Posted 03 May 2008 - 04:08 PM
Nothing definite, but resveratrol activates estrogen receptors. Eczema can be caused or exacerbated by estrogen or estrogen-like compounds; some women become allergic to their own estrogen.
Environ Toxicol Chem. 2008 Feb;27(2):442-51.Links
Interaction of stilbene compounds with human and rainbow trout estrogen receptors.Simmons DB, Trudeau VL, Marlatt VL, Moon TW, Sherry JP, Metcalfe CD.
Watershed Ecosystems Graduate Program, Trent University, Peterborough, ON, Canada.
Compounds with stilbene structures are widely used as pharmaceuticals and personal care products (PPCPs) and are present in plants. A suite of stilbene-related compounds, including PPCPs and plant-derived compounds were tested in vitro for interactions with the human and rainbow trout estrogen receptors and in vivo with rainbow trout using vitellogenin levels as a biomarker. Among the compounds with antagonistic activity, the common structural similarity was (in addition to the stilbene backbone) the presence of 4-hydroxy substitution. Stilbene-related compounds found to act as inhibitors at the estrogen receptor included the plant-derived compound resveratrol and two formulations of fluorescent whitening agents used in detergents, 4,4'-bis(2-sulfostyryl)biphenyl and diaminostilbene-1. In the yeast estrogenicity screening assay, the concentrations which caused a 50% inhibition in estrogenic response (IC50s) with the human estrogen receptor ranged from 2.56 x 10(-6) to 2.56 x 10(-6) M. In the rainbow trout estrogen receptor assay, the IC50s ranged from 7.75 x 10(-8) to 1.11 x 10(-5) M. However, in the in vivo rainbow trout vitellogenin assay, tamoxifen was the only stilbene of the compounds tested to have a significant effect as an inhibitor of estrogenicity.
PMID: 18348622 [PubMed
Shock. 2008 Feb 14 [Epub ahead of print]Links
RESVERATROL ATTENUATES HEPATIC INJURY AFTER TRAUMA-HEMORRHAGE VIA ESTROGEN RECEPTOR-RELATED PATHWAY.Yu HP, Hsu JC, Hwang TL, Yen CH, Lau YT.
*Department of Anesthesiology, Chang Gung Memorial Hospital, †College of Medicine, ‡Center for Healthy Aging Research, and §Department of Surgery, Chang Gung University, Taoyuan; ∥Department of Life Science, National Pingtung University of Science and Technology, Pingtung; and ¶Department of Physiology and Pharmacology, Chang Gung University, Taoyuan, Taiwan.
Resveratrol administration after adverse circulatory conditions is known to be protective, however, the mechanism by which resveratrol produces the salutary effects remains unknown. Recently, it was shown that resveratrol activates estrogen receptor (ER) in endothelial cells. We hypothesized that resveratrol administration in males after trauma-hemorrhage decreases cytokine production and protects against hepatic injury through an ER-dependent pathway. To study this, male Sprague-Dawley rats were subjected to trauma-hemorrhage (mean blood pressure, 40 mmHg for 90 min) then resuscitation. A single dose of resveratrol (30 mg/kg of body weight) with or without an ER antagonist (ICI 182,780), ICI 182,780, or vehicle was administered i.v. during resuscitation. Tissue myeloperoxidase activity (a marker of neutrophil sequestration), cytokine-induced neutrophil chemoattractant 1 (CINC-1), CINC-3, intercellular adhesion molecule 1, and interleukin 6 (IL-6) levels in the liver and plasma aspartate aminotransferase and alanine aminotransferase concentrations were measured at 2 and 24 h postresuscitation (n = 6 rats per group). One-way ANOVA and Tukey test were used for statistical analysis. Results showed that trauma-hemorrhage increased hepatic myeloperoxidase activity, CINC-1, CINC-3, intercellular adhesion molecule 1, and IL-6 levels and plasma aspartate aminotransferase and alanine aminotransferase concentrations. These parameters were significantly improved in the resveratrol-treated rats at both 2 and 24 h postresuscitation. Coadministration of the ER antagonist ICI 182,780 prevented the beneficial effects of resveratrol administration on postresuscitation proinflammatory responses and hepatic injury. Thus, resveratrol administration after trauma-hemorrhage attenuated hepatic injury, likely through reduction of proinflammatory mediators. Resveratrol-mediated hepatic preservation seemed to progress via an ER-related pathway.
PMID: 18277952
Shock. 2008 Feb 14 [Epub ahead of print]Links
RESVERATROL ATTENUATES HEPATIC INJURY AFTER TRAUMA-HEMORRHAGE VIA ESTROGEN RECEPTOR-RELATED PATHWAY.Yu HP, Hsu JC, Hwang TL, Yen CH, Lau YT.
*Department of Anesthesiology, Chang Gung Memorial Hospital, †College of Medicine, ‡Center for Healthy Aging Research, and §Department of Surgery, Chang Gung University, Taoyuan; ∥Department of Life Science, National Pingtung University of Science and Technology, Pingtung; and ¶Department of Physiology and Pharmacology, Chang Gung University, Taoyuan, Taiwan.
