ライフサイエンスコーパス: mutagen

1 im that cigarette smoke is a human germ cell mutagen.

2 sequence polymorphisms induced by a chemical mutagen.

3 mous transposon Activator (Ac) is a powerful mutagen.

4 reated Apc(Min/+) mice with a strong somatic mutagen.

5 r and sequences derived from the insertional mutagen.

6 5NO2 was found to be a potent direct acting mutagen.

7 sk factor for carcinogenesis because it is a mutagen.

8 These data reveal that 8-oxodGTP is a potent mutagen.

9 hanisms, which may reflect the nature of the mutagen.

10 tion of ribavirin to be that of a potent RNA mutagen.

11 afish, using mouse retroviral vectors as the mutagen.

12 nt insertion or utilizing X rays or EMS as a mutagen.

13 nosine adduct derived from acrolein, a known mutagen.

14 erichia coli to grow in the presence of this mutagen.

15 of the DOC in contrast to the particle-bound mutagens.

16 or efficient DNA repair from a wide range of mutagens.

17 by which Msd proofreads the base milieu for mutagens.

18 cell cycle and deleterious damage caused by mutagens.

19 epertoire to both purine and pyrimidine-like mutagens.

20 ke, high-temperature cooking, and associated mutagens.

21 alysis of mutation spectra of DNA exposed to mutagens.

22 igen (PCNA) that is triggered by exposure to mutagens.

23 to within an order of magnitude of chemical mutagens.

24 n complement efforts using other insertional mutagens.

25 cyclic arylamines and their bioactivation to mutagens.

26 transferable to other high-copy insertional mutagens.

27 ionizing radiation and a number of chemical mutagens.

28 be caused by smoking and other environmental mutagens.

29 lity of non-null alleles created by chemical mutagens.

30 burden analysis and testing for exposure to mutagens.

31 ising from endogenous reactions or exogenous mutagens.

32 modification due to endogenous and exogenous mutagens.

33 -deoxycytidine are predicted to be efficient mutagens.

34 easily extended by adducts formed from other mutagens.

35 via the handling and metabolism of chemical mutagens.

36 ated and more sensitive to inhibition by RNA mutagens.

37 ehensive characterizations of other germline mutagens.

38 mutation frequency in the absence of tobacco mutagens.

39 tinuously caused by endogenous and exogenous mutagens.

40 gen species to UV radiation to environmental mutagens.

41 fficacy against IQ and MeIQ tested as direct mutagens (10(-7) mol/plate), with a revertants percentag

42 s-anti-B[a]P-N(2)-dG), and one from the food mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine

43 mutational events, this study defines such a mutagen, 3'-azidothymidine [zidovudine (AZT)], used wide

44 V553I, we also demonstrate resistance to the mutagen 5-azacytidine (5-AZC) and decreased accumulation

45 mes more sensitive to treatment with the RNA mutagen 5-fluorouracil (5-FU) than wild-type (WT)-ExoN(+

46 d two mutations conferring resistance to the mutagen 5-fluorouracil (5-FU): nsp12-M611F and nsp12-V55

47 oth in the presence of ribavirin and another mutagen, 5-azacytidine.

48 in MRC-5 cells in the presence of a chemical mutagen, 5-fluorouracil.

49 e examined the mutational specificity of two mutagens, 5-azacytidine and N-methyl-N'-nitro-N-nitroso-

50 ession combined with exposure to TPA and the mutagen 7,12-dimethylbenz(a)anthracene accelerated SCC d

51 g base excision DNA repair of the endogenous mutagen 8-oxoguanine.

52 ed to study the mechanism giving rise to the mutagens 8-oxoA and FAPyA.

53 As part of our studies of lethal viral mutagens, a series of 5-substituted cytidine analogues w

54 ntexts show variability in DNA distortion at mutagen adduct sites that could compromise DNA repair at

55 In this case, the total dose of mutagen administered to the host needs to be so high tha

56 yl methanesulfonate compared to the acridine mutagen agent.

57 against ethyl methanesulfonate and acridine mutagen agents.

58 e effects should be considered not only from mutagens alone, but also including possible comutagens a

59 eloped leukemia, even after treatment with a mutagen, although some of the older mice developed a non

60 on, a chemotherapeutic agent, a clastogen, a mutagen, an inducer of fragile sites and a carcinogen.

