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Choroby spowodowane mutacjami w mitochondrialnym DNA

100%

Wojewoda M. , Zablocki K. , Szczepanowska J.

nr 2

Rola mitochondriów w odporności przeciwwirusowej

75%

Gregorczyk K. P. , Wyzewski Z. , Szulc-Dabrowska L. , Struzik J. , Szczepanowska J. , Niemialtowski M.

nr 3

Ciprofloxacin inhibits proliferation and promotes generation of aneuploidy in Jurkat cells

75%

Koziel R. , Szczepanowska J. , Magalska A. , Piwocka K. , Duszynski J. , Zablocki K.

nr 2

Ciprofloxacin is widely used in antimicrobial therapy. However it also inhibits mitochondrial topoisomerase II and therefore affects cellular energy metabolism. At a concentration exceeding 80 µg/ml ciprofloxacin induces apoptosis, while at 25 µg/ml it inhibits proliferation of Jurkat cells without any symptoms of cell death. The aim of this study was to explain the mechanisms of ciprofloxacin-evoked perturbations of the cell cycle. Human lymphoidal cells (Jurkat) were exposed to ciprofloxacin (25 µg/ml) for 4-11 days and effects of the drug on cell proliferation (light microscopy), cell cycle (flow cytometry), cell size and morphology (confocal microscopy) as well as number of chromosomes (chromosomal spread analysis) were investigated. Exposition of Jurkat cells to ciprofloxacin inhibited cell proliferation, increased proportion of cells in the G2/M-phase of the cell cycle, compromised formation of the mitotic spindle and induced aneuploidy. These observations indicate that ciprofloxacin applied at concentrations insufficient for induction of apoptosis may stop cell proliferation by inhibition of mitosis. Chromosomal instability of such cells may, at least potentially, increase a risk of cancer development.