Recorded use of pesticides in the conservation of artifacts dates back to the 16th century. Museums today are faced with a tremendous task of identification and remediation of pesticides from artifacts in order to protect museum workers and the general public. In addition, artifacts are being repatriated by Native American tribes for use in cultural ceremonies which may subject the practitioner to health risks. Arsenic and mercury salts are among the pesticides that were used that are highly persistent and toxic. The primary challenge lies in removing these hazardous and persistent metals without damaging the materials or pigments on the objects.Concentrated aqueous alpha-lipoic acid solutions were developed for removing arsenic and mercury pesticides from materials commonly used in museum artifacts. The alpha-lipoic acid solutions were reduced using natural sunlight or laboratory ultraviolet lamps to enhance the binding of arsenic. The solubility of alpha-lipoic acid in various organic and inorganic solutions was determined and environmental parameters that impact the reduction and solubility, such as pH and temperature, were examined. The kinetics of the reaction of arsenic (III) with reduced lipoic acid was examined by varying the reduced lipoic acid, base and arsenic concentration as well as temperature and stirring conditions. The results indicated that the reaction occurs at a moderate rate primarily within 8 seconds in air. The reaction is chemically rate limited enhanced at higher temperatures and lower pH. Aerobic conditions significantly decreased the extent of the reaction with increased stirring rate. This impact was minimized by using a nitrogen environment or by limiting agitation during the reaction step.The methods developed were capable of removing up to 1000 µg/cm2 arsenic (of sodium arsenite) from simulated artifacts to levels near the lower detection limit of the X-ray Fluorescence Spectrometer (1 µg/cm2) without leaving detectable residues according to Attenuated Total-Reflection Fourier Transform Infrared Spectroscopy. Similar results were achieved in removing mercury (of mercuric chloride) from non-sulfur containing materials; however, the solutions and processes developed were not capable of removing mercury from sulfur-containing materials such as wool and feathers.

Thesis (Ph.D.) - University of Glasgow, 2008. / Ph.D. thesis submitted to the Division of Infection and Immunity, Institute of Biomedical and Life Sciences, University of Glasgow, 2008. Includes bibliographical references. Print version also available.

Typescript. / Digitized by Kansas Correctional Industries

Thesis (M.S.)--Baylor University, 2008. / Includes bibliographical references (p. 60-67)

Thesis (M. Sc.)--Brock University, 2005. / Includes bibliographical references.

Thesis (M. Sc.)--Brock University, 2005. / Includes bibliographical references.

Thesis (M.S.)--Brock University, 2005. / Includes bibliographical references (leaves 68-85). Also available online (PDF file) by a subscription to the set or by purchasing the individual file.

