Book Description

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 mgD (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 mgD (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 n.