ライフサイエンスコーパス: aflatoxin

1 lites, including lovastatin, penicillin, and aflatoxin.

2 izes the secondary metabolite and carcinogen aflatoxin.

3 s with the carcinogenic secondary metabolite aflatoxin.

4 et of accumulation of aflatoxin proteins and aflatoxin.

5 in the detoxication of carcinogens including aflatoxin.

6 lovastatin and the potent natural carcinogen aflatoxin.

7 he growth of A. flavus and its production of aflatoxins.

8 s due to its ability to produce carcinogenic aflatoxins.

9 convert modified mycotoxins into their free aflatoxins.

10 Exposure to aflatoxins (0.1 to 10 muM; 5 to 10 minutes) reduced base

11 , decarboxylation, and rearrangement to give aflatoxin - a remarkable sequence of transformations.

12 s of trade; then examined how regulations of aflatoxin, a common contaminant of maize, are similar or

13 xanthone O-methylsterigmatocystin (OMST) to aflatoxin, a process we demonstrate is mediated by a sin

14 her hand, afforded no detectable increase in aflatoxins above controls, indicating that reductive deo

15 The level of aflatoxin accumulation in the filamentous fungus Aspergi

16 ts (PMS) media stimulated only low levels of aflatoxin accumulation.

17 salts (GMS) growth media strongly stimulated aflatoxin accumulation.

18 Natural occurrence of aflatoxin (AF) in agricultural soils, green leafy vegeta

19 secondary metabolite and a precursor to the aflatoxins (AF), is located in a approximately 54 kb, 23

20 d deaths per year, with dietary exposures to aflatoxin (AFB1) and subsequent DNA adduct formation bei

21 etely inhibited production of both B1 and B2 aflatoxins (AFB1 and AFB2) at a concentration of 150 mug

22 er to evaluate the possible co-occurrence of aflatoxins (AFB1, AFG1, AFB2 and AFG2), ochratoxin A (OT

23 Concentrations of the total aflatoxin, aflatoxin B1, aflatoxin B2, aflatoxin G1, afl

24 In present study aflatoxins (AFs) and ochratoxin A (OTA) were analysed in

25 etry for the extraction and determination of aflatoxins (AFs) B1, B2, G1 and G2 from food was success

26 Aflatoxins (AFs), ochratoxin A (OTA) and zearalenone (ZE

27 d fig were analysed for the incidence of any aflatoxins (AFs).

28 Total aflatoxins (AFT) and ochratoxin A (OTA) levels were esti

29 ere assayed for aflatoxin exposure using the aflatoxin-albumin adduct (AF-alb) biomarker.

30 mples were collected and analyzed for plasma aflatoxin-albumin adducts (AF-alb) using ELISA, and urin

31 We measured the concentrations of blood aflatoxin-albumin adducts from 600 people immediately af

32 illages were consistent with measurements of aflatoxin-albumin adducts.

33 By contrast, mean aflatoxin-albumin concentration in intervention villages

34 In control villages mean aflatoxin-albumin concentration increased postharvest (f

35 d of the number of people had non-detectable aflatoxin-albumin concentrations at harvest.

36 f predictive power and model performance for aflatoxin analysis and they are equally effective and ac

37 e the spectroscopic method best suitable for aflatoxin analysis in maize (Zea mays L.) grain based on

38 Our data indicate that the aflatoxin and adjacent sugar utilization clusters are pa

39 lationship was observed between Cr and total Aflatoxin and Aflatoxin B1; whereas Ochratoxin A was rel

40 The results suggest that aflatoxin and aflatrem biosynthesis may remediate oxidat

41 Aflatoxin and fumonisin are toxic food contaminants.

42 ted the association between child growth and aflatoxin and fumonisin exposure in Tanzania.

43 are potentially involved in the formation of aflatoxin and other secondary metabolites, as well as in

44 to be detected in the conversion of OMST to aflatoxin and to be established directly in the biosynth

45 conducted in individuals exposed to dietary aflatoxins and at high risk for development of liver can

46 flavus strains producing elevated levels of aflatoxins and CPA.

