Estradiol-17β as an antioxidant: Some distinct features when compared with common fat-soluble antioxidants

Ayres, Stacey A.; Tang, Maoyun; Subbiah, M.T.R.

doi:10.1016/s0022-2143(96)80008-4

Cited by 100 publications

(55 citation statements)

References 33 publications

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“…32,33 However, in our data, oestradiol has no effect on the lipid peroxidation for some unknown reason. The normal physiological level of oestrogen is 0.5 ng/ml.…”

Section: Eyecontrasting

confidence: 63%

Rapid action of oestradiol against hydrogen peroxide-induced oxidative stress in cataractous lens epithelium: an in vitro study

Gajjar¹,

Patel²,

Alapure³

et al. 2008

Eye

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Purpose To evaluate the short-term protective effects of oestradiol against damages because of oxidative stress in human lens epithelial cells (LECs). Methods The central zone of human lens epithelium was obtained from the cataract surgery and cultured in MEM culture medium. These cultured LECs were treated with 17b-oestradiol for varying time intervals from 1 to 5 min followed by treatment with H 2 O 2 (5 Â 10 À6 M) in the culture medium. Catalase activity was measured to access the oxidative stress levels. Results LECs exposed to H 2 O 2 (5 Â 10 À6 M) showed a fourfold increase in catalase activity (407.03±89.11 U/lg protein) after 6 h when compared to cultured unexposed LECs (97.124±9.4 U/lg protein). When the cultured LECs were treated with oestradiol (5 Â 10 À8 M) before H 2 O 2 treatment, the increase in catalase activity was inhibited, whereas simultaneous and post-treatments showed no effect. The catalase activity of LECs pretreated with oestradiol for 1, 2, 3 ,and 5 min was 259. 92±18.37, 200.24±14.39, 140.50±19.83, and 110.01±14.66, respectively (Po0.0001). Conclusion Antioxidative enzymes are synthesized in response to the oxidative stress signal. Upon treatment with oestrogen catalase is not synthesized. The pretreatment time of oestrogen required for its antioxidative effect can be seen within 5 min indicating non-genomic mode of action of oestrogen.

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“…32,33 However, in our data, oestradiol has no effect on the lipid peroxidation for some unknown reason. The normal physiological level of oestrogen is 0.5 ng/ml.…”

Section: Eyecontrasting

confidence: 63%

Rapid action of oestradiol against hydrogen peroxide-induced oxidative stress in cataractous lens epithelium: an in vitro study

Gajjar¹,

Patel²,

Alapure³

et al. 2008

Eye

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“…In fact, UCP3 has been proposed to play a relevant role in protection against ROS production in skeletal muscle (Vidal-Puig et al 2000, Brand et al 2002, and females have been shown to have a better ability to counteract oxidative-stress-associated pathologies induced by high-fat diet in part through greater UCP3 expression (Gó mez-Pérez et al 2008). Moreover, the intrinsic antioxidant role of E 2 (Ayres et al 1996) cannot be ruled out, especially considering the high E 2 serum levels reached by OVXCE 2 animals. Mitochondrial function and the response to oxidative stress can be strongly affected by fiber composition (Anderson & Neufer 2006, Picard et al 2008, 2012.…”

Section: Discussionmentioning

confidence: 99%

Estradiol stimulates mitochondrial biogenesis and adiponectin expression in skeletal muscle

Capllonch-Amer¹,

Sbert-Roig²,

Galmés-Pascual³

et al. 2014

Journal of Endocrinology

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Sexual dimorphism has been found in mitochondrial features of skeletal muscle, with female rats showing greater mitochondrial mass and function compared with males. Adiponectin is an insulin-sensitizing adipokine whose expression has been related to mitochondrial function and that is also expressed in skeletal muscle, where it exerts local metabolic effects. The aim of this research was to elucidate the role of sex hormones in modulation of mitochondrial function, as well as its relationship with adiponectin production in rat skeletal muscle. An in vivo study with ovariectomized Wistar rats receiving or not receiving 17b-estradiol (E 2 ) (10 mg/kg per 48 h for 4 weeks) was carried out, in parallel with an assay of cultured myotubes (L6E9) treated with E 2 (10 nM), progesterone (Pg; 1 mM), or testosterone (1 mM). E 2 upregulated the markers of mitochondrial biogenesis and dynamics, and also of mitochondrial function in skeletal muscle and L6E9. Although in vivo E 2 supplementation only partially restored the decreased adiponectin expression levels induced by ovariectomy, these were enhanced by E 2 and Pg treatment in cultured myotubes, whereas testosterone showed no effects. Adiponectin receptor 1 expression was increased by E 2 treatment, both in vivo and in vitro, but testosterone decreased it. In conclusion, our results are in agreement with the sexual dimorphism previously reported in skeletal muscle mitochondrial function and indicate E 2 to be its main effector, as it enhances mitochondrial function and diminishes oxidative stress. Moreover, our data support the idea of the existence of a link between mitochondrial function and adiponectin expression in skeletal muscle, which could be modulated by sex hormones.

