ライフサイエンスコーパス: genotoxicity

1 our mechanistic model for colibactin-induced genotoxicity.

2 itors were discovered that react strongly to genotoxicity.

3 ess magnitude and number of effects) with no genotoxicity.

4 city in normal human fibroblasts and with no genotoxicity.

5 inery and caused increased stress leading to genotoxicity.

6 1 micronucleus assays were applied to assess genotoxicity.

7 linked to the host cell biology of systemic genotoxicity.

8 lobal biological effects such as toxicity or genotoxicity.

9 lar oxidative stress, and systemic leukocyte genotoxicity.

10 y unrecognized role in cellular responses to genotoxicity.

11 tment resulted in a decrease in toxicity and genotoxicity.

12 t of compound 29 was discontinued because of genotoxicity.

13 ng is crucial for predicting their potential genotoxicity.

14 ibility of epithelial cells to 4-HNE-induced genotoxicity.

15 st levels of mammalian cell cytotoxicity and genotoxicity.

16 the molecular mechanisms of asbestos-induced genotoxicity.

17 tioxidant status, DNA damage and bone marrow genotoxicity.

18 owth and resistance to gefitinib, U0126, and genotoxicity.

19 o reduce their potential posttranscriptional genotoxicity.

20 omosomal loci with high fidelity and without genotoxicity.

21 of insertional bias, contributing to reduced genotoxicity.

22 g that may play a role in enhanced etoposide genotoxicity.

23 assay (CA) is a sensitive/simple measure of genotoxicity.

24 S), indicating the broad relevance of HRR to genotoxicity.

25 l compounds with varying carcinogenicity and genotoxicity.

26 lication and contribute to acrolein-mediated genotoxicity.

27 y transfer (LET) radiation-induced bystander genotoxicity.

28 n arsenic-induced chromosome instability and genotoxicity.

29 ricultural chemicals and drugs for potential genotoxicity.

30 eripheral blood cells were counted to assess genotoxicity.

31 utes a major human toxicity pathway known as genotoxicity.

32 C-binding factor and reduces its insertional genotoxicity.

33 rve as reporters for assessing environmental genotoxicity.

34 for the bacteria to circumvent self-induced genotoxicity.

35 M and BAN expressed a potentiating effect in genotoxicity.

36 ty that sensitize cancer cells to additional genotoxicity.

37 BPs were the driving agents of the predicted genotoxicity.

38 on have focused especially on DNA damage and genotoxicity.

39 mation of reactive oxygen species (ROS), and genotoxicity.

40 vide additional insight into benzene-induced genotoxicity.

41 lyzed fruit powders showed acute toxicity or genotoxicity.

42 A repair in preventing S. pneumoniae-induced genotoxicity.

43 netic factors that influence benzene-induced genotoxicity.

44 e, 14 was also negative in the AMES test for genotoxicity.

45 sferases that were inversely correlated with genotoxicity.

46 HOIP as a key regulator of cisplatin-induced genotoxicity.

47 This intervention decreased systemic genotoxicity, a response associated with reduced basal l

48 Cyto-genotoxicity (Ames and micronucleus assays) and potentia

49 of model Salmonella typhimurium strains for genotoxicity analysis.

50 of aldo-keto reductases and its role in the genotoxicity and carcinogenesis of B[a]P currently are u

51 r, the mechanisms involved in TiO(2)-induced genotoxicity and carcinogenicity have not been clearly d

52 ly play an important role with regard to the genotoxicity and carcinogenicity of formaldehyde.

53 The genotoxicity and carcinogenicity of tamoxifen have been

54 by AKRs in lung cells leads to ROS-mediated genotoxicity and contributes to lung carcinogenesis.

55 d as a rapid in chemico screen for potential genotoxicity and cytotoxicity in mammalian cells exposed

56 d for strong protection against BPDE-induced genotoxicity and cytotoxicity.

57 opoisomerase II activity, thereby leading to genotoxicity and cytotoxicity.

