Objectives: This study investigated the effects of estrogen-only therapy on lipid profile (through susceptibility of low density lipoproteins to oxidation) and on oxidant-antioxidant parameters in surgical menopausal women. PON genotypes are also evaluated considering that they may be associated with the personal differences observed in antioxidant effects induced by estrogen.
Methods: Thirty women who had undergone hysterectomy+bilateral ovariectomy in the last 3 years, with causes other than malignancy were included and given estrogen-only (Premarin-Wyeth Inc. 0.625 mg/day/6 months, equine conjugated estrogen). Blood samples were collected at baseline, first and sixth month of treatment. Serum (total antioxidant activity-TAO and PON activity), erythrocyte (TBARS and catalase activity), LDL and Cu2+ induced ox-LDL (TBARS and diene levels) samples were evaluated and PON1 192 polymorphisms were determined by PCR amplification & restriction enzyme digestion.
Results: At the sixth month, a higher TAO activity (p=0.016) and a lower eTBARS (p=0.028) were detected compared to the basal values. LDL and Cu induced ox-LDL TBARS levels at the sixth month of treatment were significantly (p=0.012 and 0.026, respectively) lower compared to the pretreatment values. Baseline eTBARS (p=0.007), LDL TBARS (p=0.044) and eCAT (p=0.033) activities were significantly higher in homozygote Q allele carriers compared to subjects with R allele. LDL TBARS and Cu2+ induced ox-LDLTBARS of QQ subjects (p=0.018 and 0.050) as well as LDL TBARS of QR subjects (p=0.044) showed a significant decrease with estrogen-only treatment.
Conclusions: Our study drives the attention to PON polymorphism in postmenopausal women who have risk for atherosclerosis. Although our data is limited, this study is the first that focuses on the role of PON genotypes in antiatherosclerotic effects of estrogen-only and provides important points for further studies.
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http://dx.doi.org/10.1016/j.maturitas.2005.05.017 | DOI Listing |
J Clin Endocrinol Metab
January 2025
Department of Neurology, Weill Cornell Medicine, New York NY, USA.
Accumulating evidence suggests that the effects of menopausal hormone therapy (MHT) on risk of Alzheimer's disease (AD) and all-cause dementia are influenced by timing of initiation relative to age and time-since-menopause and the type of formulation. Randomized clinical trials (RCTs) of MHT conducted in older postmenopausal women indicate an increased risk of dementia. While RCTs conducted in midlife are lacking, observational research has provided evidence for associations between midlife estrogen-only therapy (ET) use and a reduced risk of AD dementia, whereas estrogen-progestogen therapy (EPT) is associated with more variable outcomes.
View Article and Find Full Text PDFMaturitas
December 2024
Department of Clinical, Surgical, Diagnostic and Pediatric Sciences, University of Pavia, Viale Golgi 19, 27100 Pavia, Italy; Research Center for Reproductive Medicine, Gynecological Endocrinology and Menopause, IRCCS S. Matteo Foundation, Viale Golgi 19, 27100 Pavia, Italy. Electronic address:
Horm Behav
August 2024
Department of Neuroscience & Experimental Therapeutics, Albany Medical College, 47 New Scotland Avenue, MC-136, Albany, NY 12208, USA. Electronic address:
Menopause is an endocrine shift leading to increased vulnerability for cognitive impairment and dementia risk factors, in part due to loss of neuroprotective circulating estrogens. Systemic replacement of estrogen post-menopause has limitations, including risk for estrogen-sensitive cancers. A promising therapeutic approach therefore might be to deliver estrogen only to the brain.
View Article and Find Full Text PDFJAMA
May 2024
Hurvitz Brain Sciences Program, Sunnybrook Research Institute, Toronto, Ontario, Canada.
JAMA
May 2024
Claire Mellon and Associates, Portland Hospital, London, United Kingdom.
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