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Molecular basis for hycanthone drug action in schistosome parasites.
Mol Biochem Parasitol
March 2020
Department of Biochemistry & Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, United States; X-Ray Crystallography Core Laboratory, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, United States. Electronic address:
Hycanthone (HYC) is a retired drug formerly used to treat schistosomiasis caused by infection from Schistosoma mansoni and S. haematobium. Resistance to HYC was first observed in S.
View Article and Find Full Text PDFExposure to hycanthone alters chromatin structure around specific gene functions and specific repeats in Schistosoma mansoni.
Front Genet
July 2014
Département de Biologie, Université de Perpignan Via Domitia Perpignan, France ; CNRS, UMR 5244, Écologie et Évolution des Interactions (2EI) Perpignan, France.
Schistosoma mansoni is a parasitic plathyhelminth responsible for intestinal schistosomiasis (or bilharzia), a disease affecting 67 million people worldwide and causing an important economic burden. The schistosomicides hycanthone, and its later proxy oxamniquine, were widely used for treatments in endemic areas during the twentieth century. Recently, the mechanism of action, as well as the genetic origin of a stably and Mendelian inherited resistance for both drugs was elucidated in two strains.
View Article and Find Full Text PDFO6-methylguanine and O6-methylguanine-DNA [corrected] methyltransferase activity in tissues of BDF-1 mice treated with antiparasitic drugs.
Toxicol Lett
February 1998
Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Ontario, Canada.
Levels of the DNA promutagenic methylation damage, O6-methylguanine (O6-MeG) and the activity of the O6-methylguanine-DNA methyltransferase (MGMT), the enzyme responsible for repairing O6-MeG, were measured at various time intervals in tissues of BDF-I mice administered a single therapeutic dose of the antischistosomal agents hycanthone, oxaminiquine and metrifonate. Hycanthone increased O6-MeG in the liver-DNA after 6 h, then decreased by 3-fold after 48 h. Lower levels of the adduct and a slower rate of formation were found in the intestine and bladder.
View Article and Find Full Text PDFModulation of mitomycin C mutagenicity on Saccharomyces cerevisiae by glutathione, cytochrome P-450, and mitochondria interactions.
Mutat Res
April 1997
Istituto di Genetica, Università degli Studi di Parma, Italy.
It is well established that most anticancer drugs also have mutagenic effects and require metabolic activation before exerting their mutagenic/antiblastic activity. Antitumoral compound effects strongly depend on the biochemical/physiological conditions of the tumoral cells, and especially on the activation of specific drugs metabolizing enzymes and on respiration. We examined the mitomycin C-induced mutagenic effects on the D7 strain of Saccharomyces cerevisiae and on its derivative mitochondrial mutant p degrees at different contents of glutathione and cytochrome P-450, molecules able to activate/detoxicate xenobiotics.
View Article and Find Full Text PDFSalmonella strains and mammalian cells genetically engineered for expression of sulfotransferases.
Toxicol Lett
December 1995
Deutsches Institut für Ernährungsforschung, Potsdam, Germany.
Rat and human sulfotransferases (STs) were expressed in his- S. typhimurium strains. These new bacterial strains detected various mutagens which are difficult to recognize in traditional test systems, including benzylic alcohols derived from polycyclic aromatic hydrocarbons, hycanthone and 1'-hydroxysafrole.
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