58 rely dependent upon aryl-hydrocarbon-induced genotoxicity and does not involve direct aryl-hydrocarbo

59 optosis is mediated by upstream NO and ONOO- genotoxicity and downstream p53 and Fas activation and i

60 coli resulted in dose-dependent increases in genotoxicity and in mutagenesis within the lacZalpha tar

61 Estrogen metabolite-mediated genotoxicity and induction of a stem cell/progenitor cel

62 es direct evidence that AlkB suppresses both genotoxicity and mutagenesis by physiologically realisti

63 t and reliable methods for detecting exhaust genotoxicity and mutagenicity are needed to avoid the wi

64 ered the ultimate carcinogen due to its high genotoxicity and mutagenicity attributed to its ability

65 ducts induce a significantly higher level of genotoxicity and mutagenicity in nucleotide excision rep

66 portance of different forms of DNA damage in genotoxicity and mutagenicity of Cr(VI) activated by phy

67 '-deoxyguanosine (4-HNE-dG) adducts, but its genotoxicity and mutagenicity remain elusive.

68 3-epsilonG was used to quantify directly its genotoxicity and mutagenicity.

69 lean in vitro toxicity profile, including no genotoxicity and no bone marrow toxicity at the highest

70 of AAV-mediated gene therapy that influence genotoxicity and suggest that these features should be c

71 tion intermediates mediates oncogene-induced genotoxicity and that limiting such processing to mitosi

72 The stability of DCH, combined with its genotoxicity and tumorigenic properties make it an impor

73 by S. pneumoniae in vivo contributes to its genotoxicity and virulence.

74 suppressing tumor growth without displaying genotoxicity and with little toxicity to normal cells.

75 dent cell death in cancer cells with minimal genotoxicity and without evident toxicity toward normal

76 eus is the main target for radiation-induced genotoxicity and, as fewer cells are directly damaged, t

77 rogen activities), reactive modes of action (genotoxicity) and adaptive stress response pathway (oxid

78 he transit toxicity exhibited as DNA stress (genotoxicity) and membrane stress during the degradation

79 DNA so as to warrant investigation of their genotoxicity, and both anomers will be present during th

80 tathion S-transferase, metallothionein), and genotoxicity are the most sensitive tools to highlight t

81 s our own efforts to produce high-throughput genotoxicity arrays and LC-MS/MS approaches to reveal po

82 Results support the value of the ECL genotoxicity arrays together with toxicity bioassays for

83 he optimum dose significantly decreased soil genotoxicity, as evaluated with either mutant cell line.

84 is required for host responses to bacterial genotoxicity, as mutations of OGG1 acetylation sites inc

85 B lymphoblastoid cells to test the potential genotoxicity, as well as the cytotoxicity, of toxic spec

86 creased MeIQ activation based on the E. coli genotoxicity assay and 12-fold enhanced catalytic effici

87 at provides biological relevance to positive genotoxicity assay data, particularly for in vitro chrom

88 m comet tests, suggesting that the molecular genotoxicity assay is suitable for genotoxicity detectio

89 s of the in vivo erythroid micronucleus (MN) genotoxicity assay, thus enabling increased throughput a

90 In parallel, genotoxicity assays (Ames and micronucleus assays) and t

91 Finally, because TDCPP-specific genotoxicity assays have, for the most part, been negati

92 Several in vitro genotoxicity assays indicated that the selected compound

93 of polychlorinated aromatic hydrocarbons in genotoxicity assays that score for DNA deletions by intr

94 omatic hydrocarbons score negatively in most genotoxicity assays, including the Ames (Salmonella) ass

95 study reports a comparative and mechanistic genotoxicity assessment of four engineered nanomaterials

96 The genotoxicity associated with the metabolic reduction of

97 ts direct transforming function, it displays genotoxicity at several distinct levels.

