DNA damage and repair in lymphoblastoid cell lines from normal donors and fragile X syndrome patients

doi:10.1016/S0188-4409(01)00376-9

中山醫學大學機構典藏 CSMUIR > 醫學科技學院 > 生物醫學科學學系暨碩士班 > 期刊論文 > Item 310902500/18065

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/18065

Title:	DNA damage and repair in lymphoblastoid cell lines from normal donors and fragile X syndrome patients
Authors:	Wang, T.-S.;Hsieh, L.-J.;Hsu, T.-Y.;Chung, C.-H.;Li, S.-Y.
Date:	2002
Issue Date:	2017-08-01T08:18:11Z (UTC)
ISSN:	01884409
Abstract:	Background. Because lymphocytes from fragile X patients have been reported as hypersensitive to bleomycin-induced chromatid breaks and because the number of trinucleotide repeats in families with fragile X syndrome has a propensity to expand, we have investigated the possibility that fragile X cells may be hypersensitive to DNA damage and have a lower capacity for DNA repair. Methods. Lymphocytes from normal and fragile X syndrome donors were immortalized by Epstein-Barr virus transformation. Characteristics of fragile X syndrome including the folate-sensitive fragile site on chromosome Xq27.3, length of CGG repeat expansion, and FMRP expression in Epstein-Barr virus-transformed lymphoblastoid cell lines were analyzed by standard cytogenetic methods, Southern blot, and Western blot, respectively. Analysis of DNA damage and repair induced by hydrogen peroxide, bleomycin, ethyl methanesulfonate, 4-nitroquinoline-N-oxide, etoposide, and mitomycin C was carried out by single-cell gel electrophoresis assay (known as comet assay). Results. Lymphoblastoid cell lines from fragile X donors had a folate-sensitive fragile site on chromosome Xq27.3, no or low FMRP expression, and expansion of the CGG repeat. Results of comet assay showed that fragile X cells were not more sensitive to mutagen-induced DNA strand breaks and did not have lower DNA repair capacity in comparison with normal cells. Furthermore, one fragile X cell line showed hyposensitivity to DNA strand breaks induced by hydrogen peroxide, bleomycin, and ethyl methansulfonate. Conclusions. The results of this study do not support the notion that CGG trinucleotide expansion in fragile X syndrome is caused by permanent deficiency in DNA repair. © 2002 IMSS. Published by Elsevier Science Inc.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/18065 http://dx.doi.org/10.1016/S0188-4409(01)00376-9
Relation:	Archives of Medical Research 33, 128-135
Appears in Collections:	[生物醫學科學學系暨碩士班] 期刊論文

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