61 s, in the presence of continuous exposure to mutagen and accumulate mutations, as measured by inactiv

62 om the reaction of dC with glycidaldehyde, a mutagen and animal carcinogen.

63 Benzo[a]pyrene is an important environmental mutagen and carcinogen.

64 (AalphaC), a food-derived heterocyclic amine mutagen and carcinogen.

65 Aflatoxin B1 (AFB1) is a mutagen and IARC (International Agency for Research on C

66 hypothesis that RBV could act both as an RNA mutagen and inhibit viral RNA synthesis in vivo, we stud

67 It is a potent mutagen and is of concern to public health.

68 nts) to ethyl-nitrosourea (ENU), a known DNA mutagen and neural carcinogen, and measured NPC viabilit

69 of and protection from cadmium, a teratogen, mutagen and potentially lethal heavy metal.

70 -benz[de]anthracen-7-one, 3-NBA) is a potent mutagen and suspected human carcinogen identified in die

71 ic is, indeed, a potent gene and chromosomal mutagen and that its effects are mediated through the in

72 t was used to show that propionaldehyde is a mutagen and that mutation frequencies are increased in M

73 nt compartments receive different amounts of mutagen and that virions can migrate among compartments.

74 oxygen species (ROS), which represent human mutagens and are thought to be a major contributor to th

75 ad ways to the evolution of host genomes, as mutagens and as sources of genetic novelty (both coding

76 N-Nitrosamines are potent mutagens and carcinogens that can be formed during oxida

77 bacco smoke is a complex mixture of numerous mutagens and carcinogens.

78 r (NER) excises bulky DNA lesions induced by mutagens and carcinogens.

79 DNA damage caused by sunlight, environmental mutagens and certain antitumor agents.

80 DNA that are generated by various alkylating mutagens and drugs.

81 igating the effects of physical and chemical mutagens and for exploring the potential of mutation bre

82 doneness level, and intake of specific meat mutagens and heme iron are associated with lung carcinom

83 NMF distinguished all three mutagens and in the pooled analysis IR was associated wi

84 testing of viral mutational tolerance to RNA mutagens and other selective pressures.

85 ants are constantly exposed to environmental mutagens and plant cells are totipotent, an understandin

86 mplate exposes the nontemplate DNA strand to mutagens and primes unscheduled error-prone DNA synthesi

87 ction are critical for the plant response to mutagens and proper plant development.

88 sporters protect embryos and stem cells from mutagens and pump morphogens that control cell fate and

89 antly to the carcinogenicity of a variety of mutagens and raises the possibility that genome-wide LOH

90 ential for the minimization of DNA damage by mutagens and reactive oxidizing species.

91 r (PTE) lesions that are induced by chemical mutagens and refractory to DNA repair have not been prev

92 in the tentative identification of possible mutagens and the positive identification of the nonmutag

93 through treatment with chemical or physical mutagens and the selection of rare clonal variants.

94 ncluding 7,12-dimethylbenz[alpha]anthracene (mutagen) and camptothecin (topoisomerase inhibitor), as

95 ity of 2-aminoanthracene (2-AA), an indirect mutagen, and 4-nitroquinoline-N-oxide (4-NQO), a direct

96 ity of 2-aminoanthracene (2-AA), an indirect mutagen, and 4-nitroquinoline-N-oxide (4-NQO), a direct

97 nicity of 4-nitroquinoline-N-oxide, a direct mutagen, and benzo[a]pyrene, an indirect mutagen, toward

98 alleviation in response to treatment with a mutagen, and demonstrate that restriction alleviation se

99 d PAH attract much attention as carcinogens, mutagens, and as diagnostics for environmental forensics

100 Diet is a mixture of carcinogens, mutagens, and protective agents, many of which are metab

101 atalogues have the potential to identify the mutagens, and to reveal the mutagenic processes responsi

102 ity of 2-aminoanthracene (2-AA), an indirect mutagen; and 4-nitroquinoline-N-oxide (4-NQO), a direct

103 bination of this reporter-tagged insertional mutagen approach and zebrafish provides a powerful platf

104 Ribavirin is a viral mutagen approved for treatment of several virus infectio

105 emonstrated in cell culture models, but most mutagens are carcinogenic and are poorly tolerated.