98 Toxicity and genotoxicity bioassays can supplement chemical analysis-

99 ding of how proteins might mediate cisplatin genotoxicity but also should apply more generally in the

100 the role of PARP in suppression of bleomycin genotoxicity by integrins using wild-type and PARP knock

101 e than cellulose on ameliorating AOM-induced genotoxicity by up-regulating antioxidant enzyme genes,

102 Sam68 deleted cells are hypersensitive to genotoxicity caused by DNA damaging agents.

103 eted cells and animals are hypersensitive to genotoxicity caused by DNA-damaging agents.

104 mutation (SCID-X1) despite the occurrence of genotoxicity caused by the integration of first-generati

105 markers of defense and damage, biomarkers of genotoxicity (comet assay), and behavioral biomarkers (f

106 hlorination of wastewaters produced CHO cell genotoxicity comparable to chloramination, 3.9 times mor

107 Often overlooked in studies, genotoxicity could be dismissed for the investigated com

108 The molecular mechanisms (genotoxicity, cytotoxicity) were analyzed in vitro in no

109 significant correlations were observed among genotoxicity, cytotoxicity, and NAC thiol reactivity for

110 molecular genotoxicity assay is suitable for genotoxicity detection.

111 This enhancement of genotoxicity did not occur when the inactive C145A mutan

112 s, which indicates that 4-MCHM is related to genotoxicity due to its DNA damage effect on human cells

113 retention mechanism to control A3A and avert genotoxicity during innate immune responses.

114 y that generated the lowest cytotoxicity and genotoxicity employed chlorination first followed by MPU

115 racts did not induce any toxic effects (cyto-genotoxicity, estrogenic or anti-androgenic activity) in

116 Interpretation of positive genotoxicity findings using the current in vitro testing

117 tic acids, and unregulated DBPs, and the SOS genotoxicity followed the breakthrough of dissolved orga

118 Most studies have not noted genotoxicity following AAV-mediated gene delivery; there

119 ) micronucleus assay attested high levels of genotoxicity following treatment of peripheral blood lym

120 rovides new insights into the requirement of genotoxicity for DMBA-induced immunosuppression in vivo

121 5.5-5.8) than at neutral pH, suggesting that genotoxicity from arylamine metabolism by NAT could be m

122 A concentration dependent genotoxicity has been found in nanomaterials.

123 for the first time and their effect on DNA (genotoxicity) has been investigated.

124 atients due to vector integration-associated genotoxicity have been observed.

125 lofuranones, and especially as regards their genotoxicity, here we report an in silico study of the a

126 are gaps in the database for dichloromethane genotoxicity (i.e., DNA adduct formation and gene mutati

127 s had the highest degree of cytotoxicity and genotoxicity (i.e., IC(50), SSBs and DSBs) after TG expo

128 ipid and protein oxidation and inhibition in genotoxicity in a dose-response manner.

129 es may induce genetic damage, but a role for genotoxicity in biphenyl-induced carcinogenicity has not

130 himurium, and chronic cytotoxicity and acute genotoxicity in Chinese hamster ovary (CHO) cells to com

131 Although the rank order was similar for genotoxicity in CHO cells and mutagenicity in S. typhimu

132 Hs) are of significant interest due to their genotoxicity in humans.

133 air pathway counteracts acetaldehyde-induced genotoxicity in mice.

134 tagenicity of tamoxifen as a function of its genotoxicity in the cII transgene in Big Blue mouse embr

135 astly, both compounds 1r and 2r did not show genotoxicity in vitro and displayed high LD50 values in

136 ensive study of TiO(2) nanoparticles-induced genotoxicity in vivo in mice possibly caused by a second

137 To analyze hepatic genotoxicity in vivo, we transferred the fumarylacetoace

138 d at 1 and 3 years of age, were examined for genotoxicity, including centrosomal amplification, micro

139 possibility of unravelling the mechanisms of genotoxicity, including the repair of genetic damage, en

140 troviral vectors and found clear evidence of genotoxicity, indicated by numerous common integration s

