal template in BS cells. When these strands act as a template they will contain two types of breaks--those due to BrdU repair and those due to delayed maturation. The latter will be responsible for the elevated SCEs in BS cells as the DNA replication forks move through them in a manner similar to that previously reported. The possible implications of differential delays in cell proliferation in BrdU, rates of BrdU removal and extent of DNA maturation in this syndrome are discussed.

39 citations


Network Information
Related Topics (5)
DNA damage
47K papers, 2.4M citations
84% related
DNA repair
41.5K papers, 2.4M citations
83% related
DNA
107.1K papers, 4.7M citations
77% related
Mutation
45.2K papers, 2.6M citations
76% related
Carcinogenesis
60.3K papers, 3.1M citations
75% related
Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20238
202222
20215
202011
201914
201811