Oxidative Stress in the Aquatic Environment: Effects of Hypoxia and Polychlorinated Biphenyls in Fish and Bivalve Molluscs

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Title: Oxidative Stress in the Aquatic Environment: Effects of Hypoxia and Polychlorinated Biphenyls in Fish and Bivalve Molluscs
Author: Lehmann, Daniel Wade
Advisors: J. F. Levine, Committee Member
D. Shea, Committee Member
J. M. Law, Committee Chair
G. A. LeBlanc, Committee Member
Abstract: Oxidative damage is hypothesized to be an underlying cause of many chronic disease states. Acutely, oxidative damage can lead to irreversible cell injury and pathological consequences. Reactive oxygen species, while naturally occurring at low levels in biological systems, can also be brought about by severe environmental conditions such as hypoxia or by chemical contaminants. This body of work encompasses two different areas of toxicological research into the generation of radical species and the resulting oxidative damage to organisms. The first section deals with hypoxia as a causative factor in epizootic ulcerative syndrome (EUS) in Atlantic menhaden (Brevoortia tyrannus) in the estuaries of the Atlantic coast. Menhaden have a fairly large impact on the coastal environment and on tourism for the state, being integral to food webs of the estuary, coastal shelf, and an indicator of environmental degradation. Our hypothesis was that environmental exposure to hypoxic conditions in the estuaries leads to oxidative stress in Menhaden sufficient to cause tissue damage. Specific objectives of the study were two-fold: Determination of LC50 levels for both Atlantic Menhaden and the hypoxia tolerant species, Nile Tilapia (Oreochromis niloticus), at both acute (2 hour) and medium term (96 hours) exposures to hypoxia. Results indicated that tilapia have a very high tolerance and adaptability to hypoxic conditions. We could not ascertain an LC50 for tilapia as at 0.24 mg⁄L (3% saturation) we saw only 28% mortality at 2 hours. Ca++ and K+ were the only ionic alterations to blood chemistry due to exposure. Menhaden had an LC50 of 1.2 mg⁄L (16% saturation) dissolved oxygen (at 28 ppt salinity) over 1 hour and had blood chemistry dysregulation affecting Ca++, K+, Na+, and glucose levels. In the 96 hour exposures, no alterations in lipid peroxidation, glutathione, lipid soluble antioxidants, or strand breakage were detected indicating that hypoxia and reperfusion were not sufficient to cause oxidative damage or EUS in these species. In the second portion, we evaluated the effects of PCBs in Corbicula clams as possible surrogates for endangered bivalve mollusks. The Ward Transformer site, in Wake County, North Carolina was found to have Aroclor 1260 levels as high as 1.7 mg⁄kg in fish collected miles downstream from the source. Concern over the effects of PCB exposure to the native wildlife, especially at-risk populations of native bivalves, prompted the hypothesis that oxidative damage due to Aroclor exposure would cause changes in biomarkers and pathology associated with decreased health status. Specifically, we conducted a laboratory study to determine the effects of Aroclor 1260 in order to validate common biomarkers of oxidative damage in Corbicula fluminea clams, without confounding environmental factors. Secondly, we performed field deployments of Corbicula into the polluted Brier Creek system to gauge the oxidative status of animals in the field relative to a downstream gradient of Aroclor 1260 concentrations. Results from the laboratory study at 0, 1, 10, and 100 ppb indicated that exposures were detrimental to the clams. Antioxidant biomarkers responded significantly at 3 weeks exposure and morphologic changes included inflammation, anasarca, Brown cell accumulation, severe gonad atrophy, inflammation, and necrosis. In conjunction with biomarker changes, a linear relationship was seen to exist between sediment and time-weighted average water concentrations of PCBs and total oxidant scavenging capacity (TOSC) values. These studies indicated that oxidative damage occurs as a result of exposure to Aroclor 1260.
Date: 2006-06-13
Degree: PhD
Discipline: Toxicology
URI: http://www.lib.ncsu.edu/resolver/1840.16/4986

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