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1 HepG2 cells identical to that of the parent benzo(a)pyrene.
2 t induced by DMBA or by the aryl hydrocarbon benzo(a)pyrene.
3 , 8-diol, the proximate carcinogenic form of benzo(a)pyrene.
4 ce was observed for benzo(b)fluoranthene and benzo(a)pyrene.
5 droxyvitamin D(3), and of CYP1A1, induced by benzo(a)pyrene.
6 ylnitrosamino)-I-(3-pyridyl)-1-butanone plus benzo(a)pyrene.
7 hylnitrosamino)-I-(3-pyridyl)-1-butanone and benzo(a)pyrene.
8 the high molecular weight compounds such as benzo(a)pyrene.
9 ically important cross-reactants, pyrene and benzo(a)pyrene.
10 ns such as the tobacco-associated carcinogen benzo(a)pyrene.
11 n important pathway in the detoxification of benzo(a)pyrene.
12 al differences in enzymatic bioactivation of benzo(a)pyrene.
13 diol epoxide (BPDE), a bioactivated form of benzo(a)pyrene.
14 d 1 week after three oral administrations of benzo(a)pyrene (2 mg/20 g of body weight) to female A/J
15 a toward phenanthrene, fluoranthene, pyrene, benzo(a)pyrene, 2,3,7,8-tetrachlorodibenzo-p-dioxin, 1,2
16 ls-solvent, soot, and fuel oil-to which (3)H-benzo(a)pyrene ((3)H-BaP; total BaP concentrations of 1,
19 glucuronosyltransferase with activity toward benzo(a)pyrene-7, 8-diol, the proximate carcinogenic for
21 0-epoxide (N6-dA-BPDE), and N4-deoxycytidine-benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide (N4-dC-BPDE)
22 9,10-epoxide (N2-dG-BPDE); N6-deoxyadenosine-benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide (N6-dA-BPDE)
23 odiol (BPD), precursor to the potent mutagen benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide, may be an i
24 increased glucuronidating activities toward benzo(a)pyrene-7,8-diol and other metabolites that occur
27 ibitors blocked this effect, suggesting that benzo(a)pyrene-7,8-dione (BPQ), a planar PAH o-quinone g
28 tivate the tobacco-associated carcinogen (-)-benzo(a)pyrene-7R-trans-7,8-dihydrodiodiol was determine
29 a1 was inducible in Ahr(+/+) by 3 micromol/L benzo(a)pyrene, a known hydrocarbon inducer, the protein
30 to 7,12-dimethylbenz(a)anthracene (DMBA) or benzo(a)pyrene alone (complete carcinogen) or with 12-O-
32 ated meat, processed meat, HCAs, and the PAH benzo(a)pyrene and the risk of colorectal adenoma in 3,6
33 were treated with two chemical carcinogens, benzo(a)pyrene and urethane, to induce skin tumors and l
36 njugation of bay-region anti-diol epoxide of benzo(a)pyrene (anti-BPDE), which, unlike anti-BGCDE or
37 ycyclic aromatic hydrocarbons (PAHs) such as benzo(a)pyrene (B(a)P) are widely distributed environmen
38 hylanthracene (1-MA), phenanthrene (PA), and benzo(a)pyrene (B(a)P) caused significant release of 3H-
39 ion, tobacco smoke, and cooked foods include benzo(a)pyrene [B(a)P] and 2,3,7,8-tetrachlorodibenzo-p-
40 ups and treated with a mixture of 3 micromol benzo(a)pyrene [B(a)P] and 3 micromol 4-(methylnitrosami
42 ork, the two compounds were shown to inhibit benzo(a)pyrene [B(a)P]-induced pulmonary adenoma formati
43 ed black raspberry extract fractions inhibit benzo(a)pyrene [B(a)P]-induced transformation of Syrian
46 The kinetic of a photooxidation reaction of benzo(a)pyrene (BaP) carried out in controlled condition
52 Polycyclic aromatic hydrocarbons, such as benzo(a)pyrene (BaP), are known mammary carcinogens in r
53 rganic extracts of black raspberries inhibit benzo(a)pyrene (BaP)-induced cell transformation in vitr
57 ical carcinogen dimethylbenz(a)anthracene or benzo(a)pyrene (BP) followed by twice weekly application
58 12-Dimethylbenz(a)anthracene (DMBA), but not benzo(a)pyrene (BP), depletes BM hematopoietic cells in
60 blasts (MEF) to the ultimate carcinogen anti-benzo(a)pyrene (BP)-7,8-diol-9,10-epoxide (anti-BPDE) re
65 active metabolite of the tobacco carcinogen benzo(a)pyrene, can induce p53 gene mutation, down-regul
68 tly repressed DNA replication in response to benzo(a)pyrene dihydrodiol epoxide (BPDE), a genotoxin t
69 o/Delta1) cells with the DNA adducting agent benzo(a)pyrene dihydrodriol epoxide resulted in a loss o
70 umin significantly inhibited CYP1A1-mediated benzo(a)pyrene diol bioactivation in both oral SCC cells
71 ed PCR (LMPCR) we have previously shown that benzo(a)pyrene diol epoxide (BPDE) adduct formation alon
72 ytes exposed in vitro to a model carcinogen, benzo(a)pyrene diol epoxide (BPDE) by 32P-postlabeling.
