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Mechanisms of action for estrogen in cardioprotection
Published in Barry G. Wren, Progress in the Management of the Menopause, 2020
All hydroxyphenolic compounds, including estrogens, have antioxidant properties in vitro28. Since free radicals are continually generated by living cells, it was suggested that estrogens indirectly may affect cells in vivo by interacting with free radicals. The antioxidant effects of estrogens depend on the type of estrogen, and on its concentrations. Based on a number of studies28–35, the order of potency is diethyl-stilbestrol (DES) > 17α-ethinylestradiol > 2-hydroxyestradiol (catecholestrogens) > 17β-estradiol mestranol, equillins, estrone. Interestingly, 17α-estradiol, commonly regarded as a non-active estrogen, also has antioxidant properties by virtue of the hydroxyphenolic ring. Also of importance are the findings that estrogens exert antioxidant effects in vitro only at micromolar concentrations. However, in vivo 17β-estradiol may be an antioxidant at physiological (nanomolar) concentrations36.
Steroids and Brain Cell Activity During the Menstrual Cycle
Published in Diana L. Taylor, Nancy F. Woods, Menstruation, Health, and Illness, 2019
When 17β-estradiol was applied on a number of spontaneously active rat cerebral cortical neurons, the most frequently observed responses were either a decrease in the rate of spontaneous firing (44%) occurring within 1–2 min of the onset of steroid application or the absence of any change in the spontaneous activity (47%) (Phillis & O’Regan, 1988). An increase in firing rate was observed with a few neurons (9%). Firing rates returned to control levels within a few minutes of the cessation of steroid application. 17α-estradiol, a weak or inactive estrogen with no effect on reproductive function, was used as a control for the effects of the 17β-isomer. It also had a mild depressant action on the firing cerebral cortical neurons, which may have been a result of its weak ability to inhibit adenosine transport (Phillis et al., 1985).
The Biochemistry of the 17-Hydroxysteroid Dehydrogenases
Published in Ronald Hobkirk, Steroid Biochemistry, 1979
The 17-hydroxysteroid dehydrogenases consist of the 17β and 17α enzyme groups. This division is based on the stereospecificity of the enzymatic reaction at C-17 of the steroid substrate; 17β-hydroxysteroid dehydrogenases catalyze the interconversion of the 17-keto- and 17β-hydroxysteroids while 17α-hydroxysteroid dehydrogenases catalyze the interconversion of 17-keto- and 17α-hydroxysteroids. 17β-Hydroxysteroid dehydrogenase activity is present in all mammalian species, however, 17α-hydroxysteroid dehydrogenase activity is found primarily in species which excrete the 17α-epimers of estrogens and androgens. For example, in ruminants and the rabbit,10 17α-estradiol is the major urinary metabolite of 17β-estradiol. The transformation of 17β-estradiol to 17α-estradiol has been demonstrated in the rabbit both in vivo11 and in vitro.12 Using 17β-estradiol labeled with tritium at the 17α-position, Williams et al.13 showed that the in vivo conversion of this compound to 17α-estradiol proceeded via estrone and not by epimerization. Thus, in this species, the metabolism of 17β-estradiol involves both the 17β- and α-hydroxysteroid dehydrogenases. In general, the conversion of the 17β-epimers of the Cl8 and Cl9 steroids to the 17α-epimers follows the reaction sequence demonstrated with the rabbit, although Szamatowicz et al.14 has suggested (from in vitro studies with guinea pig ovaries and testes) that direct conversion of testosterone to epitestosterone by epimerization could occur.