106 ision repair, and repair of damage caused by mutagens are discussed.

107 The environmental arylamine mutagens are implicated in the etiology of various spora

108 ndividual's cumulative or recent exposure to mutagens; as a marker of individual hematopoietic progen

109 tations leading to cancer, or on the assumed mutagen-associated mutation rate, within the generally-a

110 but does not strongly depend on the assumed mutagen-associated mutation rate.

111 The mutagen-attenuated RVF MP-12 vaccine was determined to b

112 system provides the first random insertional mutagen available for germline genetic screens in mice.

113 of RAD51 to either spontaneously arising or mutagen-based DNA damage sites.

114 s were not due to differences in exposure to mutagens, because the patterns were still evident when c

115 8-dihydrodiol (BPD), precursor to the potent mutagen benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide, may

116 old in cells by gamma radiation and chemical mutagens but not by UV treatment.

117 flammatory response or the production of DNA mutagens but rather by providing carbohydrate-derived me

118 nd show that L1 is not simply an insertional mutagen, but that its retrotransposition can result in s

119 experimental animals, although it is a weak mutagen by itself.

120 These endogenous mutagens can alter genes, promote genomic rearrangements

121 Mutations that are induced by chemical mutagens can occur anywhere in the genome.

122 that paternal exposure to a wide variety of mutagens can result in transgenerational instability man

123 No anti-mutagen capacity was noted for MeIQx and Glu-P-1 (10(-5)

124 -dG, which is the major adduct of the potent mutagen/carcinogen benzo[a]pyrene.

125 tantly exposed to chemical and environmental mutagens, causing lesions that can stall replication.

126 tagen sensitivity as measured by an in vitro mutagen challenge assay has been shown to be a risk fact

127 s further showed that cell cycle response to mutagen challenge was significantly enhanced in cells tr

128 combined) for sensitivity to four different mutagen challenges.

129 s anti-tumor agent, is known as an effective mutagen, clastogen and toxicant as well as an effective

130 eomycin) to see whether sensitivity to these mutagens could be used as biomarkers for assessing risk

131 controls and used in conjunction with a meat mutagen database to estimate intake of heterocyclic amin

132 r mutations, induced by the random germ line mutagen ENU (N-ethyl-N-nitrosourea), have disclosed key

133 This set allows rapid screening of potential mutagens, environmental conditions, or genetic loci for

134 genetic screening by an enhanced retroviral mutagen (ERM)-mediated random mutagenesis in the estroge

135 ted with CBFbeta-SMMHC-transduced cells to a mutagen, ethylnitrosourea, markedly accelerated leukemog

136 The relative risks associated with mutagen exposure compared to background rates are also s

137 ge responses repress induced mutations after mutagen exposure.

138 ology applications as well as an insertional mutagen for gene discovery during development.

139 In conclusion, RBV could work as a weak mutagen for HCV RNA in HCV-infected patients.

140 However, RBV can act as a potent mutagen for some RNA viruses.

141 An insertional mutagen for use in other mouse somatic cells would facil

142 d mouse retroviral vectors have been used as mutagens for a large-scale insertional mutagenesis scree

143 hese elements as simple yet highly effective mutagens for both functional genomic and proteomic studi

144 ufficiently characterized source of chemical mutagens for consumers.

145 lications for the treatment of bacteria with mutagens, for the evolution of mutator strains in bacter

146 few studies have evaluated the role of meat mutagens formed during high cooking temperatures.

147 linked to databases for estimating intake of mutagens formed in meats cooked at high temperatures (he

148 blasts demonstrated that quercetin, a potent mutagen found in high levels in bracken fern (Pteridium

149 Environmental pollution including mutagens from wastewater effluents and discontinuity by

150 Subjects sensitive to both mutagens had a 50-fold increased risk for OPLs.

151 Thus, clinical translation of viral mutagens has been difficult, casting doubt on the clinic

152 More than 24 different types of food mutagens have been identified till date from cooked meat

153 Forward genetic screens using chemical mutagens have been successful in defining the function o

154 oviruses, acting as somatic cell insertional mutagens, have been widely used to identify cancer genes

155 nsumption (type, cooking method, and related mutagens), heme iron, nitrite/nitrate, and prostate canc

156 le of well-done meat intake and meat-derived mutagen heterocyclic amine (HCA) exposure in the risk of

157 utagenesis were observed with both the viral mutagen (i.e., G-to-C mutations) and the host restrictio

158 ency virus type 1 (HIV-1) by use of chemical mutagens [i.e., 5-azacytidine (5-AZC)] as well as by hos

159 cellular proliferation and promoted acridine mutagen ICR191-induced transformation of MCF10A cells.