141 ts of dietary ginger on oxidative stress and genotoxicity induced by streptozotocin (STZ) diabetic ra

142 Genotoxicity induced by these compounds was reduced by i

143 Genotoxicity-induced hair loss from chemotherapy and rad

144 How genotoxicity-induced HF injury is repaired remains uncle

145 amage to the colon, this study tests whether genotoxicity is elicited systemically by acute and chron

146 A mechanistic understanding of carcinogenic genotoxicity is necessary to determine consequences of c

147 additional advantage of TMB, beside its non-genotoxicity, is the electrochemical reduction property,

148 midazo[4,5-b]pyridine) and PhIP-5-sulfate (a genotoxicity marker) accumulated in liver tissue, indica

149 The objective of the study was to identify genotoxicity markers in cord blood cells from newborns e

150 leaf extract- and quercetin-induced in vitro genotoxicity may be the result of Topo II inhibition.

151 bes that are used to measure their cyto- and genotoxicity may lead to inaccurate readings.

152 ith the aim to reveal the distinct potential genotoxicity mechanisms among the different nanomaterial

153 Cytotoxicity (MTT test) and genotoxicity (micronuclei assay) were not detectable.

154 Fancc suppresses cross-linker-induced genotoxicity, modulates growth-inhibitory cytokine respo

155 [a]pyrene (BaP) provides a mechanism for the genotoxicity, mutagenicity, and carcinogenicity of PAHs.

156 tes rather than complete exhaust is used for genotoxicity/mutagenicity assessment, which may reduce t

157 TCE-associated renal genotoxicity occurs predominantly through glutathione S-

158 nergy to confer resistance to both cyto- and genotoxicities of NQO, whereas protection afforded by GS

159 ed to reactive intermediates that caused the genotoxicity of 1 in the Ames and mouse lymphoma L51784

160 FAPY adduct the prime candidate for both the genotoxicity of aflatoxin, because mammalian cells also

161 his isogenic cell line, we have revealed the genotoxicity of ambient oxygen.

162 dicals, play an important causal role in the genotoxicity of arsenical compounds in mammalian cells.

163 e examined the role of cellular vitamin C in genotoxicity of carcinogenic chromium(VI) that requires

164 rochemical protocol for direct monitoring of genotoxicity of catecholics is described.

165 study, we assessed the mutagenicity and the genotoxicity of complete diesel exhaust compared to an o

166 analyze the mammalian cell cytotoxicity and genotoxicity of concentrated organic fractions from sour

167 of graft-versus-host disease (GVHD), but the genotoxicity of conditioning remains a substantial barri

168 Asc amplified genotoxicity of Cr(VI) by altering the spectrum of DNA d

169 active Cr(III), vitamin C contributes to the genotoxicity of Cr(VI) via a direct chemical modificatio

170 s were responsible for both mutagenicity and genotoxicity of Cr(VI).

171 The predicted cyto- and genotoxicity of DBPs was calculated using published pote

172 xpression modulates cellular response to the genotoxicity of DNA double-strand breaks.

173 Arsenic inhibits DNA repair and enhances the genotoxicity of DNA-damaging agents such as benzo[a]pyre

174 dentify and characterize enzymes involved in genotoxicity of drugs and pollutants.

175 not observe a significant difference in the genotoxicity of each risk group treatment modality despi

176 ations of the c-myc oncogene showed that the genotoxicity of estrogen via AID production was not limi

177 e survival factors for TDEC that inhibit the genotoxicity of etoposide and may influence the sensitiv

178 some breaks in the MLL locus and the overall genotoxicity of etoposide are dependent on topoisomerase

179 lts elucidate a mechanism underlying the low genotoxicity of foamy virus, identify a novel insulator,

180 aycoechea et al., identify aldehyde-mediated genotoxicity of hematopoietic stem cells as a cause for

181 DNA repair factors that protect against the genotoxicity of ICLs generated by trioxsalen/ultraviolet

182 have used a cell cloning assay to study the genotoxicity of in vitro exposure of human T lymphocytes

183 oprotective effects on NHK by mitigating the genotoxicity of IR through epigenetic mechanisms.