47 gnature" cancer rates confirming exposure to aflatoxins and fumonisins.

48 Mycotoxins, such as aflatoxins and ochratoxin A, are presently considered as

49 sonator arrays to effectively identify total aflatoxins and ochratoxin A, at low concentrations (3 ng

50 d for the method were between 0.2ngL(-1) for aflatoxins and ochratoxin, and 2.0ngL(-1) for fumonisins

51 marker of the biologically effective dose of aflatoxin, and elevated levels are associated with incre

52 xposure, but effects were blocked by an anti-aflatoxin antibody only with A. flavus CM.

53 Aflatoxins are fungal metabolites that frequently contam

54 Aflatoxins are highly toxic, mutagenic, teratogenic and

55 Aflatoxins are mycotoxins secreted by Aspergillus flavus

56 Aflatoxins are potential food pollutants produced by fun

57 Aflatoxins are the most potent genotoxic and carcinogeni

58 Aflatoxins are the most thoroughly studied mycotoxins.

59 Aflatoxins are toxic secondary metabolites produced by a

60 Aflatoxins are well recognized as a cause of liver cance

61 ent with previous mutation data derived from aflatoxin-associated HCCs.

62 es responsible for detoxifying the mycotoxin aflatoxin B(1) (AFB(1)) and GST dysfunction is a known r

63 V) or C (HCV) virus, and exposure to dietary aflatoxin B(1) (AFB(1)) or alcohol consumption.

64 The levels of aflatoxin B(1) (AFB(1)) production were 1.0 and 42.7 mug

65 Dietary exposure to aflatoxin B(1) (AFB(1)), in addition to other known fact

66 ce suggests a link between the inhalation of aflatoxin B(1) (AFB(1))-contaminated grain dusts and inc

67 n attempt to understand the genetic basis of aflatoxin B(1) (AFB(1))-related susceptibility to hepato

68 inoma cases associated with high exposure to aflatoxin B(1) (AFB(1)).

69 ic trans-8,9-dihydro-8-(N7-guanyl)-9-hydroxy-aflatoxin B(1) adduct.

70 n) that occur in the complex biosynthesis of aflatoxin B(1) are mediated by cytochromes P-450.

71 The guanine N7 adduct of aflatoxin B(1) exo-8,9-epoxide hydrolyzes to form the fo

72 biosynthesis of the potent hepatocarcinogen aflatoxin B(1) in Aspergillus parasiticus.

73 high-risk population exposed unavoidably to aflatoxin B(1) in the diet.

74 ltidomain PKS central to the biosynthesis of aflatoxin B(1), a potent environmental carcinogen.

75 ylimidazo[4,5-b]pyridine and the base adduct aflatoxin B(1)-formamidopyrimidine by acylation.

76 nomius and A. parasiticus isolates produced aflatoxins B and G, but not cyclopiazonic acid (CPA).

77 (standards based on the sum of the levels of aflatoxins B(1), B(2), G(1), and G(2)) differ by more th

78 The aflatoxin B1 (5.4 mug/kg) was also found in one of the g

79 were positive for the following mycotoxins: aflatoxin B1 (50 mug/kg), alternariol monomethyl ether (

80 a component of Chinese herbal medicine), and aflatoxin B1 (a food contaminant).

81 Aflatoxin B1 (AFB) epoxide forms an unstable N7 guanine

82 ection of the mycotoxins ochratoxin A (OTA), aflatoxin B1 (AFB1) and deoxynivalenol (DON) which are s

83 as these toxins, such as ochratoxin A (OTA), aflatoxin B1 (AFB1) and deoxynivalenol (DON), are subjec

84 ution with only the specific toxin, which is aflatoxin B1 (AfB1) and mixture of AfB1 with other non-s

85 p reduced the number of revertants caused by aflatoxin B1 (AFB1) and proliferation of cells M12.C3.F6