160 In vitro, ribavirin acts as a lethal mutagen in Hantaan virus (HTNV)-infected Vero E6 cells,

161 found that the 4-HNE-DNA adduct is a potent mutagen in human cells and is preferentially formed at c

162 strate that Tnt1 is an efficient insertional mutagen in M. truncatula, and could be a primary choice

163 ific L1HS-Ta subfamily acts as an endogenous mutagen in modern humans, reshaping both somatic and ger

164 acum) Tnt1 retrotransposon as an insertional mutagen in potato.

165 ng sexual reproduction, making Tnt1 an ideal mutagen in potato.

166 mage suggests a role for L1 as an endogenous mutagen in somatic tissues.

167 ns of modification of p53 DNA exposed to the mutagen in vitro versus in vivo.

168 gions, indicating that it acts as an HCV RNA mutagen in vivo.

169 ansposons have been effectively exploited as mutagens in a variety of organisms.

170 s far greater impact than any other external mutagens in mitochondria and is fundamentally linked to

171 superfamily, are widely used as insertional mutagens in numerous plant species.

172 ement of chromatid breaks induced by various mutagens in short-term cultures of peripheral blood lymp

173 quantifying the chromatid breaks induced by mutagens in short-term cultures of peripheral blood lymp

174 lpha radiation, gamma radiation, or chemical mutagens in the presence and absence of caffeine is a ra

175 ariety of carbocyclic and heterocyclic amine mutagens including PhIP.

176 of great importance in the bioactivation of mutagens, including the N-hydroxylation of arylamines.

177 torting DNA lesions induced by a plethora of mutagens, including UV light.

178 licate ultraviolet radiation as the dominant mutagen, indicating a superficially located cell of orig

179 ygous mice (CBS(+/-) ) reduced the number of mutagen-induced aberrant colonic crypt foci.

180 ithin the same genetic background using only mutagen-induced changes as segregating markers.

181 ncreases of S and G(2) phase frequencies and mutagen-induced comets.

182 The probability of a cancer being mutagen-induced correlates across cancer sites with the

183 Levels of baseline and mutagen-induced DNA damage are intrinsically higher in P

184 We have established a mutagen-induced nonsense allele of the rat Apc gene on a

185 he conditional probabilities of cancer being mutagen-induced range between 7-96%.

186 smokers) and the probability of cancer being mutagen-induced.

187 isk and the probability of that cancer being mutagen-induced.

188 Thus, mutagen induction of LOH in embryonic stem cells suggest

189 us infection and improved resistance against mutagen/inflammation-induced colorectal tumorigenesis.

190 tations on viral replication, sensitivity to mutagen, inhibition by type I interferon (IFN), and tran

191 iation of red meat, processed meat, and meat mutagen intake with lung cancer risk in Environment And

192 red to the host needs to be so high that the mutagen is effective even in the refugia.

193 necessary to neutralize refugia and the less mutagen is necessary to achieve extinction at high migra

194 ling of a microbial pathogen with a chemical mutagen, is a potential broad-spectrum antiviral treatme

195 Genetic instability, provoked by exogenous mutagens, is well linked to initiation of cancer.

196 ed drinking water, is one of the most potent mutagens known.

197 tions induced in the initial exposure to the mutagen, many of the lines are segregating or are now fi

198 tical for adduct formation by the endogenous mutagens MDA and base propenals.

199 production of mouse mutations with the point mutagen N-ethyl-N-nitrosourea (ENU) is a key strategy fo

200 ecessive mutations generated by the chemical mutagen n-ethyl-n-nitrosourea (ENU) mapped a new mutant

201 zygous for germline mutations induced by the mutagen N-ethyl-N-nitrosourea (ENU), numerous animals di

202 ved from males mutagenized with the germline mutagen N-ethyl-N-nitrosourea (ENU), we identified a rec

203 mutagenesis screen in C57BL/6 mice using the mutagen N-ethyl-N-nitrosourea (ENU).

