Treatment of ovariectomized rats with 17β-estradiol increases hepatic delta-6 desaturase enzyme expression and docosahexaenoic acid levels in hepatic and plasma phospholipids

2013 ◽  
Vol 89 (2-3) ◽  
pp. 81-88 ◽  
Author(s):  
Alex P. Kitson ◽  
Kristin A. Marks ◽  
Brittany Shaw ◽  
David M. Mutch ◽  
Ken D. Stark
Keyword(s):  
Docosahexaenoic Acid ◽  
Ovariectomized Rats ◽  
Enzyme Expression ◽  
Plasma Phospholipids ◽  
17Β Estradiol ◽  
Delta 6 Desaturase

scholarly journals Less Carcinogenic Chlorinated Estrogens Applicable to Hormone Replacement Therapy

2021 ◽  
Vol 22 (13) ◽  
pp. 7222
Author(s):  
Yoshinori Okamoto ◽  
Hideto Jinno ◽  
Shinji Itoh ◽  
Shinya Shibutani
Keyword(s):  
Hormone Replacement Therapy ◽  
Replacement Therapy ◽  
Hormone Replacement ◽  
Metabolic Activation ◽  
Ovariectomized Rats ◽  
Estrogenic Potential ◽  
Carcinogenic Potential ◽  
Induced Tumors ◽  
Carcinogenic Effects ◽  
17Β Estradiol

Human estrogens prescribed for hormone replacement therapy (HRT) are known to be potent carcinogens. To find safer estrogens, several chlorinated estrogens were synthesized and their carcinogenic potential were determined. A pellet containing either 2-chloro-17β-estradiol (2-ClE2) or 4-chloro-17β-estradiol (4-ClE2) was implanted subcutaneously for 52 weeks into August Copenhagen Irish (ACI) rats, a preferred animal model for human breast cancer. 17β-Estradiol (E2) frequently induced mammary tumors while both 2-ClE2 and 4-ClE2 did not. Their 17α-ethinyl forms, thought to be orally active estrogens, were also synthesized. Neither 2-chloro-17α-ethinylestradiol (2-ClEE2) nor 4-chloro-17α-ethinylestradiol (4-ClEE2) induced tumors. The less carcinogenic effects were supported by histological examination of mammary glands of ACI rats treated with the chlorinated estrogens. A chlorine atom positioned at the 2- or 4-position of E2 may prevent the metabolic activation, resulting in reducing the carcinogenicity. 2-ClE2 and 4-ClE2 administered subcutaneously and 2-ClEE2 and 4-ClEE2 given orally to ovariectomized rats all showed uterotrophic potency, albeit slightly weaker than that of E2. Our results indicate that less carcinogenic chlorinated estrogens retaining estrogenic potential could be safer alternatives to the carcinogenic estrogens now in use for HRT.

The impact of exogenous estrogens on biochemical markers of endothelial dysfunction in diabetic rats with hypoestrogenia

2017 ◽  
Vol 59 (1) ◽  
pp. 46-52
Author(s):  
Tetiana Kiprich ◽  
Nataliia Gorbenko ◽  
Oleksii Borikov ◽  
Olha Ivanova ◽  
K. V. Taran
Keyword(s):  
Endothelial Dysfunction ◽  
Biochemical Markers ◽  
Diabetic Rats ◽  
Ovariectomized Rats ◽  
Receptor Modulator ◽  
17Β Estradiol ◽  
The Impact ◽  
Gender Specific ◽  
Specific Agent

It was investigated the impact of selective estrogen receptor modulator PE0607 comparing to 17β-estradiol on the biochemical markers of endothelial dysfunction in ovariectomized rats with type 2 diabetes. It was established that injection of PE0607 as well as 17β-estradiol decreases lipid peroxidation first products in serum and increases serum whole antioxidant activity and NO-synthase activity in vessels of experimental rats. These results justify the perspectives of compound PE0607 use as a potential gender-specific agent for prevention and treatment of diabetic cardiovascular disorders in women with hypoestrogenia.

scholarly journals Docosahexaenoic acid is selectively enriched in plasma phospholipids during pregnancy in Trinidadian women – Results of a pilot study

2006 ◽  
Vol 46 (1) ◽  
pp. 63-67 ◽  
Author(s):  
Graham C. Burdge ◽  
Rachel C. Sherman ◽  
ZulaikaAli ◽  
Stephen A. Wootton ◽  
Alan A. Jackson
Keyword(s):  
Pilot Study ◽  
Docosahexaenoic Acid ◽  
Plasma Phospholipids

Estradiol-induced attenuation of pulmonary hypertension is not associated with altered eNOS expression

2001 ◽  
Vol 280 (1) ◽  
pp. L88-L97 ◽  
Author(s):  
Thomas C. Resta ◽  
Nancy L. Kanagy ◽  
Benjimen R. Walker
Keyword(s):  
Pulmonary Hypertension ◽  
Chronic Hypoxia ◽  
Vascular Tissue ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Inhibitory Influence ◽  
Enos Expression ◽  
17Β Estradiol ◽  
Spermine Nonoate ◽  
Endothelial Nitric Oxide

Female rats develop less severe pulmonary hypertension (PH) in response to chronic hypoxia compared with males, thus implicating a potential role for ovarian hormones in mediating this gender difference. Considering that estrogen upregulates endothelial nitric oxide (NO) synthase (eNOS) in systemic vascular tissue, we hypothesized that estrogen inhibits hypoxic PH by increasing eNOS expression and activity. To test this hypothesis, we examined responses to the endothelium-derived NO-dependent dilator ionomycin and the NO donors S-nitroso- N-acetylpenicillamine and spermine NONOate in U-46619-constricted, isolated, saline-perfused lungs from the following groups: 1) normoxic rats with intact ovaries, 2) chronic hypoxic (CH) rats with intact ovaries, 3) CH ovariectomized rats given 17β-estradiol (E2β), and 4) CH ovariectomized rats given vehicle. Additional experiments assessed pulmonary eNOS levels in each group by Western blotting. Our findings indicate that E2β attenuated chronic hypoxia-induced right ventricular hypertrophy, pulmonary arterial remodeling, and polycythemia. Furthermore, although CH augmented vasodilatory responsiveness to ionomycin and increased pulmonary eNOS expression, these responses were not potentiated by E2β. Finally, responses to S-nitroso- N-acetylpenicillamine and spermine NONOate were similarly attenuated in all CH groups compared with normoxic control groups. We conclude that the inhibitory influence of E2β on chronic hypoxia-induced PH is not associated with increased eNOS expression or activity.

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