ライフサイエンスコーパス: BPA

1 BPA and MCOP (or its precursors) were associated with sh

2 BPA and TBBPA both interfere with skeletal muscle functi

3 BPA bioaccessibility was evaluated in six positive sampl

4 BPA concentrations were measured in prenatal (n = 375) a

5 BPA concentrations were positively associated with consu

6 BPA contents of canned tuna and sardine samples and thei

7 BPA disrupts endocrine pathways in fish, but the long-te

8 BPA exposure increased Nrf2 binding to a putative antiox

9 BPA had a high degree of variability among both males (I

10 BPA increased hepatic lipid content concomitant with inc

11 BPA induced tumor-like outgrowths in female transgenic m

12 BPA is susceptible to oxidation by Mn(III/IV) oxides, wh

13 BPA is used as a developer in thermal paper products, in

14 BPA may have toxic effects on the female reproductive sy

15 BPA selectively altered the normal developmental program

16 BPA up-regulated the levels of Drp-1 (dynamin-related pr

17 BPA was also associated with shorter luteal phase [2nd v

18 BPA was assayed in first-trimester urine samples from 38

19 BPA was detectable in 94% of women.

20 BPA was detected in 17 out of 40 samples (42.5%); in som

21 BPA was not associated with most BASC-2 scales; however,

22 BPA was not associated with WPPSI-III scores; child sex

23 BPA was positively associated with the relationship prob

24 nine phenols (four parabens, benzophenone-3, BPA, two dichlorophenols, triclosan) in spot urine sampl

25 y detection is achieved through the use of a BPA-specific aptamer as probe molecule and large electro

26 Bisphenol A (BPA) and its brominated derivative tetrabromobisphenol A

27 The endocrine disruptor bisphenol A (BPA) and the pharmaceutical 17alpha-ethinyl estradiol (E

28 Phthalates and bisphenol A (BPA) are endocrine disruptors, and previous research has

29 Phthalates and bisphenol A (BPA) are widely used industrial chemicals that may adver

30 ng batch reactors (SBRs), using bisphenol A (BPA) as the TOrC.

31 lity, and predictors of urinary bisphenol A (BPA) concentrations in 337 children from the Cincinnati,

32 Prenatal bisphenol A (BPA) exposure has been associated with adverse neurodeve

33 Human health risks due to bisphenol A (BPA) exposure through canned food consumption are an eme

34 Early-life exposure to bisphenol A (BPA) has been implicated to play a role in the developme

35 Exposure to bisphenol A (BPA) has been reported to alter global gene expression,

36 sure to nonylphenol (NP) and/or bisphenol A (BPA) has been reported to be associated with adverse bir

37 Pressures to ban bisphenol A (BPA) has led to the use of alternate chemicals such as B

38 on an innovative heterogeneous bisphenol A (BPA) immunoassay based on an electrolyte-gated organic f

39 Bisphenol A (BPA) is a high-production-volume chemical associated wit

40 Bisphenol A (BPA) is an endocrine disrupting compound that may have a

41 Bisphenol A (BPA) is an endocrine disruptor and potential reproductiv

42 Bisphenol A (BPA) is an endocrine disruptor frequently detected in hu

43 Bisphenol A (BPA) is an endocrine-disrupting compound widely used in

44 vironmental endocrine disruptor bisphenol A (BPA) is ubiquitous and associated with the increased ris

45 Bisphenol A (BPA) is widely used in the manufacture of plastics and e

46 store shelves after reports of bisphenol A (BPA) leaching from baby bottles, reusable drink bottles,

47 sure to the endocrine disruptor bisphenol A (BPA) may contribute to the development of obesity.

48 Certain phthalates and bisphenol A (BPA) show reproductive effects in animal studies and pot

49 However, bisphenol A (BPA) was identified by chemical:gene covariation as the

50 results these were assigned to bisphenol A (BPA), 2,4-di-tert-butylphenol, and a possible bisphenol

51 Bisphenol A (BPA), a chemical incorporated into plastics and resins,

52 Bisphenol A (BPA), a component of some dialysis membranes, accumulate

53 Bisphenol A (BPA), a plastics component, has been described to impart

54 gests that prenatal exposure to bisphenol A (BPA), a ubiquitous endocrine-disrupting chemical, is ass

55 increasingly used to substitute bisphenol A (BPA), a widespread environmental endocrine disruptor and

56 te the carcinogenic property of Bisphenol A (BPA), an environmental estrogen, by long-term exposure a

57 en reported between phthalates, bisphenol A (BPA), and child behavior.