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“…The first arises because estrogens are important free-radical scavengers because of the hydroxyphenolic structure of their molecules. 29 The second possible mechanism is connected with their influence on the endogenous antioxidative enzyme system. 30 Capel et al 31 were the first who suggested that sex hormones may have antioxidative properties by increasing cellular antioxidative enzyme activity.…”

Section: Discussionmentioning

confidence: 99%

Proteasome Activity as a Target of Hormone Replacement Therapy–Dependent Plaque Stabilization in Postmenopausal Women

Marfella¹,

Filippo²,

Portoghese³

et al. 2008

Hypertension

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Abstract-The molecular mechanisms of the atheroprotective effect evoked by hormone replacement therapy in postmenopausal women is not well known. Recently, we have demonstrated enhanced activity of the ubiquitinproteasome system in human atherosclerotic plaques and evidenced that it is associated with inflammatory-induced plaque rupture. Therefore, we hypothesized that hormone replacement therapy may exert the cardioprotective effects modulating the ubiquitin-proteasome activity. To investigate this possibility, this study examined the differences in inflammatory infiltration, as well as ubiquitin-proteasome activity, between asymptomatic carotid plaques of postmenopausal women with and without concomitant hormone replacement therapy. Plaques were obtained from 20 postmenopausal women treated with hormone replacement therapy (current users) and 32 nontreated women (never-users) enlisted to undergo carotid endarterectomy for extracranial high-grade (Ͼ70%) internal carotid artery stenosis. Plaques were analyzed for macrophages, T lymphocytes, human leukocyte antigen-DRϩ cells, ubiquitinproteasome system, nuclear factor B, inhibitor of nuclear factor B␤, tumor necrosis factor-␣, nitrotyrosine, matrix metalloproteinase-9, and collagen content (immunohistochemistry and ELISA). Compared with plaques from current users, plaques from never-users had more macrophages, T lymphocytes, and human leukocyte antigen-DRϩ cells (PϽ0.001); more ubiquitin-proteasome activity, tumor necrosis factor-␣, and nuclear factor B (PϽ0.001); and more nitrotyrosine and matrix metalloproteinase-9 (PϽ0.001), along with a lesser collagen content and inhibitor of nuclear factor B␤ levels (PϽ0.001). This study supports the hypothesis that hormone replacement therapy inhibits plaque ubiquitin-proteasome activity by decreasing oxidative stress generation in postmenopausal women. This effect, in turn, might contribute to plaque stabilization by inhibiting the activation of nuclear factor B-dependent inflammation, responsible for plaque rupture. Key Words: hormone replacement therapy Ⅲ atherosclerotic plaque Ⅲ inflammation Ⅲ ubiquitin-proteasome activity C ardiovascular disease is the leading cause of death in postmenopausal women. 1,2 There is a strong link between menopause and an increased incidence of cardiovascular disease, and observational studies suggest that postmenopausal hormone therapy, including various estrogen preparations with or without a progestin (most commonly a synthetic progestin), reduces cardiovascular disease risk by about half. 2,3 Hormone replacement therapy (HRT) use was also associated with a lesser extent of angiographically assessed coronary atherosclerosis. 4,5 An atheroprotective effect of estrogens is plausible and is especially attributed to a direct effect on the arterial wall, an antioxidant action, and a favorable effect on inflammation. 6 In prospective studies, administration of ovarian hormones to postmenopausal women has been shown to decrease oxidative stress markers, such as superoxide anion and peroxynitri...

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Estradiol-17β as an antioxidant: Some distinct features when compared with common fat-soluble antioxidants

Cited by 100 publications

References 33 publications

Rapid action of oestradiol against hydrogen peroxide-induced oxidative stress in cataractous lens epithelium: an in vitro study

Rapid action of oestradiol against hydrogen peroxide-induced oxidative stress in cataractous lens epithelium: an in vitro study

Estradiol stimulates mitochondrial biogenesis and adiponectin expression in skeletal muscle

Proteasome Activity as a Target of Hormone Replacement Therapy–Dependent Plaque Stabilization in Postmenopausal Women

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