Resveratrol administration after adverse circulatory conditions is known to be protective, however, the mechanism by which resveratrol produces the salutary effects remains unknown. Recently, it was shown that resveratrol activates estrogen receptor (ER) in endothelial cells. We hypothesized that resveratrol administration in males after trauma-hemorrhage decreases cytokine production and protects against hepatic injury through an ER-dependent pathway. To study this, male Sprague-Dawley rats were subjected to trauma-hemorrhage (mean blood pressure, 40 mmHg for 90 min) then resuscitation. A single dose of resveratrol (30 mg/kg of body weight) with or without an ER antagonist (ICI 182,780), ICI 182,780, or vehicle was administered i.v. during resuscitation. Tissue myeloperoxidase activity (a marker of neutrophil sequestration), cytokine-induced neutrophil chemoattractant 1 (CINC-1), CINC-3, intercellular adhesion molecule 1, and interleukin 6 (IL-6) levels in the liver and plasma aspartate aminotransferase and alanine aminotransferase concentrations were measured at 2 and 24 h postresuscitation (n = 6 rats per group). One-way ANOVA and Tukey test were used for statistical analysis. Results showed that trauma-hemorrhage increased hepatic myeloperoxidase activity, CINC-1, CINC-3, intercellular adhesion molecule 1, and IL-6 levels and plasma aspartate aminotransferase and alanine aminotransferase concentrations. These parameters were significantly improved in the resveratrol-treated rats at both 2 and 24 h postresuscitation. Coadministration of the ER antagonist ICI 182,780 prevented the beneficial effects of resveratrol administration on postresuscitation proinflammatory responses and hepatic injury. Thus, resveratrol administration after trauma-hemorrhage attenuated hepatic injury, likely through reduction of proinflammatory mediators. Resveratrol-mediated hepatic preservation seemed to progress via an ER-related pathway.
PMID: 18277952
J Reprod Med. 2002 Jun;47(6):507-9.Links
Allergic contact dermatitis from transdermal estradiol and systemic contact dermatitis from oral estradiol. A case report.Corazza M, Mantovani L, Montanari A, Virgili A.
Department of Clinical and Experimental Medicine, University of Ferrara, Via Savonarola 9, 44100 Ferrara, Italy. czm@unife.it
BACKGROUND: About 20% of patients using transdermal estradiol complain of adverse local side effects. CASE: A 47-year-old, postmenopausal woman developed eczematous lesions at the sites of application of a estradiol therapeutic transdermal system and successively at the sites of application of a gel containing estradiol. Due to the topical intolerance, the therapy was switched to oral estrogen, which caused a systemic pruritic rash. Positive patch tests with estradiol led to the diagnosis of type IV allergic dermatitis due to transdermal estradiol and to a gel containing estradiol. Systemic contact dermatitis due to oral estradiol was also diagnosed. CONCLUSION: Even though allergic contact dermatitis from estradiol is extremely rare, local side effects from estradiol systems must be kept in mind and correctly diagnosed. Patch tests allow identification of the causative agent. In the case of primary sensitization to topical estradiol, oral estrogens must be prescribed cautiously to avoid systemic reactions.
PMID: 12092023
J Am Acad Dermatol. 1995 Jan;32(1):25-31. Links
Estrogen dermatitis.Shelley WB, Shelley ED, Talanin NY, Santoso-Pham J.
Department of Medicine, Medical College of Ohio, Toledo 43699.
BACKGROUND: Autoimmune progesterone dermatitis includes pruritus, urticaria, papulovesicular eruptions, and bullous erythema multiforme. Sensitivity to estrogen has not been described, although it was probably first recognized almost 50 years ago. OBJECTIVE: Our purpose was to assess sensitization to selected hormones in women with a significant premenstrual flare of skin lesions. METHODS: Intradermal skin tests to 18 hormones and control substances were performed in seven patients and four control subjects and read for immediate urticarial and delayed type reactions. Six other control subjects had only estrone and progesterone skin tests. The effect of the antiestrogen tamoxifen on the course of the dermatosis was studied. RESULTS: Seven women exhibiting severe premenstrual exacerbations of papulovesicular eruptions, urticaria, eczema, or generalized pruritus proved to have an unrecognized sensitivity to estrogen. Five patients had a positive delayed tuberculin-type skin test to estrogen. Two patients with generalized chronic urticaria had only an urticarial reaction to intradermal estrogens. Antiestrogen therapy with tamoxifen proved effective in all five patients, whereas elimination of oral estrogen therapy cured the other two patients. CONCLUSION: Women can become sensitized to their own estrogens; the major clue is worsening of the skin problem premenstrually. Positive intradermal skin tests to estrogens are diagnostic. Tamoxifen is a specific therapy. We have named this disorder estrogen dermatitis.
PMID: 7822514