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Mechanisms of estradiol-17��-induced down-regulation of ovine uterine oxytocin receptors during the estrous cycleHazzard, Timothy McLagan 26 August 1997 (has links)
Graduation date: 1998
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Effects of estradiol-17β implants from birth to slaughter on performance, carcass, sensory traits and endocrine aspects of young bulls and steersHopkins, Trudy D. January 1986 (has links)
Call number: LD2668 .T4 1986 H66 / Master of Science
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An examination of neuroprotective effects of 17B-estradiol and extracts from Panax Quinquefolius L., Ginkgo Biloba and HypericumPerforatum against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)induced nigral-striatal neuronal degenerationChan, Wing-yan, Veronica, 陳詠恩 January 2001 (has links)
published_or_final_version / Anatomy / Master / Master of Philosophy
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Investigating the Effects of 17α-Ethynylestradiol on Mitochondrial Genome StabilityChivers, Alicia M. 23 May 2016 (has links)
Environmental toxicants are ubiquitous throughout the environment as a result of human activity. Among these toxicants, environmental estrogens are a category of particular concern due to their environmental prevalence and potency in altering reproductive traits. While many studies have addressed the detrimental effects of environmental estrogens on both aquatic and terrestrial organisms, few have analyzed the potential for these compounds to alter mitochondrial function. Mitochondria are the primary energy-generating system for all eukaryotic life, supporting all aspects of development, metabolism, and growth. Each cell within the body contains many mitochondria which in turn contain multiple copies of their own DNA genome, mitochondrial DNA (mtDNA). Mutations in mtDNA are responsible for a wide range of human diseases such as metabolic syndromes, cancers, and obesity. Among these mitochondrial diseases many are characterized by increased levels of heteroplasmy, multiple mitochondrial DNA haplotypes within an individual. Increased heteroplasmy can alter normal mitochondrial function and influence disease initiation and progression.
To date, no studies have investigated the effects of synthetic estrogens on mitochondrial genome stability. Synthetic estrogens have the capacity to bind to estrogen receptors and initiate estrogenic responses through translocation into the mitochondrion. Despite our knowledge about the relationship of heteroplasmy and disease, we still do not have a complete grasp of the mechanisms of heteroplasmic induction. Here we report our analysis of the effects of 17α-ethynylestradiol (EE2) exposure in three studies to investigate its effect on mitochondrial genome stability. Data analysis reveals a statistically significant relationship between EE2 exposure and increased heteroplasmic frequency.
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