ライフサイエンスコーパス: ddC

1 ddC (300 nM) reduced mitochondrial DNA levels from appro

2 ddC also targeted leukemic stem cells in secondary AML x

3 ddC and saline eyes were treated four times daily for 7

4 ddC demonstrated potent antiadenovirus activity in vitro

5 ddC is a selective inhibitor of the mitochondrial DNA po

6 ddC treatment inhibited mtDNA replication, oxidative pho

7 ddC was more potent than cidofovir for seven of nine ser

8 ddC was preferentially activated in AML cells compared w

9 The 3% and 2% ddC treatments were significantly more efficacious than

10 In vivo, 3% ddC, 2% ddC, and 0.5% cidofovir significantly reduced the number

11 to four topical treatment groups: 3% ddC; 2% ddC; 0.5% cidofovir; and saline.

12 vided into four topical treatment groups: 3% ddC; 2% ddC; 0.5% cidofovir; and saline.

13 In vivo, 3% ddC, 2% ddC, and 0.5% cidofovir significantly reduced th

14 g 3'-azido-2',3'-ddA (AZddA), 3'-azido-2',3'-ddC (AZddC), 3'-azido-2',3'-ddG (AZddG), AZT, and 3'-azi

15 ntrast, the rate of exonuclease removal of a ddC chain-terminated DNA occurs at least 2 orders of mag

16 sine or affect the mtDNA recovery rate after ddC treatment.

17 ic treatment with the anti-retroviral agent, ddC (Zalcitabine) with or without the concomitant delive

18 and D-FMAU, and D-dideoxynucleoside analogs, ddC and d4T.

19 As AZT and ddC are known to cause mitochondrial dysfunction, we exa

20 We find that AZT and ddC treatment leads to greater depletion of mitochondria

21 Zdv, ddI, and ddC mutations were detected frequently at baseline but w

22 e 5'-triphosphate forms of 3TC, (-)-FTC, and ddC.

23 alog prodrugs such as AraC, gemcitabine, and ddC.

24 (5-fluoro-2',3'-dideoxy-3'-thiacytidine) and ddC (2',3'-dideoxycytidine) were added to the cultures b

25 of the lymphocytes from control thymuses and ddC-induced lymphomas were positive for Thy-1.2 (pan-T),

26 stance to AZT-triphosphate (TP), ddA-TP, and ddC-TP, indicating an MDNR phenotype.

27 eralgesia caused by HIV/AIDS antiretroviral [ddC (2',3'-dideoxycytidine)] and anticancer (oxaliplatin

28 a significant concern that toxicants such as ddC impair mtDNA maintenance in both proliferating and n

29 ast to ineffective chain terminators such as ddC.

30 rrently approved for antiviral therapy: AZT, ddC, D4T, 3TC and carbovir.

31 Because ddC induced lymphomas in two different mouse models, the

32 prevents the development of neurotoxicity by ddC, as judged by amelioration of ddC-induced "neuritic

33 The high toxicity of dideoxy compounds, ddC and ddI (metabolized to ddA), may be a combination o

34 Notably, the higher toxicities of d4T, ddC, and ddA arose from their 13-36-fold tighter binding

35 Dideoxycytidine (ddC), which is known to have a delayed effect on mitocho

36 vels by treating with 2',3'-dideoxycytidine (ddC) and subsequently allowed recovery to normal levels

37 2',3'-dideoxycytidine (ddC) is a synthetic pyrimidine nucleoside analogue appro

38 analogs, Zalcitabine (2',3'-dideoxycytidine (ddC)) and Lamivudine (beta-d-(+)-2',3'-dideoxy-3'-thiacy

39 deoxythymidine (D4T), 2',3'-dideoxycytidine (ddC), (-)-beta-L-2',3'-dideoxy-3'-thiacytidine (3TC), (-

40 tion caused by beta-d-2',3'-dideoxycytidine (ddC), 2',3'-didehydro-2',3'-dideoxythymidine, and 2',3'-

41 nalogs such as beta-D-2',3'-dideoxycytidine (ddC), beta-2'-fluoro-5-methyl-arabinofuranosyluracil (FM

42 e to CTNAs, including 2',3'-dideoxycytidine (ddC), cytarabine (ara-C) and zidovudine (Azidothymidine,

43 tion NRTIs, including 2',3'-dideoxycytidine (ddC), were originally and are still pursued as anticance

44 ed a nucleoside analog 2'3'-dideoxycytidine (ddC), which is phosphorylated to the activated antimetab

45 w-level resistance to 2',3'-dideoxycytidine (ddC).

46 We show that among the dideoxynucleosides, ddC appears to be the most neurotoxic, followed by ddI a

47 nsitivity to other nucleoside analogs (i.e., ddC, ddI, and d4T).