An insight into the neuroprotective effects and molecular targets of pomegranate (Punica granatum
) against Alzheimer’s disease
Published in Nutritional Neuroscience, 2023
Namy George, Majed AbuKhader, Khalid Al Balushi, Bushra Al Sabahi, Shah Alam Khan
Pirzadeh et al. in 2020 have reviewed in detail the chemical constituents present in the pomegranate fruit extract which proved to contain approximately 85.4% water, 10.6% sugar, 1.4% pectin and 0.2–1% polyphenols [30]. Most of the antioxidant property of the fruit is due to the water-soluble tannins found in the peel which accounts for nearly 92% of the total antioxidant activity. Tannins are capable of undergoing hydrolysis with and without the help of enzymes. Ellagitannins (ETs), gallotannins and punicalagin are some of the hydrolyzable tannins present in the different parts of the pomegranate. As a matter of fact, the hydrolzyed products like ellagic acid are partly metabolized by gut bacteria producing demethyellagic acid glucuronide, urolithin derivatives and several other metabolites. These metabolites could also be responsible for the health benefits of the consumption of pomegranate [44]. Furthermore, pomegranate seed oil (PSO) consists of fatty acids such as punicic acid, linoleic acid and oleic acids (Figure 1). The major constituents of PSO are steroidal and non-steroidal estrogens. Steroidal estrogen in the seed oil comprises tocopherol, testosterone, stigmasterol, β-estrolsitosterol, 17-α-estradiol and the nonsteroidal estrogen comprises coumestrol and campestral [30]. There is a high variation seen in the pomegranate’s bioactive constituents depending upon the environmental conditions it is grown [5].
Primary choice of estrogen and progestogen as components for HRT: a clinical pharmacological view
Published in Climacteric, 2022
CEEs are primarily produced by extraction from the urine of pregnant mares (which may also raise the question of animal welfare), where the lowest layer contains 50–65% sodium estrone sulfate, the middle layer contains up to 30% different (not all specified) equine (i.e. not human) estrogens and the upper layer contains the second important content of the mixture, 20–35% sodium equilin sulfate. The main components of CEE, as well as of so-called ‘conjugated estrogens’ (also from horses or in part synthetically produced), are sodium estrone sulfate and sodium equilin sulfate. These components can vary between 52.5–61.5% and 22.5–30.5%, respectively, according to the United States Pharmacopeia 27 (USP 27) defined in Martindale [11], one of the main sources for clinical pharmacologists regarding the description of drug properties. The total of the combined two should be between 79.5 and 88% [11]. For standardization, the registration offices only ask in terms of these two estrogens. In addition, these mixtures should contain 13.5–19.5% 17-α-dihydro-equilin, 2.5–9.5% 17-α-estradiol and 0.5–4.0% of 17β-dihydro-equilin, all as sulfates [11].
Paraben concentrations found in human body fluids do not exert steroidogenic effects in human granulosa primary cell cultures
Published in Toxicology Mechanisms and Methods, 2020
Elena Herrera-Cogco, Bruno López-Bayghen, Dinorah Hernández-Melchor, Almena López-Luna, Cecilia Palafox-Gómez, Leticia Ramírez-Martínez, Estheisy López-Bello, Arnulfo Albores, Esther López-Bayghen
The apparent toxicity of parabens has been described at two levels: estrogenic activity and mitochondrial toxicity. Parabens have been proposed to act as estrogens by binding to the uterine estrogen receptor (ER), as demonstrated in a mouse model (Routledge et al. 1998). Moreover, parabens are shown to promote ER-dependent transcriptional activity in yeast and MCF-7 cells (Routledge et al. 1998; Okubo et al. 2001), with a side-chain length dependency. Methylparaben (MPB) is the least potent disruptor, while butylparaben (BPB) is the most potent ‘estrogen’, 5-fold lower than that of 17α-estradiol (Routledge et al. 1998). In vivo, parabens are associated with weak estrogenic activity (6-fold lower than 17β-estradiol) in the vitellogenin assay in fish (10 mg/kg) and in uterotrophic assays in rodents (400–600 mg/kg) (Routledge et al. 1998; Hossaini et al. 2000; Alslev et al. 2005). According to the National Toxicology Program review for BPB, the overall mean applied exposure for women is about 0.12 mg/kg (Masten and Program 2005), which is 80- to 5000-fold less than doses used in the in vivo models.