Aberrations In Mouse Bone Marrow Cells Research Articles

Retraction: Stanimirovic Z, Aleksic N, Kulic M, Maletic M. Fumagillin-induced chromosome aberrations in mouse bone-marrow cells, Arch Biol Sci. 2010;62(1):47-55, DOI: 10.2298/ABS1001047S

This is a notice of retraction of the article: Fumagillin-induced chromosome aberrations in mouse bone-marrow cells, published in the Archives of Biological Sciences in 2010, Vol. 62, Issue 1. The Editor-in-Chief has been informed that this paper plagiarizes an earlier paper: Kulic M, Aleksic N, Stanimirovic Z, Ristic S, Medenica S. Examination of genotoxic effects of fumagillin in vivo. Genetika. 2009;41(3):329-38. The results presented in the article that is being retracted partially overlap with the results in the original article without appropriate justification, permission or crossreferencing. Further, Figs. 1 and 2 in the retracted article also appear in: Stanimirovic Z, Stevanovic J, Kulic M, Stojic V. Frequency of chromosomal aberrations in the evaluation of genotoxic potential of dicyclohexylamine (fumagillin) in vivo. Acta Veterinaria. 2006;56(4):353-66. and in Stanimirovic Z, Stevanovic J, Bajic V, Radovic I. Evaluation of genotoxic effects of fumagillin by cytogenetic tests in vivo. Mutat Res. 2007;628(1):1-10. These figures (in the retracted article) have been subsequently tampered with and therefore present falsified results. After confirmation of this fact, the Editor-in-Chief of the Archives of Biological Sciences has decided to retract the paper immediately. We apologize to the readers of the journal that it took so many years to notice this error and to retract the paper. We request readers of the journal to directly get in touch with the editorial office and the editors of the journal for similar cases in the future, so that they can be handled promptly. <br><br><font color="red"><b> Link to the retracted article <u><a href="http://dx.doi.org/10.2298/ABS1001047S">10.2298/ABS1001047S</a></b></u>

In vitro and in vivo induction of chromosome aberrations by alpha- and beta-zearalenols: Comparison with zearalenone

Zearalenone (ZEN) is a non-steroidal estrogenic mycotoxin produced by Fusarium fungi. It contaminates different components of the food chain and can cause serious economic and public health problems. The major metabolites of ZEN in various animal species are alpha- and beta-zearalenol (α-, β-ZOL). Some in vivo studies have shown that these two metabolites are as toxic as the mother molecule (ZEN), but other investigations have demonstrated that α- and β-ZOL are less toxic than ZEN. Thus, the aim of the present study was to evaluate cytotoxicity and genotoxicity of α- and β-ZOL in vivo, in mouse bone-marrow cells and in vitro, in cultured HeLa cells, and to compare it with ZEN. ZEN showed the same cytotoxicity as α-ZOL and both are more cytotoxic than β-ZOL. Genotoxicity of ZEN and its derivatives was assessed by the chromosome aberration assay. Our results show that ZEN as well as α- and β-ZOL increased the percentage of chromosome aberrations in mouse bone-marrow cells and in HeLa cells. In the two systems, ZEN and α-ZOL exhibited the same range of genotoxicity and both were more genotoxic than β-ZOL. Furthermore, our results show that either ZEN or its two metabolites inhibited cell viability in a dose-dependent manner. We conclude that biotransformation of ZEN may be considered as only a partial detoxification pathway since the resulting metabolites remain relatively toxic.