204 opulations after treatment with the powerful mutagen N-ethyl-N-nitrosourea.

205 ue-Dawley rat that had been treated with the mutagen N-ethyl-N-nitrosourea.

206 ns against direct-acting and indirect-acting mutagens, namely 4-nitro-o-phenylenediamine, sodium azid

207 ing to the conclusion that generation of the mutagen nitrogen dioxide is peculiar to cell culture sys

208 repeat tract in a non-B conformation is the mutagen, not the sequence per se in the right-handed B h

209 iguous base-pairing capacity is an efficient mutagen of the PV genome.

210 In addition, mutagen or cancer-specific mutational background models

211 late the mutation rate, either by the use of mutagens or by selection (or genetic manipulation) of fi

212 ve been studied because of their activity as mutagens or drugs, but little is known regarding their i

213 natures that are causally linked to specific mutagens or susceptibility loci.

214 not affect viral replication, sensitivity to mutagen, or inhibition by IFN-beta compared to WT MHV.

215 ted with ultraviolet (UV) light and chemical mutagens, or by insertional mutagenesis.

216 NA, and these thymine analogs are well known mutagens, our observations raise the possibility that ha

217 sts, which are more exposed to environmental mutagens over time.

218 ugia, i.e., compartments that receive little mutagen, prevent extinction?

219 functional food ingredient with interesting mutagen preventing properties.

220 of the DNA bacteriophage T7 was grown with a mutagen, producing a genomic rate of 4 nonlethal mutatio

221 The essential oil showed mutagen-protective efficacy against IQ and MeIQ tested a

222 e), C. lechleri essential oil was tested for mutagen-protective properties (concentration range: 0.01

223 Mutagens related to meat cooking and processing, and var

224 case control study, we used two assays with mutagens relevant to tobacco exposure (benzo[a]pyrene di

225 at are known to be strong, moderate and weak mutagens, respectively.

226 overed novel mutations in genes that include mutagen sensitive 206, single-strand annealing reducer,

227 d-joining (MMEJ) component, polymerase theta/mutagen-sensitive 308 (mus308), exhibits a sporadic thin

228 ere solely sensitive to MMS and define 8 new mutagen-sensitive genes (mus212-mus219).

229 The remaining 16 mutants define 14 new mutagen-sensitive genes (mus314-mus327).

230 an interaction between the gene (mus309, for mutagen-sensitive) encoding the Drosophila Bloom's syndr

231 of epidemiologic and genetic studies linking mutagen sensitivity and cancer risk.

232 We developed the first model incorporating mutagen sensitivity and epidemiologic factors to predict

233 re was a dose response between the degree of mutagen sensitivity and risk of SCCHN in non-Hispanic Wh

234 hly heritable, thereby validating the use of mutagen sensitivity as a cancer susceptibility factor.

235 Increased mutagen sensitivity as measured by an in vitro mutagen c

236 city, we validated our previous finding that mutagen sensitivity as measured by the frequency of chro

237 When mutagen sensitivity data were incorporated, the AUC incr

238 r predisposition factor, the heritability of mutagen sensitivity has not been clearly established.

239 This is the first study to examine mutagen sensitivity in a premalignant condition.

240 provides further support to the notion that mutagen sensitivity increases the risk of cancer.

241 Despite numerous studies showing that mutagen sensitivity is a cancer predisposition factor, t

242 us epidemiologic studies have suggested that mutagen sensitivity is a cancer susceptibility factor fo

243 nce is becoming increasingly convincing that mutagen sensitivity is a risk factor for cancer developm

244 the strongest and most direct evidence that mutagen sensitivity is highly heritable, thereby validat

245 notype and provided compelling evidence that mutagen sensitivity is highly heritable.

246 of genetic and environmental factors on the mutagen sensitivity phenotype and provided compelling ev

247 of genetic and environmental factors on the mutagen sensitivity phenotype.

248 Mutagen sensitivity was measured in peripheral blood lym

249 Mutagen sensitivity, a measurement of chromatid breaks i

250 We measured DNA damage, mutagen sensitivity, and reactive oxygen species (ROS) i

251 Mutagen sensitivity, measured by quantifying the chromat

252 r studies are required to fully characterize mutagen sensitivity, which could have important implicat

253 s study is to identify genetic predictors of mutagen sensitivity.

