No description available.

Made available in DSpace on 2014-06-11T19:27:18Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-07-08Bitstream added on 2014-06-13T18:31:18Z : No. of bitstreams: 1 zanoli_jcc_me_araca.pdf: 862916 bytes, checksum: 14a8c6ca70d93c05133bf28113b4bac8 (MD5) / Abamectina é uma lactona macrocíclica pertencente à família das avermectinas, utilizada mundialmente como agente antiparasitário em animais de criação e estimação, além do emprego agrícola como princípio ativo dos inseticidas e nematicidas. Mitocôndrias são responsáveis pela conversão da energia liberada pelo transporte de elétrons e armazenamento como energia de ligação na molécula de ATP, um componente metabólico essencial. Interferências em sua síntese ou utilização caracterizam mecanismos pelos quais os xenobióticos podem expressar toxicidade aguda ou crônica. Neste trabalho, os efeitos da abamectina na bioenergética de mitocôndrias isoladas de fígado de rato foram avaliados. Nas concentrações utilizadas (5 a 25 µM), abamectina causou inibição da cadeia respiratória, sem afetar a atividade das enzimas NADH desidrogenase, succinato desidrogenase e o potencial de membrana, comportando-se de maneira semelhante à oligomicina e ao atractilosídeo. A principal atuação da abamectina foi reduzir o potencial mitocondrial de fosforilação oxidativa, diminuindo os níveis de ATP provavelmente como resultado de sua ação direta sobre a FoF1-ATPase, uma vez que inibiu a atividade desta enzima, e/ou sobre o translocador de ADP/ATP. A inibição mais acentuada da atividade fosfohidrolase em mitocôndrias intactas desacopladas do que em mitocôndrias rompidas juntamente com a inibição da despolarização do potencial de membrana induzida pelo ADP sugerem que a abamectina atuou inibindo mais especificamente o translocador de ADP/ATP do que a FoF1-ATPase / Abamectin is a macrocyclic lactone belonging to the avermectin family, used worldwide as antiparasitic agent in farm animals and pets, and agricultural employment as the active ingredient of insecticides and nematicides. Mitochondria are responsible for converting the energy released by electron transport and storage as the binding energy molecule ATP, an essential metabolic component. Interference in its synthesis or utilization characterize mechanisms by which xenobiotics can express acute or chronic toxicity. In this study, the effects of abamectin in the bioenergetics of mitochondria isolated from rat liver were evaluated. At the concentrations used (5-25 mM), abamectin caused inhibition of the respiratory chain without affecting the activity of enzymes NADH dehydrogenase, succinate dehydrogenase and the membrane potential, behaving similarly to oligomycin and Atractyloside. The main activity of abamectin was to reduce the potential of mitochondrial oxidative phosphorylation, decreasing ATP levels probably as a result of its direct action on the Fo-F1 ATPase, since it inhibited the activity of this enzyme, and/or the ADP/ATP translocator. The more pronounced inhibition of the fosfohydrolase activity in intact uncoupled mitochondria than in disrupted mitochondria, in addition to the inhibition of the ADP-stimulated depolarization of mitochondrial membrane potential suggest that abamectin acted more specifically by inhibiting the ADP/ATP translocator than the FoF1-ATPase

No description available.

by Ai-Dong Qi. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (p. 219-256). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web.

Thesis (Ph. D.)--University of Washington, 2002. / Vita. Includes bibliographical references (leaves 90-103).

No description available.

Osteoarthritis is the end result of damage to articular cartilage, which lacks the ability to self-repair. Tissue engineering of cartilage is a promising field of study that aims to promote healing of cartilage in vivo by manipulation of the chondrocytes that maintain the tissue, or through in vitro production of new cartilage for implantation into cartilage defects. Tissue-engineered cartilage constructs require mechanical stimulation to produce matrix components in quantities and proportions similar to native cartilage tissue, and adenosine triphosphate (ATP) is thought to be an autocrine/paracrine biochemical mediator of these mechanical forces on the cell, after its release from chondrocytes under mechanical stress. This study determined culture conditions for chondrocytes in 3D agarose scaffolds from mature donors undergoing total joint arthroplasty for the treatment of osteoarthritis, then supplemented these cells in vitro with exogenous ATP in concentrations varying from 50 nM to 1 mM in the presence of the radioisotopes [35S] and [3H]-proline, with radioisotope incorporation acting as markers of proteoglycan and collagen synthesis respectively. The basal concentrations of ATP in the chondrocyte cultures as well as the ATP half-life in the cultures were determined by lucifer/luciferase assay and luminometry. The P2Y receptor expression on the populations of chondrocytes from 8 donors was determined by flow cytometry, with largely varied individual expression and heterogeneity of P2Y1 and P2Y2 receptors. Exogenous ATP was found to increase synthesis of matrix components by 200% of the control cultures at doses of 100 nM to 1 µM. Patients with worse arthritis patterns, who were on chronic narcotic medications and who smoked were more likely to have a negative response to the exogenous ATP supplementation. The basal concentration of ATP in the cultures was less than 1 nM, and the ATP half-life varied from 1-2 hours, depending on the expression of P2Y1 receptors expressed by the donor’s chondrocyte population (R2 = 0.99). Supplementation of exogenous ATP to tissue-engineered cartilage in vitro appears to be a promising technique for improving the matrix synthesis of these constructs. / Thesis (Master, Mechanical and Materials Engineering) -- Queen's University, 2011-01-28 10:49:47.118

Thesis (Ph. D.)--University of Hong Kong, 2009. / Includes bibliographical references (leaves 142-172) Also available in print.

Thesis (Ph. D.)--University of Washington, 1998. / Vita. Includes bibliographical references (leaves [90]-105).

Thesis (Ph. D.)--University of Texas at Austin, 1999. / Vita. Includes bibliographical references (leaves 93-109). Available also in a digital version from Dissertation Abstracts.