Chicken Cytochrome P450, Family 19, Subfamily A, Polypeptide 1 ELISA Kit (DEIA-BJ2938)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Serum, plasma, cell culture supernatants, body fluid and tissue homogenate
Species Reactivity
Intended Use
Chicken Cytochrome P450, Family 19, Subfamily A, Polypeptide 1 ELISA Kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of the Cytochrome P450, Family 19, Subfamily A, Polypeptide 1. This ELISA kit is for research use only, not for therapeutic or diagnostic applications.
Contents of Kit
2. ENZYME CONJUGATE: 6.0 mL or 10 ml
3. STANDARD A-F: 1 vial each
7. WASH SOLUTION (100 x): 10 mL
All components of this kit are stable at 2-8°C until the kit's expiration date.
Detection Range
50-1000 pg/mL
1.0 pg/mL


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Bioaccumulation and biochemical effects of ethylhexyl methoxy cinnamate and its main transformation products in zebrafish


Authors: Zhou, Ranran; Lu, Guanghua; Yan, Zhenhua; Bao, Xuhui; Zhang, Peng; Jiang, Runren

The purpose of this study was to investigate the bioaccumulation and biochemical responses exposed to one of the main organic ultraviolet (UV) pollutants in the environment, ethylhexyl methoxy cinnamate (EHMC), and its main transformation product, either alone or in combination in zebrafish (Danio rerio). Four-month-old zebrafish were exposed to EHMC (34.4, 344 nmol/L) solution for 14 days, the species and contents of EHMC transformation products in zebrafish were determined and 3,5-dichloro-2-hydroxyacetophenone (3,5DCl(2)HAcP) was the one with the highest concentration in transformation products. Then, zebrafish were exposed to EHMC, 3,5DCl(2)HAcP alone and mixed solution for 21 days. At 7, 14 and 21 d, the related indexes of antioxidant defense system were determined. Results showed that both EHMC and 3,5DCl(2)HAcP can lead to the increase of malondialdehyde (MDA) and glutathione (GSH) contents, superoxide dismutase (SOD), catalase (CAT) and glutathione reductase (GR) activities in visceral mass compared with the corresponding control group, thus produced oxidative stress effect in organism and 3,5DCl(2)HAcP even showed stronger oxidative stress than EHMC. The effects of the two lower concentration co-exposure groups were similar and more significant to that of single exposure groups, while excessive oxidative stress occurred at the highest co-exposure group indicated by the decrease of GSH content, SOD, CAT, GR activities and the continued increase of MDA content. At 21 d, estradiol (E-2), vitellogenin (Vtg) and testosterone (T) contents, estrogen receptor (Esr), progesterone receptor (Pgr), androgen receptor (Ar), Vtgl, P450 aromatase (Cyp19a1) and 17 beta-hydroxysteroid dehydrogenase (Hsd17b3) expression were all significantly increased when exposed to 3,5DCl(2)HAcP alone, showing complex estrogen and androgen effects. When exposed to EHMC alone, E-2 and Vtg contents, Esr, Pgr, Vtgl, Cyp19a1 and Hsd17b1 gene expression levels decreased significantly, and T content and Ar and Hsd17b3 expression increased significantly, indicated that EHMC can produce anti-estrogen and androgen effect. Last, the decrease of estrogen effect and increase of androgen effect in co-exposure group suggested that 3,5DCl(2)HAcP might weaken the estrogen effect and promote the androgen effect of EHMC.

CTBP1/CYP19A1/estradiol axis together with adipose tissue impacts over prostate cancer growth associated to metabolic syndrome


Authors: Massillo, Cintia; Dalton, Guillermo Nicolas; Porretti, Juliana; Scalise, Georgina Daniela; Farre, Paula Lucia; Piccioni, Flavia; Secchiari, Florencia; Pascuali, Natalia; Clyne, Colin; Gardner, Kevin; De Luca, Paola; De Siervi, Adriana

Metabolic syndrome (MeS) increases prostate cancer (PCa) risk and aggressiveness. C-terminal binding protein 1 (CTBP1) is a transcriptional co-repressor of tumor suppressor genes that is activated by low NAD(+)/NADH ratio. Previously, our group established a MeS and PCa mice model that identified CTBP1 as a novel link associating both diseases. We found that CTBP1 controls the transcription of aromatase (CYP19A1), a key enzyme that converts androgens to estrogens. The aim of this work was to investigate the mechanism that explains CTBP1 as a link between MeS and PCa based on CYP19A1 and estrogen synthesis regulation using PCa cell lines, MeS/PCa mice and adipose co-culture systems. We found that CTBP1 and E1A binding protein p300 (EP300) bind to CYP19A1 promoter and downregulate its expression in PC3 cells. Estradiol, through estrogen receptor beta, released CTBP1 from CYP19A1 promoter triggering its transcription and modulating PCa cell proliferation. We generated NSG and C57BL/6J MeS mice by chronically feeding animals with high fat diet. In the NSG model, CTBP1 depleted PCa xenografts showed an increase in CYP19A1 expression with subsequent increment in intratumor estradiol concentrations. Additionally, in C57BL/6J mice, MeS induced hypertrophy, hyperplasia and inflammation of the white adipose tissue, which leads to a proinflammatory phenotype and increased serum estradiol concentration. Thus, MeS increased PCa growth and Ctbp1, Fabp4 and IL-6 expression levels. These results describe, for the first time, a novel CTBP1/CYP19A1/Estradiol axis that explains, in part, the mechanism for prostate tumor growth increase by MeS.

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