139 resultados para estradiol (E2)

em Repositório Institucional UNESP - Universidade Estadual Paulista "Julio de Mesquita Filho"


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Pós-graduação em Ciência e Tecnologia Animal - FEIS

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Chronic ethanol intake is associated with sex hormone disturbances, and it is well known that melatonin plays a key role in regulating several reproductive processes. We report the effects of ethanol intake and melatonin treatment (at doses of 100. μg/100. g. BW/day) on sex hormones and steroid receptors in the ovaries, oviducts and uteri of ethanol-preferring rats. After 150 days of treatment, animals were euthanized, and tissue samples were harvested to evaluate androgen, estrogen, progesterone and melatonin receptor subunits (AR, ER-α and ER-β, PRA, PRB and MT1R, respectively). Melatonin decreased estradiol (E2) and increased progesterone (P4) and 6-sulfatoxymelatonin (6-STM), while an ethanol-melatonin combination reduced both P4 and E2. Ovarian AR was not influenced by either treatment, and oviduct AR was reduced after ethanol-melatonin combination. Oviduct ER-α, ER-β and uterine ER-β were down-regulated by either ethanol or melatonin. Conversely, ovarian PRA and PRB were positively regulated by ethanol and ethanol-melatonin combination, whereas PRA was down-regulated in the uterus and oviduct after ethanol consumption. MT1R was increased in ovaries and uteri of melatonin-treated rats. Ethanol and melatonin exert opposite effects on E2 and P4, and they differentially regulate the expression of sex steroid receptors in female reproductive tissues. © 2013 Elsevier Inc.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Among the sexual hormones the estrogens are receiving major attention due to their biological activity. Such biological response is atributed to the best conformation recognized by their receptors, resulting in maximum responses. The estrogens are also considered responsible for most of disruptor´s effects caused by their presence in aquatic ecosystems. The 17β-estradiol hormone is produced by vertebrates during the reproductive phase of their lives and its presence has been detected in superficial waters. The objective of this study was to evaluate the cause-effect of tilapia exposition to the hormone 17β-estradiol through the analysis of biotransformation enzymes in liver and gills, complemented with the quantification of 17β-estradiol and estrone in water samples collected from fish ponds integrated to swine production. The present study was conducted under laboratory conditions, in a randomized experimental design with three levels of 17β-estradiol (E2) (0, 5, 15 µg L-1), with three replicates. After 7 days of exposure time, liver and gills were extracted to analyze three isoforms of cytochrome P450: EROD, BROD, PROD and the activity of Glutathione S-Transferase (GST). The results showed that the EROD activity (CYP1A), normally induced by the metabolism of aromatic compounds, did not present statistical differences among the treatments exposed to E2, what means that the hormone did not induce isoform 1A in fish under these particular experimental conditions. PROD activity was significantly altered in both concentrations, by means of 5 and 15 µg L-1, when compared to control. This result can indicate an important role of PROD on the metabolism of E2 present in water. Regarding to the BROD activity, it could be observed differences statistically significant between control and both groups of treatments. Two or more CYP isoforms can contribute to the metabolism of the same compound, what makes BROD a candidate as a next bioindicator of the exposure to E2 in aquatic ecosystems. Analysis of variance could confirm the effect of E2 statistically significant on the GST activity in liver tissues with >90% of significance (Prob>F = 0.0753). Furthermore, it was possible to observe that the values of GSTs activities in liver and gills in both, control and treatments, follow a tendency, that means, enzymatic activity in gills increase as the increasing of the activity in the liver tissues. In this study, the 17β–estradiol was found in measurable concentrations in three sampled points, and these values were similar to the findings of other authors at different locations in Brazil. In addition, those values are much higher than the minimum concentration that presented observable effects (10 ng L-1).

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Progesterone (P-4), 17 beta- estradiol (E2) and androstenedione (A4) plasma concentrations were correlated with palpated corpora lutea (CL), recovered embryos and viable embryos in 13 Nelore cows induced to superovulate with FSH, starting on Day 10 of the estrous cycle. Administration of FSH increased the number of ovulations and recovered embryos. Plasma P4, E2 and A4 levels on Day O and of P4 on Days 10 and 11 of the cycle were not correlated with the superovulatory response. Determination of CL by palpation per rectum was used to estimate the number of recovered embryos. Plasma P4 levels higher than 1 ng/ml on the induced estrus day (Day 14) had an adverse effect on the embryo viability rate. Plasma E2 concentrations on Day 14 were positively correlated with the number of viable embryos collected, a correlation that has not been previously reported. The present data indicate that plasma P4 and E2 concentrations in FSH-PGF2 alpha-treated Nelore cows are useful for the identification of 2 different populations of Nelore donors and are correlated with superovulatory response and, particularly, with the number of viable embryos.

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In the aquatic environment, biotransformation enzymes are established biomarkers for assessing PAH exposure in fish, but little is known about the effect of 17β-estradiol (E2) on these enzymes during exposure to benzo(a)pyrene (BaP). In this study, Nile tilapia (Oreochromis niloticus) were exposed for 3, 5, and 10 days to BaP (300 μg L(-1)) and E2 (5 μg L(-1)). These substances were applied isolated or mixed. In the mixture experiment, fish were analyzed pre- and postexposure in order to better understand whether preexposure to the hormone masks the responses activated by PAH or vice versa. Phase I enzymes ethoxyresorufin-O-deethylase (EROD), pentoxyresorufin-O-depenthylase (PROD), and benzyloxyresorufin-O-debenzylase (BROD) activities as well as the phase II enzyme glutathione S-transferase (GST) were analyzed. Isolated E2 treatment decreased EROD activity after 3 days, but this enzyme activity returned to control values after 5 and 10 days of exposure. Isolated BaP treatment significantly induced EROD activity after 3 and 5 days, and the activity returned to control levels after ten exposure days. Combined treatment (E2 + Bap) significantly increased EROD activity, both in the pre- and postexposure. This increase was even higher than in the isolated BaP treatment, suggesting a synergism between these two compounds. When E2 and BaP were used singly, they did not change BROD and PROD activities. However, combined treatment (E2 + Bap) significantly increased PROD activity. Isolated BaP treatment increased GST activity after 10 days. However, this response was not observed in the mixture treatment, suggesting that E2 suppressed the GST induction modulated by BaP. The results put together indicated that E2 altered the biotransformation pathway regarding enzymes activated by BaP in Nile tilapia.

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Androgen exposure during sexual development induces alterations in steroidal target tissues. The objective of this study was to evaluate the uterine responsiveness to estradiol after perinatal androgenization. Pregnant Wistar rats were exposed to corn oil or testosterone propionate at 0.05, 0.1, or 0.2 mg/kg from gestational day 12 until postnatal day 21. Female offspring was challenged with estradiol (E2 ) after weaning (0.4 mg/kg) and at adulthood (10 or 100 µg/day), when the pituitary response was also evaluated. At adulthood, control and 0.05 mg/kg groups presented a uterine weight increment when exposed to 100 µg/day of E2 , 0.1 mg/kg group only responded to 10 µg/day of E2 , and the 0.2 mg/kg group showed increased uterine weight at both doses. The pituitary weight was similarly increased after estradiol stimulation in all experimental groups. In conclusion, testosterone propionate exposure induced an abnormal stimulation of uterine tissue growth by estrogen stimulus without affecting pituitary response. More studies are needed to clarify whether these alterations are capable of impairing the reproductive capacity of the female tract. © 2015 Wiley Periodicals, Inc. Environ Toxicol, 2015.

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