Fumagillin-induced chromosome aberrations in mouse bone-marrow cells

The genotoxicity of fumagillin was evaluated assessing the mitotic index and chromosome aberrations in mouse bone-marrow cells. Mice were given fumagillin orally in doses 5, 10 and 20 mg/kg bw. All doses significantly (p<0.001) reduced the mitotic index. The medium and maximum doses led to significant (p<0.01 and p<0.001, respectively) increases in numeric aberrations. The highest dose induced both structural and numeric aberrations (p<0.001), and insertions on the first pair of autosomes that were amplified in the 1C and 1E regions. These results pointed to the genotoxic potential of fumagillin in the range of medium and maximum doses applied. <br><br><font color="red"><b> This article has been retracted. Link to the retraction <u><a href="http://dx.doi.org/10.2298/ABS150320032E">10.2298/ABS150320032E</a><u></b></font>

In vivo antimutagenic effect of vitamins C and E against rifampicin-induced chromosome aberrations in mouse bone-marrow cells

The genotoxic effect of rifampicin (RMP), one of the most active antituberculosis agents is studied. Also, the possible protection provided by the natural antioxidant vitamins C (VC) and E (VE) against the genotoxic effect of RMP is assessed. Mice were orally treated by gavage with 10, 50, 150 and 300 mg RMP kg −1 body weight (bw). Also, oral treatment was conducted with RMP plus the vitamins. Mice received 300 mg RMP kg −1 bw plus 100, 200 and 400 mg VC or VE kg −1 bw. Samples were taken 24 h after the treatment. Repeated treatments with: (1) the therapeutic dose of RMP (10 mg kg −1 bw); (2) RMP plus a dose of 25, 50 and 75 mg VC kg −1; (3) RMP plus 10, 20 and 40 mg VE kg −1 bw for 30 consecutive days were conducted. The tested doses of RMP induced a significant increase in the percentage of chromosome aberrations. However, a lower percentage of chromosome aberrations was observed when animals were treated with the therapeutic dose for 30 consecutive days. The obtained results revealed that chromosome aberrations induced by RMP decreased to a significant extent when mice were treated with RMP plus VC. The repeated doses of VC reduced the percentage of chromosome aberrations induced by RMP in a significant and dose-dependent manner. On the other hand, repeated doses of VE were not very effective in reducing the percentage of chromosome aberrations induced by RMP. Only the highest dose (3×40 mg kg −1 bw) showed a significant effect ( P<0.01). The results on the induction of chromosome damage clearly show that only VC appears able to efficiently protect the bone-marrow cells when given together with RMP, while no significant reduction in the yield of chromosome aberrations was observed for VE in combination with the antituberculosis drug.

Effects of H-2 genes on mutagen-induced micronuclei and chromosome aberrations in mouse bone-marrow cells

The induction of chromosome aberrations, micronuclei and SCEs was studied in hepatocytes of F344 rats exposed in vivo to hepatocarcinogens. Hepatocytes were isolated and allowed to proliferate in Williams' medium E supplemented with epidermal growth factor. Cells were fixed after a culture period of 48 h. Oral administration of dimethylnitrosamine at doses of 2.5–20 mg/kg body weight (bw) induced (1) chromosome aberrations in up to 27% of the metaphase cells 2–48 h after its administration, (2) SCEs with a frequency of up to 0.9 per chromosome 2–48 h after its administration, and (3) micronuclei in up to 2.9% of the cells 16–48 h after its administration. Oral administration of 2-acetylaminofluorene at doses of 6.25–200 mg/kg bw induced (1) chromosome aberrations in up to 35% of the metaphase cells after 2–48 h, (2) SCEs at up to 0.9 per chromosome and (3) micronuclei in up to 2.5% of the cells with a maximum after 4 h. Oral administration of CCl4, a non-genotoxic hepatocarcinogen, at a dose of 1600 mg/kg bw did not induce chromosome aberrations, SCEs or micronuclei within 4–72 h. Intraperitoneal injections of Trp-P-1, Glu-P-1, MeIQx, IQ and nitro-IQ resulted in chromosome aberrations in up to 16% of the metaphase cells and SCEs at up to 0.9 per chromosome, while injections of Trp-P-2 and Glu-P-2 produced SCEs at up to 0.7 and 1.1 per chromosome, respectively. The present method of in vivo cytogenetic assay using rats without partial hepatectomy or mitogen treatment in vivo should be useful for evaluating the tumor-initiating activities of hepatocarcinogens.

Cytosar-induced micronuclei and chromosomal aberrations in mouse bone-marrow cells

Cytosar-induced micronuclei and chromosomal aberrations in mouse bone-marrow cells