000133442 001__ 133442
000133442 005__ 20260217205500.0
000133442 0247_ $$2doi$$a10.1016/j.mrgentox.2024.503753
000133442 0248_ $$2sideral$$a138120
000133442 037__ $$aART-2024-138120
000133442 041__ $$aeng
000133442 100__ $$0(orcid)0000-0003-2936-242X$$aCatalán, Julia$$uUniversidad de Zaragoza
000133442 245__ $$aChromosome-specific induction of micronuclei and chromosomal aberrations by mitomycin C: Involvement of human chromosomes 9, 1 and 16
000133442 260__ $$c2024
000133442 5060_ $$aAccess copy available to the general public$$fUnrestricted
000133442 5203_ $$aCytogenetic studies have shown that human chromosomes 1, 9, and 16, with a large heterochromatic region of highly methylated classical satellite DNA, are prone to induction of chromatid breaks and interchanges by mitomycin C (MMC). A couple of studies have indicated that material from chromosome 9, and possibly also from chromosomes 1 and 16, are preferentially micronucleated by MMC. Here, we further examined the chromosome-specific induction of micronuclei (MN; with and without cytochalasin B) and chromosomal aberrations (CAs) by MMC. Cultures of isolated human lymphocytes from two male donors were treated (at 48 h of culture, for 24 h) with MMC (500 ng/ml), and the induced MN were examined by a pancentromeric DNA probe and paint probe for chromosome 9, and by paint probes for chromosomes 1 and 16. MMC increased the total frequency of MN by 6–8-fold but the frequency of chromosome 9 -positive (9+) MN by 29–30-fold and the frequency of chromosome 1 -positive (1+) MN and chromosome 16 -positive (16+) MN by 12–16-fold and 10–17-fold, respectively. After treatment with MMC, 34–47 % of all MN were 9+, 17–20 % 1+, and 3–4 % 16+. The majority (94–96 %) of the 9+ MN contained no centromere and thus harboured acentric fragments. When MMC-induced CAs aberrations were characterized by using the pancentromeric DNA probe and probes for the classical satellite region and long- and short- arm telomeres of chromosome 9, a high proportion of chromosomal breaks (31 %) and interchanges (41 %) concerned chromosome 9. In 83 % of cases, the breakpoint in chromosome 9 was just below the region (9cen-q12) labelled by the classical satellite probe. Our results indicate that MMC specifically induces MN harbouring fragments of chromosome 9, 1, and 16. CAs of chromosome 9 are highly overrepresented in metaphases of MMC-treated lymphocytes. The preferential breakpoint is below the region 9q12.
000133442 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttps://creativecommons.org/licenses/by/4.0/deed.es
000133442 590__ $$a2.5$$b2024
000133442 592__ $$a0.668$$b2024
000133442 591__ $$aGENETICS & HEREDITY$$b95 / 192 = 0.495$$c2024$$dQ2$$eT2
000133442 593__ $$aHealth, Toxicology and Mutagenesis$$c2024$$dQ2
000133442 591__ $$aTOXICOLOGY$$b66 / 106 = 0.623$$c2024$$dQ3$$eT2
000133442 593__ $$aGenetics$$c2024$$dQ3
000133442 591__ $$aBIOTECHNOLOGY & APPLIED MICROBIOLOGY$$b104 / 177 = 0.588$$c2024$$dQ3$$eT2
000133442 594__ $$a4.4$$b2024
000133442 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000133442 700__ $$aJärventaus, Hilkka
000133442 700__ $$aFalck, Ghita C.-M.
000133442 700__ $$0(orcid)0000-0002-1946-1187$$aMoreno, Carlos$$uUniversidad de Zaragoza
000133442 700__ $$aNorppa, Hannu
000133442 7102_ $$11001$$2420$$aUniversidad de Zaragoza$$bDpto. Anatom.,Embri.Genét.Ani.$$cÁrea Genética
000133442 773__ $$g896 (2024), 503753 [9 pp.]$$pMutat. res., Genet. toxicol. environ. mutagen.$$tMUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS$$x1383-5718
000133442 8564_ $$s1694934$$uhttps://zaguan.unizar.es/record/133442/files/texto_completo.pdf$$yVersión publicada
000133442 8564_ $$s2476480$$uhttps://zaguan.unizar.es/record/133442/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000133442 909CO $$ooai:zaguan.unizar.es:133442$$particulos$$pdriver
000133442 951__ $$a2026-02-17-20:21:49
000133442 980__ $$aARTICLE