58 We examined the association of bisphenol A (BPA), benzophenone-3 (BP-3), triclosan (TCS), and parabe

59 nol F diglycidyl ether (BFDGE), bisphenol A (BPA), bisphenol B (BPB), bisphenol F (BPF) and bisphenol

60 Three selected chemicals, bisphenol A (BPA), diethylhexyl phthalate (DEHP) and mineral oil hydr

61 e direct effects of exposure to bisphenol A (BPA), mono-n-butyl phthalate (Pht), and polychlorinated

62 sure to ban or limit the use of bisphenol A (BPA), production of alternatives such as bisphenol AF (B

63 ), whereas the ICC was 0.39 for bisphenol A (BPA).

64 ee and single step detection of Bisphenol A (BPA).

65 early-life exposure to low-dose bisphenol A (BPA).

66 eceipts, contain high levels of bisphenol A (BPA).

67 In contrast, Bisphenol-A (BPA) elicited a non-monotonic response.

68 Bisphenol-A (BPA) is an environmentally ubiquitous estrogen-like endo

69 disrupting chemicals, including bisphenol-A (BPA), induce non-monotonic dose response (NMDR) relation

70 sequencing in d-200 dorsal prostates across BPA doses.

71 Additionally, BPA and TNF-alpha levels in cord blood were inversely as

72 During the additions, BPA oxidation rate decreases by 3 orders of magnitude, a

73 ealth record-based "best practice advisory" (BPA) that prompted primary care providers to perform HCV

74 -1 as a potential therapeutic target against BPA-mediated impaired mitochondrial dynamics and neurode

75 uld be considered when determining aggregate BPA exposure.

76 ord-integrated provider best practice alert [BPA], and direct patient solicitation) or assigned to re

77 lectronic health record best practice alert [BPA], and patient solicitation), evaluated hepatitis C v

78 BP-3 and BPA were associated with significantly lower TT in male

79 dy to report an association of both BP-3 and BPA with serum TT in adolescents.

80 nificantly lower TT in male adolescents, and BPA was associated with significantly higher TT in femal

81 antitative (79 elements total) analyses, and BPA, using isotopic dilution and MEPS pre-concentration

82 Serum free-BPA and BPA-glucuronide were quantitated in sera of individual P

83 easures of urinary phthalate metabolites and BPA and circulating total 25(OH)D in a prospective cohor

84 We measured 11 phthalate metabolites and BPA in pooled urine from three specimens spaced througho

85 lysis, we reported that DEHP metabolites and BPA were significantly associated with an approximate 20

86 esults support a role for exposure to NP and BPA and possibly inflammation in increasing oxidative/ni

87 We aimed to investigate urinary NP and BPA levels in relation to biomarkers of oxidative/nitrat

88 inerals, electrolytes, most polyphenols, and BPA, is reasonably reproducible in 24-h urine samples th

89 ed to the use of alternate chemicals such as BPA analogues bisphenol S (BPS) and bisphenol AF (BPAF)

90 The association between BPA and BRIEF-P scores was modified by child sex (BPAxse

91 ed significant positive associations between BPA and fat weight [SMD=0.67 (95% CI: 0.53, 0.81)], trig

92 Associations between BPA and TT differed according to sex in adolescents, wit

93 The observed associations between BPA, MnBP, and behavior in boys are consistent with prev

94 sure and 8-OHdG and 8-NO2Gua levels, between BPA and 8-isoPF2alpha levels, and between maternal CRP l

95 nisms explains the NMDR relationship between BPA and Ca(2+) entry in beta-cells.

96 mechanisms described a broader impact beyond BPA exposure and can be applied to understand other mode

97 ty and teratogenic effects of the bisphenols BPA, BPS, BPF, and BPAF in zebrafish embryo-larvae and a

98 On the other hand, Drp-1 inhibition blocked BPA-mediated Drp-1 translocation, leading to decreased a

99 Results of that analysis indicate that both BPA and EE have dose- and sex-specific impacts on the ce

100 g technique is used to determine the bounded BPA level by measuring the sample/electrode interfacial

101 f BPA from thermal paper receipts occurs but BPA pharmacokinetics following dermal exposure is not un

