Expression of the estrogen receptor alpha (ERα) and the androgen receptor (AR) in CAMA-1, MCF-7, and MCF7-AR1 breast cancer cell lines at the protein level

Cell extracts were prepared during exponential proliferation in maintenance medium containing 10% fetal bovine serum. Immunoblots were performed as described in Materials and methods. A representative immunoblot. Relative expression of sex steroid receptors quantified to actin content. Each bar represents the mean ± standard error of the mean of four independent experiments. Double asterisk indicates < 0.01 versus wild-type MCF-7 cells as determined by an analysis of variance followed by a Bonferroni test.<p><b>Copyright information:</b></p><p>Taken from "1,1-dichloro-2,2-bis(-chlorophenyl)ethylene (-DDE) disrupts the estrogen-androgen balance regulating the growth of hormone-dependent breast cancer cells"</p><p>http://breast-cancer-research.com/content/10/1/R16</p><p>Breast Cancer Research : BCR 2008;10(1):R16-R16.</p><p>Published online 14 Feb 2008</p><p>PMCID:PMC2374972.</p><p></p

-DDE modulates the expression of sex-steroid-dependent genes in CAMA-1 cells at the mRNA level

mRNA levels were determined by a semiquantitative polymerase chain reaction after a 24-hour treatment with hormones and antiandrogens (or vehicles) as described in Materials and methods. mRNAs for , , , and were quantified relative to mRNA. A representative gel electrophoresis is shown below each panel. Each bar represents the mean ± standard error of the mean of six independent experiments. Double asterisk indicates < 0.01 versus control, †† indicates < 0.01 versus Etreatment, and ‡ and ‡‡ indicate, respectively, < 0.05 and < 0.01 versus E+DHT treatment as determined by an analysis of variance with specific contrasts. AR, androgen receptor; DHT, dihydrotestosterone; E, 17β-estradiol; ERα, estrogen receptor alpha; OHF, hydroxyflutamide; -DDE, 1,1-dichloro-2,2-bis(-chlorophenyl)ethylene.<p><b>Copyright information:</b></p><p>Taken from "1,1-dichloro-2,2-bis(-chlorophenyl)ethylene (-DDE) disrupts the estrogen-androgen balance regulating the growth of hormone-dependent breast cancer cells"</p><p>http://breast-cancer-research.com/content/10/1/R16</p><p>Breast Cancer Research : BCR 2008;10(1):R16-R16.</p><p>Published online 14 Feb 2008</p><p>PMCID:PMC2374972.</p><p></p

-DDE modulates the expression of sex-steroid-dependent genes in CAMA-1 cells at the protein level

Immunoblots were performed after 24 hours of treatment with hormones and antiandrogens (or vehicles) as described in Materials and methods. Cyclin D1 , ERα , and AR protein levels were quantified relative to actin content. Each bar represents the mean ± standard error of the mean of six independent experiments. A representative immunoblot is shown below each panel. Single asterisk indicates < 0.05 and double asterisk < 0.01 versus control; † and †† indicate, respectively, < 0.05 and < 0.01 versus Etreatment; and ‡ and ‡‡ indicate, respectively, < 0.05 and < 0.01 versus E+DHT treatment as determined by an analysis of variance with specific contrasts. AR, androgen receptor; DHT, dihydrotestosterone; E, 17β-estradiol; ERα, estrogen receptor alpha; OHF, hydroxyflutamide; -DDE, 1,1-dichloro-2,2-bis(-chlorophenyl)ethylene.<p><b>Copyright information:</b></p><p>Taken from "1,1-dichloro-2,2-bis(-chlorophenyl)ethylene (-DDE) disrupts the estrogen-androgen balance regulating the growth of hormone-dependent breast cancer cells"</p><p>http://breast-cancer-research.com/content/10/1/R16</p><p>Breast Cancer Research : BCR 2008;10(1):R16-R16.</p><p>Published online 14 Feb 2008</p><p>PMCID:PMC2374972.</p><p></p

Effects of Intravenous Benzo[a]Pyrene Dose Administration on Levels of Exposure Biomarkers, DNA Adducts, and Gene Expression in Rats

<div><p>The effects of benzo[a]pyrene (BaP) administration on biomarkers of exposure and early effects were studied in male Sprague-Dawley rats intravenously injected with doses of 0.4, 4, 10, or 40 μmol BaP/kg . Blood, tissues, and excreta were collected 8 and 24 h posttreatment. BaP and several of its metabolites were simultaneously measured in blood, tissues and excreta by ultra-high-performance liquid chromatography (UHPLC)/fluorescence. DNA adducts of BaP diol epoxide (BaPDE) in lungs were quantified using an ultrasensitive immunoassay with chemiluminescence detection. Expression of selected genes in lungs of treated rats (lung RNA) compared to control rats was also assessed by quantitative real-time polymerase chain reaction. There was a dose-dependent increase in blood, tissue, and excreted levels of BaP metabolites. At 8 and 24 h postinjection, BaP and hydroxyBaP were found in higher concentrations in blood and tissues compared to other analytes. However, diolBaP were excreted in greater amounts in urine and apparently more rapidly than hydroxyBaP. Mean percentages (± SD) of injected dose excreted in urine as 4,5-diolBaP during the 0–8 h and 0–24 h period posttreatment were 0.16 ± 0.027% and 0.14 ± 0.083%, respectively. Corresponding values for 3-OHBaP were 0.0045 ± 0.0009% and 0.026 ± 0.014%. BaP-diones were not detectable in blood, tissues, and excreta; 7,8-diolBaP and BaPtetrol were found to be minor metabolites. There was also a dose-dependent increase in DNA adduct formation in lung. Analysis of gene expression further showed a modulation of <i>Cyp1a1, Cyp1b1, Nqo1, Nrf2, Fos</i>, and <i>Ahr</i> expression at 10- and 40-μmol/kg doses, but not at the lower doses. This study provided a better assessment of the influence of absorbed BaP doses on biological levels of diolBaP and OHBaP exposure biomarkers and association of the latter with early biological alterations, such as DNA adducts and gene expression.</p></div

Distribution of the infant blood lead levels at 12 months.

<p>Distribution of the infant blood lead levels at 12 months.</p

Univariate analyses of variables associated with malaria risk at 12 months.

<p>Univariate analyses of variables associated with malaria risk at 12 months.</p

Negative binomial regression on factors associated with <i>P</i>.<i>falciparum</i> density (logarithm of parasite density at lead assessment).

<p>Negative binomial regression on factors associated with <i>P</i>.<i>falciparum</i> density (logarithm of parasite density at lead assessment).</p

Logistic regression on the possibility of having a positive blood smear at 12 months.

<p>Logistic regression on the possibility of having a positive blood smear at 12 months.</p

Linear regression on factors associated with <i>P</i>.<i>falciparum</i> density at 12 months (logarithm of parasite density at lead assessment).

<p>Linear regression on factors associated with <i>P</i>.<i>falciparum</i> density at 12 months (logarithm of parasite density at lead assessment).</p

Demographic and clinical characteristics of the infants.

<p>Demographic and clinical characteristics of the infants.</p