73 al aberrations induced in vitro by activated benzo(a)pyrene diol epoxide (BPDE) in lymphocyte culture
74 he levels of DNA adducts induced in vitro by benzo(a)pyrene diol epoxide (BPDE), a bioactivated form
76 e prototype polycyclic aromatic hydrocarbon, benzo(a)pyrene diol epoxide [B(a)PDE], or B(a)PDE plus U
77 gene by a variety of carcinogens, including benzo(a)pyrene diol epoxide, benzo(g)chrysene diol epoxi
78 four dose levels each of gamma-irradiation, benzo(a)pyrene diol epoxide, N-methyl-N-nitro-N-nitrosog
79 Higher tail moments of gamma-radiation and benzo(a)pyrene diol epoxide-induced comets were signific
85 formation of Syrian hamster embryo cells and benzo(a)pyrene diol-epoxide [B(a)PDE]-induced activator
86 ximum tolerated concentrations of (+/-) anti-benzo(a)pyrene diol-epoxide, no induced mitochondrial mu
87 lity of p53 codons 157, 248, 249, and 250 to benzo(a)pyrene-diol-epoxide (BPDE), an active metabolite
90 e powerful polycyclic hydrocarbon carcinogen benzo(a)pyrene display transversion point mutations in t
92 y two of 92 samples had detectable levels of benzo(a)pyrene-equivalents (a combined measure of carcin
96 +/+) mice were treated with a single dose of benzo(a)pyrene, followed by twice weekly applications of
97 east tissues treated in vitro with 4 micro M benzo(a)pyrene in 76 cancer cases and 60 noncancer contr
99 to 7,12-dimethylbenz(a)anthracene (DMBA) and benzo(a)pyrene in C3H/HeN mice and resulted in a state o
103 were significant predictors of the level of benzo(a)pyrene-induced adducts in the breast tissues.
104 enethyl isothiocyanate (PEITC-NAC) inhibited benzo(a)pyrene-induced lung tumorigenesis in A/J mice, a
106 nstrate that NQO2 protects against DMBA- and benzo(a)pyrene-induced skin carcinogenesis and suggest t
109 d keratinocytes to the chemical stress agent benzo(a)pyrene led to induction of NQO1 and stabilizatio
111 rase UGT1A7 catalyzes the glucuronidation of benzo(a)pyrene metabolites and other bulky aromatic comp
114 a variety of agents (the chemical carcinogen benzo(a)pyrene, oncogenes c-myc and ZNF217, and/or domin
117 reaction was observed after incubation with benzo(a)pyrene oxidation products that was attributed to
118 thracene, chrysene, benzo(b)fluoranthene and benzo(a)pyrene (PAH4) that have been chosen as indicator
119 xhibited even higher activity toward certain benzo(a)pyrene phenols, including the major 3- and 9-phe
120 extract, aromatic and polar DEP fractions, a benzo(a)pyrene quinone, and a phenolic antioxidant induc
121 e-trans-7,8-dihydrodiol-9,10-epoxide and not benzo(a)pyrene quinones contributed to increased benzo(a
122 tic Daphnia magna, anthracene, chrysene, and benzo(a)pyrene resulted in no or limited acute toxicity
123 or age and personal measurements of airborne benzo(a)pyrene, the largest reductions in levels of S-GS
126 ransferase (UGT)-mediated glucuronidation of benzo(a)pyrene-trans-7,8-dihydrodiol (BPD), precursor to
127 dies, we show that benzo(a)pyrene metabolite benzo(a)pyrene-trans-7,8-dihydrodiol-9,10-epoxide and no
128 pyrene-trans-7S,8S-dihydrodiol [(+)-BPD] and benzo(a)pyrene-trans-7R,8R-dihydrodiol [(-)-BPD] forms o
129 n liver microsomal incubations with purified benzo(a)pyrene-trans-7S,8S-dihydrodiol [(+)-BPD] and ben
130 e reactivity of photodegradation products of benzo(a)pyrene vs. DNA has been assessed using both geno
132 o be the ultimate carcinogenic metabolite of benzo(a)pyrene, was about 9-625-fold higher as compared
134 sed the concentration of five PAHs including benzo(a)pyrene, which increased approximately 2-fold.
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