86 Aflatoxin B1 (AFB1) and/or hepatitis B and C viruses are

87 HCCs occur in geographical regions with high aflatoxin B1 (AFB1) exposure, concomitant with hepatitis

88 There is a prompt need for determination of aflatoxin B1 (AFB1) in food products to avoid distributi

89 Aflatoxin B1 (AFB1) is a human hepatotoxin and hepatocar

90 Aflatoxin B1 (AFB1) is a mutagen and IARC (International

91 , exposure to the genotoxic hepatocarcinogen aflatoxin B1 (AFB1) is a significant factor in the genes

92 Among them, Aflatoxin B1 (AFB1) is the most toxic.

93 r for determination and quantification of an aflatoxin B1 (AFB1) level using a reduced graphene oxide

94 Aflatoxin B1 (AFB1) producing fungi contaminate food and

95 is initiated through metabolic activation of aflatoxin B1 (AFB1) to its epoxide form that reacts with

96 rochemical aptasensor for trace detection of aflatoxin B1 (AFB1) was developed by using an aptamer as

97 isk of liver cancer upon exposure to dietary aflatoxin B1 (AFB1), a carcinogenic product of the mold

98 maximum limits (MLs) of 5 and 2mugkg(-1) for aflatoxin B1 (AFB1), respectively.

99 High expression of the aflatoxin B1 (AFB1)-8,9-epoxide-conjugating glutathione

100 5% of NNK-induced, 59% of VC-induced, 58% of aflatoxin B1 (AFB1)-induced, 14% of N-ethyl-N-nitrosoure

101 ue has been developed for the preparation of aflatoxin B1 (AFB1)-tagged liposomes encapsulating a vis

102 diol epoxide, N-hydroxy-2-aminofluorene, and aflatoxin B1 8,9-epoxide in (1) naked intact genomic DNA

103 , sodium azide, mitomycin C, benzo[a]pyrene, aflatoxin B1 and 2-aminofluorene, were compared with the

104 Samples containing aflatoxin B1 are allowed to migrate by capillary action

105 The device is capable of detecting aflatoxin B1 at levels down to 20 ng and could serve as

106 The compound is responsive to Aflatoxin B1 at parts per billion level, which makes it

107 Aflatoxin B1 content was significantly correlated with t

108 The visual limit of detection for aflatoxin B1 decreased to 0.6ng/mL compared to 11ng/mL w

109 has been applied to label-free detection of aflatoxin B1 in a competitive immunoassay format, with t

110 Mean concentrations of aflatoxin B1 in groundnuts in household stores in interv

111 r has a potential for quick determination of aflatoxin B1 in paprika samples.

112 inogenic mycotoxin and secondary metabolite, aflatoxin B1 in the filamentous fungus and an important

113 Aflatoxin B1 induced substitutions of guanines in a GpC

114 hesis of the potent environmental carcinogen aflatoxin B1 involves ca. 15 steps beyond the first poly

115 nigmatic step in the complex biosynthesis of aflatoxin B1 is the oxidative rearrangement of versicolo

116 ch was tested by determining zearalenone and aflatoxin B1 mycotoxins.

117 Cell survival and mutagenesis following aflatoxin B1 treatment was assayed in strains defective

118 In this paper we report the sensing of aflatoxin B1(AFB1) by field effect capacitive method usi

119 e between 0.05mugL(-1) (for aflatoxin G1 and aflatoxin B1) and 15mugL(-1) (for deoxynivalenol and fum

120 hratoxin A and aflatoxin M1 (a metabolite of aflatoxin B1), as well as other aflatoxins, under compet

121 certain mycotoxins, such as deoxynivalenol, aflatoxin B1, aflatoxin B2, aflatoxin G1, aflatoxin G2,

122 Concentrations of the total aflatoxin, aflatoxin B1, aflatoxin B2, aflatoxin G1, aflatoxin G2,

123 centration of 0.48+/-0.05ngL(-1) followed by aflatoxin B1, aflatoxin G1 and ochratoxin A.

124 tify 14 fungus secondary metabolites, namely aflatoxin B1, aflatoxin G1, aspergillic acid, aspyrone,

125 A method for aflatoxin B1, B2, G1 and G2 determination and confirmati

126 etection method for the determination of the aflatoxin B1, B2, G1 and G2 in peanuts, rice and chilli

127 biosynthesis of the environmental carcinogen aflatoxin B1, is one of the multidomain iterative polyke

128 ]anthracene, benzo[a]pyrene-7,8-dihydrodiol, aflatoxin B1, naphthalene, and styrene, with high turnov

129 zone containing immobilized antibodies; then aflatoxin B1-tagged, dye-containing liposomes are allowe

130 ohol and tobacco consumption and exposure to aflatoxin B1.