102 Impaired mitochondrial dynamics by BPA resulted in increased reactive oxygen species and ma

103 ort the induction of an adaptive response by BPA co-exposure that alters the microcellular environmen

104 For some cells, BPA caused rapid Ca(2+) transient loss without marked ch

105 serial urine samples to accurately classify BPA exposure and consider sociodemographic and environme

106 A complete BPA dose-response analysis of prostate lesions across mu

107 tors, and urinary creatinine concentrations, BPA, but not BPF or BPS, was significantly associated wi

108 CD-1 mice exposed to 4 to 40,000 mug/kg/day BPA or 0.02 to 2 mug/kg/day EE from conception until 12-

109 ant CD-1 mice were administered 25mug/kg/day BPA via osmotic minipumps from gestational day 8 through

110 The developed biosensor can detect BPA level in 20s and exhibits a large linear range from

111 We were able to detect BPA spiked in human serum as well as in maternal and cor

112 repeating the dermal exposure had detectable BPA-d16 in urine for 9 days, showed linear cumulative ex

113 ve sensing method that successfully detected BPA at femto molar (fM) levels, which is an improvement

114 Developmental BPA exposures heighten prostate cancer susceptibility in

115 d pyrosequencing revealed that developmental BPA exposure induced hypomethylation of the Nrf2 and Sre

116 In conclusion, dialyzer BPA content may contribute to BPA burden in patients on

117 e the pharmacokinetics of dermal and dietary BPA exposure, six male participants handled simulated re

118 Compared to dietary BPA exposure, dermal absorption of BPA leads to prolonge

119 ted with Sphingobium sp. BiD32, a documented BPA-degrading culture.

120 to carcinoma in rats given neonatal low-dose BPA with adult T+E but not in rats given adult T+E alone

121 By the last cycle of the day, enhanced BPA removal was lost, although it returned with the next

122 sed to simulate human digestion and evaluate BPA bioaccessibility in canned seafood for the first tim

123 Normal kidneys rapidly excrete BPA, but insufficient excretion may sensitize patients w

124 For BPA, we observed a nonsignificant inverse association wi

125 f DEHP metabolites and 1.22 (1.01, 1.47) for BPA] at median 10 wk and 26 wk, respectively.

126 for repeated mailing, 30.9% versus 3.6% for BPA, and 63.5% versus 2.0% for patient solicitation) and

127 epeated mailing, 13.2 [95% CI, 3.6-48.6] for BPA, and 32.9 [95% CI, 19.3-56.1] for patient solicitati

128 ntrations of 1.0, 1.0, 0.10, and 50 mg/L for BPA, BPF, BPAF, and BPS, respectively.

129 ve lower estimated pKa values than those for BPA.

130 oning were measured at several pH values for BPA, BPAF, and BPS.

131 cretion over 5 days, and had detectable free BPA-d16 in serum.

132 Proportions of free BPA-d16 in urine following dermal exposure (0.71%-8.3% o

133 at doses that yield undetectable serum free BPA.

134 lateral prostates despite undetectable free BPA 1 hr postexposure.

135 Serum free-BPA and BPA-glucuronide were quantitated in sera of indi

136 n volumes and disposal of products made from BPA, polycarbonate plastic and epoxy resins, BPA has ent

137 The rank order for toxicity was BPAF > BPA > BPF > BPS.

138 The rank order for estrogenicity was BPAF > BPA = BPF > BPS.

139 PA concentrations in 31 cashiers who handled BPA receipts were as likely to decrease as to increase a

140 estrogenic effects on gene expression, high BPA exposure activity ratios across all test sites, and

141 Higher BPA, BPF, and BPS concentrations were observed in obese

142 neurobehavioral outcomes with a doubling in BPA concentration and sex-specific associations.

143 tion with an interquartile range increase in BPA and phthalate concentrations and were weighted to re

144 We found that 4 hr post-damage initiation, BPA exposure and co-exposure transiently condensed chrom

145 Interestingly, BPA-mediated inhibitory effects on NSC proliferation and

146 c lobes was conducted that included internal BPA dosimetry, progression to adenocarcinoma with aging

147 Intracellular BPA in PBMCs increased after chronic hemodialysis with p

148 ning relevant levels of BPA (isotope-labeled BPA-d16) for 5 min, followed by hand-washing 2 h later.

