Increasing resistance to praziquantel, the only available antischistosomal drug, is always developed by schistosomes. The recent description of stem cell-like neoblasts in schistosomes led to the idea of applying antineoplastic drugs as antischistosomal agents that may inhibit stem cell divisions and retard worm regeneration. Here, we explored the in vitro and in vivo effect of some antineoplastic drugs on S. mansoni worm and the host mouse liver. S. mansoni worms' viability was tested after exposure to either praziquantel or one of the antitumor drugs (hydroxyurea, cisplatin, methotrexate, and colchicine) in vitro for 24 and 48 h. The effect of two of them (hydroxyurea and cisplatin) on worm burden, tegument ultrastructure, and host liver structure and function was tested in vivo in S. mansoni-infected mouse model. All drugs affected variably the worm burden in vitro. Hydroxyurea and cisplatin, like praziquantel, damaged the worm tegument, reduced worm burden, and viable schistosome eggs, decreased anti-schistosome IgG, reduced egg-induced hepatic granuloma size and cellularity, restored liver organization and improved liver function as represented by serum alanine aminotransferase and albumin. In conclusions, a single dose of hydroxyurea and cisplatin had anti-schistosome effects and may offer a safe promising alternative to control of schistosomiasis. A direct link between antitumor drugs and inhibition of schistosome neoblasts remains to be proven.
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http://dx.doi.org/10.1016/j.biopha.2018.01.098 | DOI Listing |
FEMS Yeast Res
December 2024
Faculty of Science, Department of Molecular Biology and Genetics, Istanbul University, Istanbul, Turkey.
Fission yeast is the ideal model organism for studying telomere maintenance in higher eukaryotes. Telomere length has been directly correlated with life expectancy and the onset of aging-related diseases in mammals. In this study, we developed a novel simple, and reproducible method to measure the telomere length, by investigating the effect of Caffeine and Cisplatin on the telomere length in fission yeast.
View Article and Find Full Text PDFbioRxiv
September 2024
Department of Biological Sciences, University of Massachusetts Lowell, 198 Riverside Dr. Lowell MA, 01854.
Organisms rely on coordinated networks of DNA repair pathways to protect genomes against toxic double-strand breaks (DSBs), particularly in germ cells. All repair mechanisms must successfully negotiate the local chromatin environment in order to access DNA. For example, nucleosomes can be repositioned by the highly conserved Nucleosome Remodeling and Deacetylase (NuRD) complex.
View Article and Find Full Text PDFCell Mol Life Sci
April 2024
Department of Hepatology and Gastroenterology, Medizinische Klinik m. S. Hepatologie und Gastroenterologie, Charité, Universitätsmedizin Berlin, Campus Virchow-Klinikum (CVK) and Campus Charité Mitte (CCM), Augustenburger Platz 1, Forum 4, Raum 2.0704a, 13353, Berlin, Germany.
Background And Aim: Cellular senescence of hepatocytes involves permanent cell cycle arrest, disrupted cellular bioenergetics, resistance to cell death, and the release of pro-inflammatory cytokines. This 'zombie-like' state perpetuates harmful effects on tissues and holds potential implications for liver disease progression. Remarkably, senescence exhibits heterogeneity, stemming from two crucial factors: the inducing stressor and the cell type.
View Article and Find Full Text PDFInt J Mol Sci
April 2024
Department of Otolaryngology and Head and Neck Surgery, McGill University, Montreal, QC HC3 1E2, Canada.
DNA Repair (Amst)
February 2024
Department of Medical Biology, Amsterdam University Medical Centers (location AMC), Meibergdreef 9, 1105 AZ Amsterdam, the Netherlands; Cancer Center Amsterdam, Amsterdam, the Netherlands. Electronic address:
DNA double-strand breaks initiate the DNA damage response (DDR), leading to the accumulation of repair proteins at break sites and the formation of the-so-called foci. Various microscopy methods, such as wide-field, confocal, electron, and super-resolution microscopy, have been used to study these structures. However, the impact of different DNA-damaging agents on their (nano)structure remains unclear.
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