184 The genotoxicity of PAH o-quinones may play a role in the ca

185 We investigated changes in the toxicity and genotoxicity of PAH-contaminated soil from a former manu

186 locking element that significantly decreases genotoxicity of retroviral integration.

187 Also, hAGT did not enhance the genotoxicity of S-(2-haloethyl)glutathiones that mimic t

188 Here, we evaluated the genotoxicity of selected food products in Finland.

189 tch repair (MMR) strongly enhances cyto- and genotoxicity of several chemotherapeutic agents and envi

190 ining a pyridone are not responsible for the genotoxicity of the clb cluster.

191 nation and to determine the cytotoxicity and genotoxicity of the concentrated organic fractions from

192 Toxicity and genotoxicity of the residues from solvent extracts of th

193 hydrocarbons (PAHs), but it can increase the genotoxicity of the soil despite removal of the regulate

194 iol does not significantly contribute to the genotoxicity of the very potent carcinogen DB[a,l]P in h

195 Next to the acute toxicity, the genotoxicity of these compounds was investigated.

196 ombine to protect E. coli from the potential genotoxicity of this DNA adduct.

197 erturbations may be responsible for both the genotoxicity of this lesion and its ability to be recogn

198 To explore the mechanism of the lower genotoxicity of TOR, the formation of DNA adducts induce

199 We investigated the genotoxicity of UVA1 versus UVB in the overall genome an

200 The genotoxicity of zidovudine has been established in exper

201 ythroid MN assay is capable of screening for genotoxicity on BM in a physiologically reflective manne

202 lts from the HUSTLE protocol suggest minimal genotoxicity or carcinogenicity with long-term hydroxyur

203 ma, or for other diseases that are driven by genotoxicity or the molecular response to oxidative stre

204 wards alterations that have occurred through genotoxicity or through epigenetic modifications.

205 ment resulted in an increase in toxicity and genotoxicity over the course of a treatment cycle, where

206 dy investigates TiO(2) nanoparticles-induced genotoxicity, oxidative DNA damage, and inflammation in

207 stress responses to oxidative stress (Nrf2), genotoxicity (p53) and inflammation (NF-kappaB) and the

208 he formation of unregulated DBPs with higher genotoxicity potencies.

209 imilar functions and similar carcinogenicity/genotoxicity profiles.

210 s with similar functions and carcinogenicity/genotoxicity profiles.

211 screening with a battery of DT40 mutants for genotoxicity profiling, we found that column treatment i

212 iolet irradiation, but not by other forms of genotoxicity, providing a novel mechanism for stress-med

213 In vitro toxicity studies for genotoxicity, reactive oxygen species formation, and cel

214 epeats (LTRs) may have significantly reduced genotoxicity relative to the conventional retroviral vec

215 anaemia is probably due to aldehyde-mediated genotoxicity restricted to the HSPC pool.

216 other aspects of cellular damage, including genotoxicity, resulting from exposure to NO under long-t

217 ditional cytotoxicity (live/dead) assay, the genotoxicity results from the single cell array based as

218 In a umu genotoxicity screen, cytochrome P450 2W1 catalyzed the a

219 n macroscopic surfaces opens new avenues for genotoxicity screening and enabled the first use of pure

220 Arrays suitable for genotoxicity screening are reported that generate metabo

221 the potential to become a valuable tool for genotoxicity screening for chemical safety evaluation, a

222 A damage could serve as a basis for in vitro genotoxicity screening for new organic compounds.

223 thick DNA-polyion films used in voltammetric genotoxicity screening sensors showed that concentration

224 Genotoxicity screening sensors that measure DNA damage f

225 e and DNA-adduct formation rates relevant to genotoxicity screening.

226 n of ECL arrays for high-throughput in vitro genotoxicity screening.