149 nistic framework that may connect early-life BPA to later-life predisposition to prostate carcinogene

150 Nevertheless, Mn oxides may limit BPA migration in near-surface environments and have pote

151 Observational studies have linked BPA exposure to kidney and cardiovascular injury in huma

152 The lowest BPA dose initiated maximal hormonal carcinogenesis in la

153 with greatest hypomethylation at the lowest BPA doses.

154 s, the natural logarithm of SpG-adj maternal BPA concentration was inversely associated with infant A

155 specific gravity-adjusted (SPG-adj) maternal BPA concentrations and infant AGD, adjusting for covaria

156 We observed no association between maternal BPA and infant AGD-AF.

157 These findings demonstrate that maternal BPA exposure has dose- and sex-specific effects on pancr

158 Mean BPA levels increased after one hemodialysis session with

159 We measured BPA concentration in urine samples collected at approxim

160 demonstrated that abiotic processes mediate BPA transformation and mineralization in the absence of

161 ngi, algae and even higher plants metabolize BPA, but anaerobic microbial degradation has not been do

162 ulfone membranes released significantly more BPA into the culture medium and induced more cytokine pr

163 ats were briefly exposed to 0.1 to 5,000 mug BPA/kg BW on postnatal days (PND) 1, 3, and 5.

164 as previously observed in vivo, while 1 muM BPA significantly inhibited ductal growth.

165 tion rate, 12 sequential additions of 80 muM BPA are performed at pH 7.

166 At environmentally relevant doses (1 nM), BPA significantly increased ductal growth, as previously

167 ure to phthalates (p-trend < 0.0001) but not BPA; participants with high consumption (>/= 34.9% TEI f

168 ss are a function of prenatal exposure to NP/BPA and inflammation in 241 mother-fetus pairs.

169 The observed BPA, however, could be an impurity of tetrabromo-BPA (TB

170 Dermal absorption of BPA from thermal paper receipts occurs but BPA pharmacok

171 o dietary BPA exposure, dermal absorption of BPA leads to prolonged exposure and may lead to higher p

172 pt paper results in measurable absorption of BPA or the BPA alternatives bisphenol S (BPS) and 4-hydr

173 ereas there were significant associations of BPA exposure with general and abdominal obesity, BPF or

174 We examined the associations of BPA, BPF, and BPS exposure with obesity in U.S. adults.

175 range increase of urinary concentrations of BPA (1.53; 95% CI: 1.04, 2.25) and MEP (monoethyl phthal

176 samples were analyzed for concentrations of BPA and nine phthalate metabolites several times during

177 Urinary concentrations of BPA and several phthalate metabolites were significantly

178 The effect size and incremental costs of BPA intervention (excluding startup costs) support more

179 In some studies, the daughters of BPA-exposed dams have shorter AGD than controls.

180 In this study, aerobic degradation of BPA, BPAF, and BPS at 100 mug/kg soil and 22 +/- 2 degre

181 weaned on PND21 and exposed to same dose of BPA via their drinking water through PND35.

182 onic fibroblasts, exposure to a high dose of BPA was associated with changes in the cellular microenv

183 e found that exposure to increasing doses of BPA affected Ca(2+) entry in an NMDR manner.

184 Both doses of BPA significantly impaired insulin secretion in male but

185 For example, a doubling of BPA concentration was associated with 1-point (95% CI: 0

186 A doubling of BPA concentration was associated with poorer SRS-2 score

187 This effect of BPA was blocked by Fulvestrant, a full estrogen antagoni

188 uscle microsomes, we examined the effects of BPA and TBBPA on ryanodine receptor type 1 (RyR1), dihyd

189 We also observed dose-specific effects of BPA on islets in males.

190 patients with CKD to adverse the effects of BPA.

191 nvironment changes induced by co-exposure of BPA and KBrO3 versus either agent alone.

192 sed to two relevant human exposure levels of BPA (10mug/kg/d-LowerB and 10mg/kg/d-UpperB).

193 lated receipts containing relevant levels of BPA (isotope-labeled BPA-d16) for 5 min, followed by han

194 itment to the Srebp-1c promoter in livers of BPA-exposed mice was observed.

195 predictive understanding of the longevity of BPA and its transformation products in environmental sys

196 r rapid, sensitive and on-site monitoring of BPA in food samples.

197 ipt contained 1-2% by weight of the paper of BPA, BPS, or BPSIP.

198 , raising concern about the pervasiveness of BPA.