131 sitive foci) in the liver of rats exposed to aflatoxin B1.

132 highly related to hepatitis B infection and aflatoxin B1.

133 observed between Cr and total Aflatoxin and Aflatoxin B1; whereas Ochratoxin A was related to Cu and

134 inones versicolorin A and B readily afforded aflatoxins B1 and B2.

135 Fluorescence emission of aflatoxins B1 and G1 was enhanced by post-column chemica

136 arker - ergosterol and important mycotoxins (aflatoxins B1, B2, G1 and G2, and ochratoxin A) were als

137 d and characterized for the determination of aflatoxins (B1, B2, G1 and G2) in rice.

138 ed), were investigated for their contents of aflatoxins (B1, B2, G1 and G2), patulin, and ergosterol.

139 Aflatoxin B2 was the most frequently detected mycotoxin

140 oxins, such as deoxynivalenol, aflatoxin B1, aflatoxin B2, aflatoxin G1, aflatoxin G2, ochratoxin A,

141 ations of the total aflatoxin, aflatoxin B1, aflatoxin B2, aflatoxin G1, aflatoxin G2, ochratoxin A,

142 d inhibited the production of ochratoxin and aflatoxin-B2.

143 prime candidate for both the genotoxicity of aflatoxin, because mammalian cells also have similar byp

144 (P = 0.036) in median urinary levels of this aflatoxin biomarker compared with those taking placebo.

145 h chemopreventive agents modulated levels of aflatoxin biomarkers in the study participants in manner

146 has allowed a molecular characterization of aflatoxin biosynthesis and its regulation.

147 The 27 genes involved in aflatoxin biosynthesis are clustered within a 70 kb regi

148 Genetic studies on aflatoxin biosynthesis in Aspergillus flavus and A. para

149 crystal structure of the PksA PT domain from aflatoxin biosynthesis with a heptaketide mimetic tether

150 coding for growth and development of fungus, aflatoxin biosynthesis, binding, transport, and signalin

151 rmation on physiological factors involved in aflatoxin biosynthesis, but it has been difficult to und

152 known about the global factors that regulate aflatoxin biosynthesis, but there is a clear link betwee

153 Binding of AflR, a positive regulator of aflatoxin biosynthesis, to the ordA promoter showed a po

154 of AflM in the complex enzymatic network of aflatoxin biosynthesis.

155 % conversion) to a so far unknown product of aflatoxin biosynthesis.

156 hromosome III, including the known genes for aflatoxin biosynthesis.

157 a xanthone precursor does not take place in aflatoxin biosynthesis.

158 here is a clear link between development and aflatoxin biosynthesis.

159 e fungus to regain completely its ability of aflatoxin biosynthesis.

160 f aflR, the transcriptional regulator of the aflatoxin biosynthetic gene cluster.

161 roducing polyketide synthase, PksA, from the aflatoxin biosynthetic pathway in Aspergillus parasiticu

162 a suggest that the order of genes within the aflatoxin cluster determines the timing and order of tra

163 and laboratory animals, chronic exposure to aflatoxins compromises immunity and interferes with prot

164 equally effective and accurate in predicting aflatoxin concentration in maize.

165 cal density is inversely proportional to the aflatoxin concentration in the sample.

166 nd three atoxigenic isolates of A. flavus in aflatoxin conducive and non-conducive media with varying

167 uracy and reliability for rapid screening of aflatoxin contaminated maize samples.