Inadequate concentrations of progesterone during gestation can result in impaired embryonic growth and losses. These losses may be attributed to an overactive mechanism of progesterone catabolism or improper luteal function, which results in low concentration of progesterone. Progesterone catabolism occurs to the greatest extent by the liver, which holds a vast supply of cytochrome P450 enzymes and aldo-keto reductases that are involved in steroid inactivation. Insulin is a hormone produced by the pancreas that is involved in glucose uptake and metabolism. Progesterone catabolism is decreased in the presence of elevated insulin levels. Lipoic acid is a naturally occurring antioxidant and multienzyme cofactor which has been shown to increase insulin sensitivity and enhance glucose uptake in a number of species. The objectives of the current experiments were to 1) determine if administering a racemic mixture of lipoic acid by gavage at a dose of 32 mg/kg BW would increase peripheral progesterone concentrations, decrease progesterone clearance rates, or modulate cytochrome P450 2C (CYP2C), cytochrome P450 3A (CYP3A), or aldo-keto reductase 1 C (AKRIC) hepatic enzyme activity, and 2) determine if dosing lipoic acid directly into the rumen at 32 mg/kg BW or 64 mg/kg BW would increase progesterone in the blood, decrease progesterone clearance rates, or modulate insulin. In the first trial, Katahdin cross ovariectomized ewes were randomly assigned to a control or a lipoic acid treatment group. In this experiment, a controlled internal drug release (CIDR) device was inserted in all ewes and serum samples were collected daily for five days to determine progesterone. Liver biopsies were performed on day 10 to measure CYP2C, CYP3A, and AKRI C activity. Following liver biopsies, CIDRs were removed and an intensive blood sampling was performed to measure progesterone decay from peripheral circulation. We found that while lipoic acid does not have an effect on peripheral progesterone concentrations or hepatic enzyme activity, lipoic acid supplemented ewes have decreased progesterone clearance rates compared to control ewes. In the second trial, ovariectomized Katahdin cross ewes were randomly assigned to a control, low lipoic acid (32 mg/kg BW), or a high lipoic acid (64 mg/kg BW) treatment group. A CIDR was inserted in all ewes and blood samples were taken daily for 4 days. Following CIDR removal on day 11, an intensive blood sampling was performed to measure progesterone decay from peripheral circulation. One week following CIDR removal, ewes underwent an intravenous glucose tolerance test. It was found that lipoic acid supplementation did not affect progesterone concentrations, progesterone clearance, or insulin area under the curve. There was a treatment effect such that high lipoic acid dosed ewes had higher area under the curve for glucose when compared to control and low lipoic acid dosed ewes. Although no differences in progesterone concentrations were seen in the second trial, we speculate that the administration method rather than the efficacy of lipoic acid may account for the lack of differences observed. This theory is based on evidence from our first trial that oral lipoic acid supplementation did in fact reduce progesterone catabolism, as well as published data demonstrating that ruminally dosed lipoic acid is less effective than the equivalent oral dose.

Call number: LD2668 .T4 1979 M34 / Master of Science

The studies presented in this work were completed with the goal ofgaining greater insight into the roles of protein oxidation in brain aging and age-relatedcognitive impairment. Aging is associated with the impairment of physiological systemssuch as the central nervous system (CNS), homeostatic system, immune system, etc.Functional impairments of the CNS is associated with increased susceptibility to developmany neurodegenerative diseases such as Alzheimer's diseases (AD), Parkinson's disease(PD), and amyotrophic lateral sclerosis (ALS). One of the most noticeable functionalimpairments of the CNS is manifested by cognitive decline. In the past three decades, thefree radical theory of aging has gained relatively strong support in this area. Excessiveproduction reactive oxygen species (ROS) was demonstrated as a contributing factor inage-related memory and synaptic plasticity dysfunction. This dissertation use proteomicsto identify the proteins that are oxidatively modified and post-translationally altered inaged brain with cognitive impairment and normal aging brain.Ongoing research is being pursued for development of regime to preventoxidative damage by age-related oxidative stress. Among which are those that scavengefree radicals by antioxidants, i.e. ??-lipoic acid (LA), and protecting the brains byreducing production of neurotoxic substance, i.e. reducing production of amyloid ??(A??).Therefore, proteomics were also used to identify the alteration of specific proteins in agedbrain treated with LA and antisense oligonucleotides again amyloid protein precursor.This dissertation provides evidences that certain proteins are less oxidatively modifiedand post-translationally altered in cognitively impaired aged brain treated with LA andantisense oligonucleotides against the A?? region of amyloid precursor protein (APP)(AO).Together, the studies in this dissertation demonstrated that increased oxidativestress in brain play a significant role in age-related cognitive impairment. Moreover, suchincreased oxidative stress leads to specific protein oxidation in the brain of cognitiveimpaired subject, thereby leading to cognitive function impairment. Moreover, thefunctional alterations of the proteins identified by proteomics in this dissertation mayleads to impaired metabolism, decline antioxidant system, and damaged synapticcommunication. Ultimately, impairment of these processes lead to neuronal damages andcognitive decline. This dissertation also show that several of the up-regulated andoxidized proteins in the brains of normal aging mice identified are known to be oxidizedin neurodegenerative diseases as well, suggesting that the expression levels of certainproteins may increase as a compensatory response to oxidative stress. This compensationwould allow for the maintenance of proper molecular functions in normal aging brainsand protection against neurodegeneration.