199 Receipts were analyzed for the presence of BPA or alternatives considered for use in thermal paper.

200 omparing the highest with lowest quartile of BPA, 1.02 (0.70-1.47) for BPF, and 1.22 (0.81-1.83) for

201 altered cellular excitability as a result of BPA-induced Vm hyperpolarization.

202 s suggest that there are multiple sources of BPA exposure in young children.

203 rothermal effect for long-range transport of BPA molecules toward electrode surface.

204 ighting health concerns regarding the use of BPA alternatives.

205 the effect of Mn oxide structural changes on BPA oxidation rate, 12 sequential additions of 80 muM BP

206 sulfone or BPA-free polynephron dialyzers on BPA levels in 69 prevalent patients on hemodialysis: 28

207 environmental exposure to phthalates and/or BPA to disrupt circulating vitamin D levels in pregnancy

208 dialysis with BPA-containing polysulfone or BPA-free polynephron dialyzers on BPA levels in 69 preva

209 ry levels of seven PEs metabolites, six PBs, BPA, and six dialkyl phosphate metabolites in five-hundr

210 We recently demonstrated that perinatal BPA exposure is associated with higher body fat, impaire

211 icients (ICCs) as a measure of within-person BPA variability and to identify sociodemographic and env

212 Once they enter the human body, PEs, BPA, PBs, and OPs are metabolized and/or conjugated and

213 sure of Greek preschool-age children to PEs, BPA, PBs, and OPs by investigating the urinary levels of

214 posure was linked to three main sources: PEs-BPA to plastic, PBs-diethyl phthalate to personal hygien

215 At this time point, BPA exposure and co-exposure also reduced the change in

216 We envision repurposing poly(BPA carbonate) for the production of value-added polymer

217 Pre-BPA and post-BPA screening rates were compared, and care of newly dia

218 ths prior to BPA to 72% over the 1 year post-BPA.

219 Pre-BPA and post-BPA screening rates were compared, and care

220 e estimated the association between prenatal BPA exposure and child neurobehavior at 3 y of age in a

221 Indeed, prenatal BPA exposure preferentially altered adult estrogen-respo

222 Our results suggest that prenatal BPA exposure may contribute to developmental origins of

223 isphenol A (2,2-bis[4-hydroxyphenyl]propane, BPA), the monomer used to produce polycarbonate plastic

224 hly sensitive methods are needed to quantify BPA in various matrices including water, serum, and food

225 Here, we quantify BPA oxidation rates and the formation of its predominant

226 BPA, polycarbonate plastic and epoxy resins, BPA has entered terrestrial and aquatic environments.

227 ic (Drp-1siRNA) inhibition of Drp-1 reversed BPA-induced mitochondrial dysfunctions, fragmentation, a

228 ynephron dialyzers reduced predialysis serum BPA (from 70.6+/-8.4 to 47.1+/-7.5 ng/ml, P<0.05).

229 not significantly increase predialysis serum BPA levels, although a trend toward increase was detecte

230 er but with different kind of sauces, showed BPA levels ranging from <1microgkg(-1) (limit of quantif

231 Specifically, BPA reduces growth during early development, followed by

232 ld successfully recover the levels of spiked BPA.

233 ntal leaching for Pb, Ba, Cr, Cu, Mn and Sr; BPA was detected in samples from polycarbonate container

234 excretion rates and creatinine-standardized BPA concentrations.

235 Similarly structured BPA analogues are widely used but far less is known abou

236 inear regression with continuous and tertile BPA concentrations.

237 This biosensor was applied to test BPA in canned food samples and could successfully recove

238 however, could be an impurity of tetrabromo-BPA (TBBPA) or TBBPA-based flame retardants.

239 cts to BPA and that BPAF is more potent than BPA, further highlighting health concerns regarding the

240 zed at a rate that is 12.6 times slower than BPA and accumulates in solution.

241 These results demonstrate that BPA degradation by environmentally relevant Mn(III/IV) o

242 We demonstrate that BPA deposition in the eggs of rainbow trout (Oncorhynchu

243 rogramming events, we have demonstrated that BPA exposure generates reactive oxygen species and promo

244 on in the absence of oxygen, indicating that BPA is susceptible to degradation under anoxic condition

245 The results suggest that BPA bioaccessibility was slightly lower in samples with

246 ly shorter AGD in daughters, suggesting that BPA may alter the hormonal environment of the female fet

247 The BPA had associated educational materials, order set, and

248 The BPA intervention had the lowest incremental cost per com

249 The BPA probes are converted to the corresponding benzocouma

250 In the BPA trial, data from 14,475 patients (BC, n = 8928; cont

251 sults in measurable absorption of BPA or the BPA alternatives bisphenol S (BPS) and 4-hydroxyphenyl 4

252 We thus show that these BPA alternatives induce similar toxic and estrogenic eff

253 ittle is known about exposure of cashiers to BPA and alternative compounds in receipt paper.