168 Consumption of aflatoxin-contaminated food and commodities poses seriou

169 Eighteen aflatoxin-contaminated maize samples were incubated with

170 pectra were more marked and pronounced among aflatoxin contamination groups than those of FT-NIR spec

171 genomics program are to reduce and eliminate aflatoxin contamination in food and feed and to discover

172 ess whether postharvest measures to restrict aflatoxin contamination of groundnut crops could reduce

173 package of postharvest measures to restrict aflatoxin contamination of the groundnut crop; ten contr

174 Aflatoxin contamination, caused by fungal pathogen Asper

175 used significant increases in the total free aflatoxin content, 15+/-8% and 13+/-5%, respectively.

176 , leading to an underestimation of the total aflatoxin content.

177 hese results show that a small proportion of aflatoxins could be associated to matrix substances in p

178 KR7A subfamily was purified from liver as an aflatoxin dialdehyde reductase AKR7A1.

179 This aflatoxin-DNA adduct excretion product serves as a bioma

180 E-31 also significantly reduces formation of aflatoxin-DNA adducts and decreases size and number of a

181 CDDO-Im treatment reduces levels of aflatoxin-DNA adducts by approximately 40% to 90% over t

182 Aflatoxin-driven mutagenesis is initiated through metabo

183 sidents of Qidong who had been monitored for aflatoxin exposure and HBV infection.

184 -this to model the multiplicative effects of aflatoxin exposure and hepatitis B in causing HCC.

185 The aflatoxin exposure and the toxic affects of aflatoxins o

186 Thus, aflatoxin exposure apparently remains a substantial publ

187 s polymerase in cellular tolerance following aflatoxin exposure has not been established.

188 dditional health risk that may be related to aflatoxin exposure in children, a hypothesis that merits

189 ions where it has been studied, the existing aflatoxin exposure results in changes in nutrition and i

190 ols in neighboring villages were assayed for aflatoxin exposure using the aflatoxin-albumin adduct (A

191 h the next highest level of evidence include aflatoxin exposure, and heavy alcohol and tobacco use.

192 ing from hepatitis B and C viral infections, aflatoxin exposure, chronic alcohol use or genetic liver

193 of the risk factors for human liver cancer (aflatoxin exposure, hepatitis B virus-associated liver i

194 ure 24, previously hypothesized to stem from aflatoxin exposure, indeed likely represents AFB1 exposu

195 antially reduce the disease burden caused by aflatoxin exposure.

196 dong County, China, a region of well-studied aflatoxin exposure.

197 cination programs and efforts to both reduce aflatoxin exposures and to attenuate the toxicological c

198 We determined optimal aflatoxin extraction conditions in terms of concentratio

199 ell experiments for their ability to support aflatoxin formation in the blocked mutant DIS-1, defecti

200 Having secured the role of HOMST in aflatoxin formation, the mechanism of the second oxidati

201 the physiological factors known to influence aflatoxin formation.

202 eration of monolithic columns for extracting aflatoxin from real food samples by combining the superi

203 ribute to poor child health and development: aflatoxin, fumonisin, and deoxynivalenol.

204 cation Limits were between 0.05mugL(-1) (for aflatoxin G1 and aflatoxin B1) and 15mugL(-1) (for deoxy

205 0.48+/-0.05ngL(-1) followed by aflatoxin B1, aflatoxin G1 and ochratoxin A.

206 total aflatoxin, aflatoxin B1, aflatoxin B2, aflatoxin G1, aflatoxin G2, ochratoxin A, lead, cadmium,

207 deoxynivalenol, aflatoxin B1, aflatoxin B2, aflatoxin G1, aflatoxin G2, ochratoxin A, T-2 toxin and

208 secondary metabolites, namely aflatoxin B1, aflatoxin G1, aspergillic acid, aspyrone, betaine, chrys

209 n, aflatoxin B1, aflatoxin B2, aflatoxin G1, aflatoxin G2, ochratoxin A, lead, cadmium, mercury, arse

210 l, aflatoxin B1, aflatoxin B2, aflatoxin G1, aflatoxin G2, ochratoxin A, T-2 toxin and zearalenone, w

211 d-type strain and a mutant (649) lacking the aflatoxin gene cluster fail to produce aflatoxin or tran

212 B binding at promoters of seven genes in the aflatoxin gene cluster that carry CREs.

213 III in the region previously containing the aflatoxin gene cluster.

214 aled the silencing effect is specific to the aflatoxin gene cluster.