48 ocular administration are needed to evaluate ddC as a topical antiviral treatment for adenoviral ocul

49 Following ddC exposures, we measured cell viability, mtDNA copy nu

50 The in vitro IC(50) for ddC ranged from 0.18 to 1.85 microg/mL, whereas those fo

51 Furthermore, ddC preferentially inhibited mtDNA replication in a subs

52 ral sensitivity that is exacerbated in gp120+ddC as compared to either treatment alone.

53 of HIV-gp120 to the rat sciatic nerve (gp120+ddC).

54 nsitivity to mechanical stimuli in the gp120+ddC model and reversal of some measures of thigmotaxis.

55 A approximately equal to d4T >> ddA (ddI) >> ddC.

56 e nuclease-dependent removal of incorporated ddC from replicating genomic DNA.

57 ion of L-OddC, L-SddC, L-Fd4C, L-FMAU, and L-ddC were compared with D-deoxynucleoside analogs, AraC,

58 Immunohistochemical studies revealed little ddC-associated alteration in DRG phenotype, as compared

59 After 13 days of 1 muM ddC exposure, proliferating and differentiated HepaRG ha

60 Cells exposed to 12 muM ddC contained even less mtDNA.

61 everely impaired by day 8, with 1 and 12 muM ddC, whereas differentiated cells displayed defects of s

62 leak linked respiration (day 14) with 12 muM ddC.

63 within 24 hr, which is in contrast to 300 nM ddC, which had no effect on cell growth for the first 4

64 he 50% inhibitory concentrations (IC(50)) of ddC and cidofovir were determined using standard plaque-

65 oxicity by ddC, as judged by amelioration of ddC-induced "neuritic pruning," neuronal mitochondrial d

66 igh correlation between the internal dose of ddC and the incidence of thymic lymphoma in both mouse m

67 and evaluated for toxicity, plasma levels of ddC, and pathological changes.

68 , we evaluated the carcinogenic potential of ddC in two different mouse models.

69 Removal of ddC was too slow to measure (<0.00002 s(-1)).

70 phosphorylated metabolites, whereas that of ddC and the L-deoxycytidine analogs may not involve dCMP

71 ong antiviral efficacy of 3TC versus that of ddC.

72 ats treated with perineural HIV-gp120 and/or ddC and there is a reduction in intraepidermal nerve fib

73 tment regimens that included ddI plus AZT or ddC plus AZT in situations in which the T215Y and/or M41

74 eared during drug regimens containing ddI or ddC, with prior or concurrent AZT treatment.

75 hat the failure of the exonuclease to remove ddC may play a major role in its greater toxicity.

76 riptase-resistant, azidothymidine-resistant, ddC/ddI-resistant, nivirapine-resistant, and other clini

77 Each pair of enantiomers of Se-ddC and Se-FddC was separated by an amylose chiral colum

78 s vary more than 500,000-fold for the series ddC > ddA (ddI) > 2',3'-didehydro-2',3'-dideoxythymidine

79 the utility of the HepaRG cell line to study ddC-induced toxicity in isogenic proliferating (undiffer

80 Systemic ddC treatment alone is associated with a persistent mech

81 n, and both are considerably less toxic than ddC.

82 Previous studies indicated that ddC has the potential to cause thymic lymphoma in C57BL/

83 ein was detected in only 20% (23/115) of the ddC-induced lymphomas with mostly minimal expression in

84 d as NKT (e.g. adefovir and cidofovir), two (ddC and ddI) manifested significantly higher affinity fo

85 After 13 days of 1 uM ddC exposure, proliferating and differentiated HepaRG ha

86 Cells exposed to 12 uM ddC contained even less mtDNA.

87 severely impaired by day 8, with 1 and 12 uM ddC, whereas differentiated cells displayed defects of s

88 -leak linked respiration (day 14) with 12 uM ddC.

89 3) is the major transporter interacting with ddC and ddI.

90 he delayed increase in lactate observed with ddC exposure, CldAdo-treated cells exhibited a 2-2.4-fol

91 The mice were treated with ddC by gavage at 500 and 1000 mg/kg/day for up to 6 mont

92 hildren and adolescent patients treated with ddC.

93 n animal models of human AML, treatment with ddC decreased mtDNA, electron transport chain proteins,

94 Treatment with ddC for 36 days and with FTC for 12 days resulted in eff

95 e (Ara-C), zidovudine (AZT) and zalcitabine (ddC)-we show that TDP1 is capable of removing the covale

96 ine (Zdv), didanosine (ddI), or zalcitabine (ddC) was acceptable.

97 ated with zidovudine (AZT) plus zalcitabine (ddC) and didanosine (ddI) develop AZT resistance mediate

98 rs of magnitude in the sequence zalcitabine (ddC) > didanosine (ddI metabolized to ddA) > stavudine (

99 IC(50) values for Zdv, zalcitabine (ddC), didanosine (ddI), 3TC, and stavudine (d4T) were de

100 he findings support the clinical use of Zdv, ddC, ddI, and d4T but not of 3TC for the antiretroviral

101 -type HIV-1 were equally susceptible to Zdv, ddC, ddI, and d4T.