254 sion, dialyzer BPA content may contribute to BPA burden in patients on hemodialysis.

255 duce similar toxic and estrogenic effects to BPA and that BPAF is more potent than BPA, further highl

256 lowing question: does early-life exposure to BPA affect the obesity-related outcomes body weight, fat

257 ernal and/or ancestral embryonic exposure to BPA affects liver metabolism leading to development-dist

258 ht to determine whether in utero exposure to BPA altered the global CpG methylation pattern of the ut

259 m may prove useful in monitoring exposure to BPA and other small molecules in various matrices.

260 These results suggest that exposure to BPA from thermal paper should be considered when determi

261 Exposure to BPA in utero has been linked to female reproductive diso

262 Low-level exposure to BPA is ubiquitous in human populations due to its widesp

263 c review suggest that early-life exposure to BPA may increase adiposity and circulating lipid levels

264 Despite ubiquitous human exposure to BPA, and the wide-spread clinical use of EE as oral cont

265 potential source of occupational exposure to BPA, BPS, and BPSIP.

266 et for estrogens, and that oral exposures to BPA and EE can have estrogen-like immunomodulatory affec

267 cal and nonbiological processes that lead to BPA transformation and degradation, and identifies resea

268 In the 3 years prior to BPA implementation, 52,660 baby boomers were seen in pri

269 care provider visit in the 6 months prior to BPA to 72% over the 1 year post-BPA.

270 The sensor is responsive to BPA down to femto molar levels, but not to structurally

271 alf-lives of <1 day in both soils similar to BPA.

272 (0-7.5 h) were monitored for free and total BPA-d16.

273 few cashiers had detectable levels of total BPA or BPS in serum, whereas BPSIP tended to be detected

274 llowing dermal exposure (0.71%-8.3% of total BPA-d16) were generally higher than following the dietar

275 ticipants still had detectable urinary total BPA-d16 after 1 week.

276 After dietary exposure, urine total BPA-d16 peaked within 5 h and quickly cleared within 24

277 Higher first-trimester BPA exposure was associated with significantly shorter A

278 ecimens are required to characterize typical BPA exposure.

279 y lead to higher proportions of unconjugated BPA in systemic circulation.

280 Urinary BPA concentrations, which decreased over childhood, had

281 Urinary BPA, BPF, and BPS concentrations were measured using on-

282 t association between occupation and urinary BPA excretion among males.

283 Child urinary BPA concentrations were not associated with child anthro

284 ified based on occupation to compare urinary BPA excretion levels.

285 ship between longitudinally measured urinary BPA and phthalate metabolite concentrations during gesta

286 enstrual cycle-specific estimates of urinary BPA and phthalate metabolites were not associated with d

287 likely to have detectable levels of urinary BPA compared to individuals with unlikely occupational e

288 have significantly higher levels of urinary BPA excretion (geometric mean (GM): 5.45 mug/L, 95% CI:

289 ransformed serum TT and quartiles of urinary BPA, BP-3, TCS, and parabens in male and female children

290 Prenatal urinary BPA concentration was associated with some aspects of ch

291 found associations between prenatal urinary BPA concentrations and FMI, %BF, and WC.

292 Prenatal urinary BPA concentrations were positively associated with child

293 The GM urine BPA concentration was 2.78 ng/mL among males and 2.44 ng

294 The mean urine BPA concentrations in 31 cashiers who handled BPA receip

295 In utero BPA exposure altered the global CpG methylation profile

296 Utilizing BPA as a model exposure, pregnant CD-1 mice were adminis

297 ux of Ca(2+) from loaded microsomes, whereas BPA exhibited little or no activity at these targets.

298 urther work is required to determine whether BPA induces similar DNA lesions in vivo at environmental

299 sign, we studied the effect of dialysis with BPA-containing polysulfone or BPA-free polynephron dialy

300 24 hr post-damage initiation by KBrO3, with BPA-only samples timed to coincide with these designated