215 rated that AtfB binds to the nor-1 (an early aflatoxin gene) promoter at a composite regulatory eleme

216 ficant decrease in transcript levels of five aflatoxin genes and at least two key global regulators o

217 he position of aflR is likely preventing the aflatoxin genes from being expressed in 649 x wild-type

218 ated with activation of transcription of the aflatoxin genes.

219 Hepatotoxic aflatoxins have found a worthy adversary in two new fami

220 oped-country approaches to the management of aflatoxins impractical in developing-country settings, b

221 t assay (ELISA) methods for the detection of aflatoxin in spice paprika matrix.

222 rch has only focused on the presence of free aflatoxins in agricultural commodities.

223 estigate the occurrence of possible modified aflatoxins in maize.

224 e method was applied to the determination of aflatoxins in peanut (9), rice (5) and chilli (10) sampl

225 The absence of aflatoxins in samples confirm the protector effects of t

226 -liquid microextraction for determination of aflatoxins in soybean juice by HPLC.

227 ction with hepatitis B virus and exposure to aflatoxins in the diet act synergistically to amplify ri

228 Experimentally, aflatoxin-induced hepatocarcinogenesis can be inhibited

229 of guanines in a GpC context, as observed in aflatoxin-induced liver cancers.

230 DNA adducts and decreases size and number of aflatoxin-induced preneoplastic hepatic lesions in rats

231 y potent chemopreventive agent that inhibits aflatoxin-induced tumorigenesis in rat liver.

232 ding of AtfB to the promoters occurred under aflatoxin-inducing but not under aflatoxin-noninducing c

233 Aflatoxin is a liver toxin and carcinogen contaminating

234 Contamination of crops with aflatoxin is a serious global threat to food safety.

235 Promotion of the HIV epidemic by aflatoxin is postulated but not yet established.

236 sts that fumonisin contamination rather than aflatoxin is the most likely factor in maize promoting H

237 ne dietary consumption of foods that contain aflatoxins is the second leading cause of environmental

238 CATC(AFB)GATCT).d(AGATCGATGT) containing the aflatoxin lesion in the correctly paired (AFB)G.C contex

239 taminated with high (246-510ppb; 141-422ppb) aflatoxin levels, respectively.

240 pment of an immunosensor for the analysis of aflatoxin M(1) directly in milk samples.

241 se of this approach, the detection limit for aflatoxin M(1) in milk was estimated to be 8 ng L(-1), w

242 microelectrode array (MEA) immunosensor for aflatoxin M(1) is presented in this paper.

243 d selectivity studies using ochratoxin A and aflatoxin M1 (a metabolite of aflatoxin B1), as well as

244 d immunoassay has been developed to quantify aflatoxin M1 (AFM1) at ultra-trace levels in milk sample

245 lectrochemiluminescence (ECL) aptasensor for aflatoxin M1 (AFM1) detection by a closed bipolar electr

246 The extraction of aflatoxin M1 (AFM1) from cheese is generally carried out

247 The rapid and sensitive detection of aflatoxin M1 (AFM1) in milk by using surface plasmon res

248 immunosorbent assay (CL-ELISA) for detecting aflatoxin M1 (AFM1) was developed.

249 Aflatoxin M1 (AFM1), a potentially carcinogenic compound

250 inting efficiencies against ochratoxin A and aflatoxin M1 of 1.84 and 26.39, respectively, even under

251 values were between 0.02 and 10.14ng/mL for aflatoxins M1, B1, B2, G1, G2, ochratoxins A and B, HT-2

252 posure to fumonisin alone or coexposure with aflatoxins may contribute to child growth impairment.

253 rence, oltipraz, an established modulator of aflatoxin metabolism in humans, is 100-fold weaker than

254 changes in mRNA levels of genes involved in aflatoxin metabolism were measured in rat liver followin

255 The aflatoxin moiety intercalated above the 5' face of the m

256 primary endpoint was modulation of levels of aflatoxin-N(7)-guanine adducts in urine samples collecte

257 nic acid did not lead to an increase in free aflatoxins, neither did treatment with a protease.

