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the end point of unscheduled dna synthesis (uds) is measured by determining the uptake of labelled nucleosides in cells that are not undergoing scheduled (s-phase) dna synthesis.
končna točka preizkusa nenačrtne sinteze dna (uds) se meri z določanjem sprejema označenih nukleozidov v celicah, v katerih ne poteka načrtna (faza s) sinteza dna.
this effect was not confirmed in vivo in the mouse micronucleus test in the rat unscheduled dna synthesis (uds) test.
tega učinka niso potrdili in vivo pri testu mikronukleusa pri miših in pri testu nenačrtovane sinteze dna (uds – unscheduled dna synthesis) pri podganah.
there was no evidence of in vivo genotoxicity (mouse micronucleus assay and mouse liver unscheduled dna synthesis assay).
in vivo ni bilo znakov genotoksičnosti (test mikronukleusa pri miših in test nenačrtovane sinteze dnk pri miših).
this method is a replicate of the oecd tg 486, unscheduled dna synthesis (uds) test with mammalian liver cells in vivo (1997).
ta metoda ustreza metodi oecd tg 486, unscheduled dna synthesis (uds) test with mammalian liver cells in vivo (1997).
gemzar (gemcitabine) is a pyrimidine antagonist (an antimetabolite) that is metabolised intracellularly to active diphosphate and triphosphate nucleosides which inhibit dna synthesis.
zdravilo gemzar (gemcitabin) je antagonist pirimidina (antimetabolit), ki se metabolizira znotraj celic v aktivni difosfat in trifosfat nukleozid, ki zavirata sintezo dnk.
first, dfdcdp inhibits ribonucleotide reductase, which is uniquely responsible for catalysing the reactions that produce deoxynucleoside triphosphates (dctp) for dna synthesis.
najprej dfdcdp zavira ribonukleotidno reduktazo, ki je katalizira samo reakcije, ki tvorijo dezoksinukleozidne trifosfate (dctp) za sintezo dnk.
the main effects were anaemia, leucopenia, decreased platelet counts and panmyelopathy and reflect the basic mode of action of the compound (inhibition of dna synthesis).
glavni učinki so bili anemija, levkopenija, zmanjšanje števila trombocitov in panmielopatija; učinki odražajo temeljni način delovanja spojine (zaviranje sinteze dna).
accumulation of ara-gtp in leukaemic blasts allows for preferential incorporation of ara-gtp into deoxyribonucleic acid (dna) leading to inhibition of dna synthesis.
kopičenje ara-gtp v levkemičnih blastnih celicah omogoča želeno vgraditev ara-gtp v deoksiribonukleinsko kislino (dna), kar vodi v zavrtje sinteze dna.
the mechanism of action is not completely understood, but it appears that ara-ctp acts primarily through inhibition of dna synthesis.
načina delovanja ne razumemo v celoti, vendar kaže, da ara-ctp deluje predvsem preko zaviranja sinteze dna.
it also inhibits viral dna synthesis by causing dna chain termination due to a lack of the 3’-hydroxyl group necessary for dna elongation.
zavira tudi sintezo virusne dna, ker povzroči zaključitev verige dna zaradi pomanjkanja 3'-hidroksilne skupine, potrebne za podaljševanje dna.
in addition hydroxycarbamide causes an immediate inhibition of dna synthesis by acting as a ribonucleotide reductase inhibitor, without interfering with the synthesis of ribonucleic acid or protein.
poleg tega hidroksikarbamid neposredno ovira sintezo dna, ker deluje kot inhibitor ribonukleotid reduktaze, ne da bi posegal v sintezo ribonukleinske kisline ali proteinov.
antiviral activity: entecavir inhibited hbv dna synthesis (50% reduction, ec50) at a concentration of 0.004 µm in human hepg2 cells transfected with wild-type hbv.
protivirusna aktivnost: pri transfekciji humanih hepg2 celic z divjim tipom hbv entekavir zavira sintezo hbv dna (50% zmanjšanje, ec50) pri koncentraciji 0,004 μm.