ライフサイエンスコーパス: 3-methylcholanthrene

1 phenobarbital, oltipraz, and, in particular, 3-methylcholanthrene.

2 inducing CYP1A1 mRNA were benzo[e]pyrene and 3-methylcholanthrene.

3 ethylchrysene, 11,12-dihydroxy-11,12-dihydro-3-methylcholanthrene, 1,2-dihydroxy-1,2-dihydro-6-methyl

4 ness to oltipraz (2- to 5-fold increase) and 3-methylcholanthrene (10- to 30-fold increase).

5 tal (2 mmol/L), oltipraz (50 micromol/L), or 3-methylcholanthrene (2.5 micromol/L) revealed UGT1A1-in

6 Advanced 10-day 3-methylcholanthrene 205 intracranial tumors could be cu

7 For treatment of 10-day 3-methylcholanthrene 205 pulmonary metastases, systemic

8 Administration of 3-methylcholanthrene (3-MC) to these mice (Nrf1(flox/flo

9 gned to determine whether tumor induction by 3-methylcholanthrene (3-MC), a carcinogenic hydrocarbon,

10 duced lung tumors following exposure to BaP, 3-methylcholanthrene (3-MC), and urethane.

11 ague-Dawley rats were injected with PB, PCN, 3-methylcholanthrene (3-MC), or vehicle for 4 days.

12 al exposure of liver slices to the model POP 3-methylcholanthrene (3-MC; 25 muM) at levels of hydrost

13 3-Methylcholanthrene (3MC) is an aryl hydrocarbon recept

14 the aryl-hydrocarbon receptor (AhR) agonist 3-methylcholanthrene (3MC) is involved in the antimigrat

15 hydrocarbon environmental toxicants such as 3-methylcholanthrene and 2,3,7,8-tetrachlorodibenzo-p-di

16 eased by pretreatment with the CYP1A inducer 3-methylcholanthrene and decreased by coincubation with

17 esignated AHR repressor (AHRR) is induced by 3-methylcholanthrene and represses the transcriptional a

18 -1 stimulators, such as beta-naphthoflavone, 3-methylcholanthrene, and tBHQ, significantly upregulate

19 Polycyclic aromatic hydrocarbons such as 3-methylcholanthrene are toxic to rat epidermal cells in

20 SMCs with 0.3 or 3 microM hydrogen peroxide, 3-methylcholanthrene, benzo[a]pyrene-7,8-diol, 3-hydroxy

21 Lung tumorigenesis was induced using a 3-methylcholanthrene/butylated hydroxytoluene (BHT; 3,5-

22 ter embryo fibroblasts with a single dose of 3-methylcholanthrene caused the activation of the transf

23 rative analysis of the antitumor response to 3'-methylcholanthrene-induced tumors, which either grow

24 compared the incidence and immunogenicity of 3'methylcholanthrene-induced sarcomas in syngeneic wild-

25 Incubations of 3-methylcholanthrene-induced colon slices dosed with 50

26 We subjected a heterozygous 3-methylcholanthrene-induced murine sarcoma cell line to

27 ntigens expressed by cell lines derived from 3-methylcholanthrene-induced sarcomas of (C57BL/6J X SPR

28 lted in significantly increased incidence of 3-methylcholanthrene-induced spontaneous sarcoma develop

29 hormone (insulin and glucagon) and chemical (3-methylcholanthrene) induction agents in a microfluidic

30 mma or IFN-alpha reduce expression of H60 on 3'-methylcholanthrene (MCA) sarcomas from 129/Sv mice.

31 In mice with 10-day established pulmonary 3-methylcholanthrene (MCA) 205 metastases, accumulation

32 injection of ethyl carbamate (urethane), or 3-methylcholanthrene (MCA) and butylated hydroxytoluene

33 n a low dose (10 microg/g of body weight) of 3-methylcholanthrene (MCA) develop no lung tumors unless

34 rian hamster embryo fibroblasts initiated by 3-methylcholanthrene (MCA), and was shown to be a single

35 Using the carcinogen 3-methylcholanthrene (MCA), we demonstrate with Fourier

36 D73 deficiency suppressed the development of 3-methylcholanthrene (MCA)-induced fibrosarcomas through

37 were induced in Rosa26-Foxm1 mice using the 3-methylcholanthrene (MCA)/butylated hydroxytoluene (BHT

38 thin 1 week of treatment with the carcinogen 3-methylcholanthrene (MCA; 10 microg/g body weight), lun

39 ore reduced the effects of both oltipraz and 3-methylcholanthrene on the P1 reporter.

40 Comparative effects of oltipraz and 3-methylcholanthrene on transfected cytochrome P4501A1 r

41 Treatment with 3-methylcholanthrene or oltipraz had no effect compared

42 Clofibrate, 3-methylcholanthrene, or beta-naphthoflavone treatment o

43 Previously, we reported the absence of 3-methylcholanthrene- or oltipraz-responsive elements in

44 well as other known P450 inducers, including 3-methylcholanthrene, pregnenolone-16alpha-carbonitrile,

45 sion of AhR agonists beta-naphthoflavone and 3-methylcholanthrene, respectively, into partial agonist

46 ciferase activities expressed from basal and 3-methylcholanthrene-responsive UGT1A7 gene reporter con

47 coma cell lines compared with that in edited 3'-methylcholanthrene sarcoma cell lines (i.e., some une

48 was more heterogeneous in groups of unedited 3'-methylcholanthrene sarcoma cell lines compared with t

49 ls by TCDD but not by beta-naphthoflavone or 3-methylcholanthrene was significantly diminished.