258 urred under aflatoxin-inducing but not under aflatoxin-noninducing conditions and correlated with act

259 eyed for the presence of 22 mycotoxins (four aflatoxins, ochratoxin A, diacetoxiscyrpenol (DAS), thre

260 method for the simultaneous determination of aflatoxins, ochratoxin A, zearalenone, deoxynivalenol, f

261 he prevalence and level of human exposure to aflatoxins on a global scale have been reviewed, and the

262 we examined the effects of acute exposure to aflatoxins on airway cell physiology.

263 aflatoxin exposure and the toxic affects of aflatoxins on immunity and nutrition combine to negative

264 g the aflatoxin gene cluster fail to produce aflatoxin or transcripts of the aflatoxin pathway genes.

265 s infection, toxins (for example, alcohol or aflatoxin) or metabolic influences, and (2) mutations oc

266 the basis of mutagenesis experiments in the aflatoxin pathway and these biochemical precedents, tota

267 l to produce aflatoxin or transcripts of the aflatoxin pathway genes.

268 All aflatoxins, patulin and ergosterol were determined by hi

269 e contaminated with trace or zero amounts of aflatoxins, patulin and ergosterol, so they posed no ris

270 ng the final Claisen-type cyclization to the aflatoxin precursor, norsolorinic acid anthrone.

271 he PKS ACP, leading to the production of the aflatoxin precursor, norsolorinic acid.

272 as was its 9-deoxy analogue, an established aflatoxin precursor.

273 ood contaminated by mycotoxins, particularly aflatoxins (predominantly found in peanut, maize, rice,

274 Aflatoxin production by Aspergillus flavus is exacerbate

275 The lack of aflatoxin production in the diploid was not due to a uni

276 This way, fungal biomass development and aflatoxin production were dependent on TEO concentration

277 ay and examined for their ability to support aflatoxin production.

278 esis of the first isolatable intermediate in aflatoxin production.

279 tion and spread of histone H4 acetylation in aflatoxin promoters and the onset of accumulation of afl

280 RE1, AGCC(G/C), are highly conserved in five aflatoxin promoters that demonstrate AtfB binding.

281 Aflatoxin promotes hepatocellular cancer, and fumonisin

282 n promoters and the onset of accumulation of aflatoxin proteins and aflatoxin.

283 ing large amounts of maize have very similar aflatoxin regulations: nations with strict standards ten

284 Aflatoxins secreted by respiratory A. flavus may impair

285 in sub-Sahara Africa and Asia, where dietary aflatoxins significantly enhance the carcinogenic effect

286 n the biosynthesis of the fungal carcinogen, aflatoxin, six cytochromes P450 are encoded by the biosy

287 top pairs of maize-trading nations do total aflatoxin standards (standards based on the sum of the l

288 Glucose stimulated transcription of the aflatoxin structural genes ver-1 and nor-1 to similar in

289 ntibodies through simultaneous imprinting of aflatoxin subtypes B1, B2, G1, and G2.

290 nsformation of a NaBH4-reduced adduct to the aflatoxin system via the Nef-cyclization process was ach

291 hogenic fungus infecting maize and producing aflatoxins that are health hazards to humans and animals

292 The recoveries of aflatoxins that were spiked into food samples were 86.38

293 in significantly inhibited the production of aflatoxins; the 0.5% level had a greater than 96% inhibi

294 Humans are exposed to hepatocarcinogenic aflatoxins through ingestion of moldy foods, a consequen

295 either of these compounds was converted into aflatoxin under conditions where the anthraquinones vers

296 etabolite of aflatoxin B1), as well as other aflatoxins, under competitive conditions.

297 Exposure to aflatoxin was associated with childhood chronic hepatome

298 against fungal amylase and the occurrence of aflatoxins were determined in edible beans.

299 nly since early 1960s when the first studied aflatoxins were found to be carcinogenic.

300 re mainly contaminated with ochratoxin A and aflatoxins, whereas Italian samples with deoxynivalenol

301 assium hydroxide caused a total reduction of aflatoxins, while trifluoromethanesulfonic acid did not