227 the latter in vitro and was negative in the genotoxicity screens with a satisfactory oral safety pro

228 dependent inhibition and was negative in the genotoxicity screens with a satisfactory oral safety pro

229 bs at the base contain rapidly dividing, yet genotoxicity-sensitive transit-amplifying cells (TAC) th

230 Results show that the genotoxicity sensors can be used to estimate relative DN

231 available evidence from animal experiments, genotoxicity studies and clinico-epidemiological observa

232 ia and evaluated in various cytotoxicity and genotoxicity studies in human retinal pigment epithelium

233 Recent work employing genotoxicity studies suggests that National Institute fo

234 e use of a single cell array based assay for genotoxicity study of nanomaterials using normal human f

235 o) activation of MeIQ with another bacterial genotoxicity system (Salmonella typhimurium umu).

236 The conventional genotoxicity testing methods are laborious, take time an

237 The regulatory requirements for genotoxicity testing rely on a battery of genotoxicity t

238 on of TGx-DDI for high-throughput cell-based genotoxicity testing using nCounter technology.

239 enabling new strategies for drug discovery, genotoxicity testing, and environmental health.

240 or genotoxicity testing rely on a battery of genotoxicity tests, which generally consist of bacterial

241 MNPs exhibited significantly higher genotoxicity than BMs and promoted the expression of Bax

242 malian cells, are likely more susceptible to genotoxicity than prokaryotes in the ecosystem when expo

243 Thus, TOR is likely to have lower genotoxicity than TAM.

244 e more sensitive (6-fold) to benzene-induced genotoxicity than the female NQO1+/+ mice.

245 gation but rather by initiating a cumulative genotoxicity that deregulated DNA synthesis.

246 nscriptase inhibitor exposures induced fetal genotoxicity that was persistent for 3 years.

247 esult in low-level protection from cyto- and genotoxicities, this protection is greatly enhanced by c

248 NAT2 genetic polymorphisms on metabolism and genotoxicity, tissue-specific expression and the elucida

249 In this study, we evaluated the genotoxicity to Chinese hamster ovary (CHO) cells induce

250 nd I(-) levels may yield organics with lower genotoxicity to CHO cells than chlorine-based disinfecti

251 ed by dextran sulfate sodium administration, genotoxicity to peripheral leukocytes and erythroblasts

252 Q) was tested for potential cytotoxicity and genotoxicity upon A549 lung cancer cells and Human Umbil

253 as well as their ability to induce cyto and genotoxicity upon interaction with biological systems by

254 The soil extract fractions were tested for genotoxicity using the DT40 chicken lymphocyte bioassay

255 rmine the biodistribution, toxickinetic, and genotoxicity variances in murine animals.

256 determine if mammalian cell cytotoxicity and genotoxicity varied in response to different chlorinatio

257 Genotoxicity was also observed in colon mucosa of mice g

258 ed from E faecalis-infected macrophages; its genotoxicity was assessed in human colon cancer (HCT116)

259 MTT assay and flow cytometry analysis, while genotoxicity was assessed in vitro by alkaline comet, DN

260 A statistically significant increase in genotoxicity was measured in the unfractionated soil ext

261 Additionally, genotoxicity was measured using the SOS-Chromotest (dete

262 Moreover, this systemic genotoxicity was observed in mice with subclinical infla

263 HBQ-induced genotoxicity was shown as increased levels of 8-hydroxy-

264 els of peripheral leukocyte and erythroblast genotoxicity were also observed.

265 orine, the lowest levels of cytotoxicity and genotoxicity were observed with MPUV radiation.

266 Cytostatic effects, including genotoxicity, were cell- and metal-dependent, apart from

267 ly tested for its capacity to confer reduced genotoxicity when restored by short-term oral transfer.

268 based approaches likely underestimate Cr(VI) genotoxicity when standard ATM-activating carcinogens ar

269 Insertional mutagenesis and genotoxicity, which usually manifest as hematopoietic ma

270 Both genotoxicity with and without metabolic activation and t