Browsing by Subject "Ultraviolet radiation"
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Item Open Access Factors Affecting Ultraviolet Exposure in Coastal Waters of the Florida Keys: Effects on Nearshore and Offshore Coral Reef Tracts(2007-05) Rosenfeld, CarlaWe have investigated how the loss of chromophoric dissolved organic matter (CDOM) in the water column due to photobleaching allows for increased penetration of UV radiation near coral reefs in the Florida Keys. Extended exposure to UV may contribute to coral bleaching episodes. CDOM serves as the primary control on UV exposure of corals in this region because it strongly absorbs UV radiation, especially damaging UVB wavelengths. An important fraction of the CDOM pool in Florida Keys coastal waters is transported from Florida Bay, but local CDOM sources including seagrasses, mangroves, and Sargassum colonies may also be substantial. CDOM samples collected along transects near the reefs and from mangrove leaf and Sargassum incubation experiments were exposed to simulated solar radiation for up to 120 hours. Calculated photobleaching rates (k305) of CDOM produced by mangrove leaf litter and Sargassum colonies (approx. 0.02 hr^-1) were an order of magnitude greater than rates measured for the water column samples (0.002 hr^-1). However, our experiments indicate that photobleaching of CDOM in natural waters near the reefs can still be substantial during summer months and may allow UVB levels at 4 m depth (typical depth of fringing reefs) to increase by as much as 20%. Corals located in shallower waters (2 m) along the reef line may experience up to a 40% increase in UVB exposure due to loss of CDOM.Item Open Access Role of Mitochondrial Dynamics and Autophagy in Removal of Helix-Distorting Mitochondrial DNA Damage(2012) Bess, Amanda SmithMitochondria are the primary energy producers of the cell and play key roles in cellular signaling, apoptosis and reactive oxygen species (ROS) production. Mitochondria are the only organelles that contain their own genome which encodes for a small subset of electron transport chain (ETC) proteins as well as the necessary tRNAs and ribosomal subunits to translate these proteins. Over 300 pathogenic mitochondrial DNA (mtDNA) mutations have been shown to cause a number of mitochondrial diseases emphasizing the importance of mtDNA maintenance and integrity to human health. Additionally, mitochondrial dysfunction and mtDNA instability are linked to many wide-spread diseases associated with aging including cancer and neurodegeneration. Mitochondria lack the ability to repair certain helix-distorting lesions that are induced at high levels in mtDNA by important environmental genotoxins including polycyclic aromatic hydrocarbons, ultraviolet C radiation (UVC) and mycotoxins. These lesions are irreparable and persistent in the short term, but their long-term fate is unknown. Degradation of mitochondria and mtDNA is carried out by autophagy. Autophagy is protective against cell stress and apoptosis resulting from exposure to mitochondrial toxicants suggesting that it plays an important role in removal of unstable mitochondria that can serve as a source of ROS or initiate apoptotic cell death. Furthermore, dysfunctional mitochondria can be specifically targeted for degradation by the more specific process of mitophagy influenced in part by the processes of mitochondrial dynamics (i.e., fusion and fission).
The goals of this dissertation were to investigate the long-term fate of helix-distorting mtDNA damage and determine the significance of autophagy and mitochondrial dynamics in removal of and recovery from persistent mtDNA damage. Removal of irreparable mtDNA damage and the necessity of autophagy, mitophagy, fusion and fission genes in removal of this damage were examined using genetic approaches in adult Caenorhabditis elegans. In order to investigate the significance of autophagy, fusion and fission genes in recovery from mtDNA damage-induced mitochondrial dysfunction in vivo, an experimental method was developed to specifically induce persistent mtDNA damage and mitochondrial dysfunction without persistent nDNA damage in developing C. elegans. Additionally, the effect of persistent helix-distorting DNA damage on mitochondrial morphology, mitochondrial function and autophagy was investigated in C. elegans and in mammalian cell culture. The rate and specificity of mitochondrial degradation was further examined in cell culture using live-cell fluorescence microscopy and transmission electron microscopy.
Removal of UVC-induced mtDNA damage was detectable by 72 hours in C. elegans and mammalian cell culture, and required mitochondrial fusion, fission and autophagy, providing genetic evidence for a novel mtDNA damage removal pathway. UVC exposure induced autophagy with no detectable effect on mitochondrial morphology in both systems; mitochondrial function was inhibited in the C. elegans system but not in the cell culture system in which the degree of mtDNA damage induced was less. Furthermore, mutations in genes involved in these processes as well as pharmacological inhibition of autophagy exacerbated mtDNA damage-mediated larval arrest, illustrating the in vivo relevance of removal of persistent mtDNA damage. Mutations in genes in these pathways exist in the human population, demonstrating the potential for important gene-environment interactions affecting mitochondrial health after genotoxin exposure.