254 -epoxide (BPDE)-induced chromatid breaks (by mutagen-sensitivity assay) and DNA damage (by comet assa

255 ith those linked to a specific environmental mutagen, specifically ionizing radiation or cigarette sm

256 igated the association between meat and meat mutagens, specifically PhIP, and prostate cancer risk in

257 The results show that mutagens such as fast neutrons (used for the induction o

258 Mutagens, such as UV light, were implicated in unexpecte

259 entify mutated genes, and argue that the two mutagens target the same set of genes.

260 nes (1,6- and 1,8-DNPs) are much more potent mutagens than 1-nitropyrene (1-NP).

261 ethyltransferase (M.EcoRII) and that it is a mutagen that can form productive base pairs with either

262 m transfer DNA (T-DNA) is an effective plant mutagen that has been used to create sequence-indexed T-

263 5-aza-2'-deoxycytidine (KP1212), a selective mutagen that induces A-to-G and G-to-A mutations in the

264 These agents define a specific class of mutagen that promotes template-switching and acts by sta

265 and could be extended to the arylamine food mutagens that are biologically relevant in humans.

266 Reactive oxygen species are ubiquitous mutagens that have been linked to both disease and aging

267 etroviruses are powerful insertional somatic mutagens that have been used for many landmark discoveri

268 ng in enhanced sensitivity of CVB3 to lethal mutagens that is dependent on the size of the viral popu

269 Mutagens that strongly and specifically affect this clas

270 transposons are "copy-and-paste" insertional mutagens that substantially contribute to mammalian geno

271 erited DNA repair deficiencies or exposed to mutagens, the pleotropic effects of these contexts could

272 use they were derived without carcinogens or mutagens, these bipotential LPC lines provide novel tool

273 ss of viral drug resistance: resistance to a mutagen through increased fidelity.

274 Fast neutron radiation has been used as a mutagen to develop extensive mutant collections.

275 transposon system has been used as a somatic mutagen to identify candidate cancer genes.

276 y transposon to act as a somatic insertional mutagen to identify genes involved in solid tumour forma

277 wide BiFC screen with an enhanced retroviral mutagen to identify new LMP1-binding proteins.

278 se screens to compare the efficiency of each mutagen to isolate mutants and to identify mutated genes

279 The diminished ability of FP mutagens to hemolyse and aggregate red blood cells due t

280 The use of transposons as insertional mutagens to identify cancer genes in mice has generated

281 d 4-nitroquinoline-N-oxide (4-NQO), a direct mutagen toward Salmonella typhimurium TA 98 and TA 100.

282 d 4-nitroquinoline-N-oxide (4-NQO), a direct mutagen toward Salmonella typhimurium TA 98 and TA 100.

283 d 4-nitroquinoline-N-oxide (4-NQO), a direct mutagen toward Salmonella typhimurium TA 98 and TA 100.

284 ect mutagen, and benzo[a]pyrene, an indirect mutagen, toward Salmonella typhimurium TA 98 and TA 100.

285 A mutagen-treated CHO cell line, in which LRP-1 is express

286 e of perinatal lethality was observed in the mutagen-treated cohort compared with an untreated backcr

287 Surprisingly, our results demonstrate mutagen treatment did not increase mitochondrial point o

288 embryonic stem cells to nontoxic amounts of mutagens triggers a marked increase in the frequency of

289 ype E. coli in <24 h, outperforming chemical mutagens, ultraviolet light and the mutator strain XL1-R

290 the type and concentration of flavonoids and mutagen used.

291 ith the proposed mechanism of action for the mutagens used.

292 s potential as a random germline insertional mutagen useful for in vivo gene trapping in mice.

293 -frame exon traps in the enhanced retroviral mutagen vector.

294 The positive identification of mutagens was hampered by a lack of commercially availabl

295 omatic hydrocarbons (PAHs) and other organic mutagens were assessed by quantification of urinary PAH

296 summary, red meat, processed meat, and meat mutagens were independently associated with increased ri

297 Each mutagen, whether used alone or in combination, resulted

298 fusion peptide (FP) and four closely related mutagens with a lipid bilayer.

299 ting HIV-1 infection in which use of a viral mutagen would over multiple rounds of replication lead t

300 densely ionizing radiation than by chemical mutagens, x-rays, or endogenous aging processes.