Ecological risk assessment and its application to elasmobranch conservation and management.

Ecological risk assessments (ERAs) are employed to quantify and predict the vulnerability of a particular species, stock or population to a specific stressor, e.g. pollution, harvesting, climate change, by-catch. Data generated from ERAs are used to identify and prioritize species for implementation of effective conservation and management strategies. At this time, ERAs are of particular importance to elasmobranchs, given the ecological importance and documented global population declines of some elasmobranch species. Here, ERAs as a tool for elasmobranch conservation and management are reviewed and a theoretical roadmap provided for future studies. To achieve these goals, a brief history of ERAs and approaches used within them (in the context of elasmobranchs) are given, and a comprehensive review conducted of all ERA studies associated with elasmobranchs published between 1998 and 2011. The hazards assessed, species evaluated and methodological approaches taken are recorded. Chronological and geographical patterns suggest that this tool has grown in popularity as a commercial fishery management instrument, while also signalling a recent precautionary approach to elasmobranch management in commercial fisheries globally. The analysis demonstrates that the predominant parameters incorporated in previous ERAs are largely based on life-history characteristics, and sharks have received the majority of attention; batoids (including skates) have received less attention. Recreational fishing and habitat degradation are discussed as hazards which warrant future investigation through ERA. Lastly, suggestions are made for incorporating descriptive ecological data to aid in the continued development and evolution of this management tool as it applies to future elasmobranch conservation.

Characterization of hydrogen peroxide toxicity in cultured rat forebrain neurons.

We investigated the ability of hydrogen peroxide (H2O2) to cause apoptotic cell death in cultured rat forebrain neurons and the potential mechanisms by which oxidative stress triggers delayed neuronal death. H2O2 (25 microM for 5 min) reduced cell viability to 34.5 +/- 8.3% of untreated controls 20 h after exposure, and resulted in a significant proportion of neurons which exhibited apoptotic nuclear morphology. Using single cell fluorescence assays, we measured H2O2-induced changes in DNA strand breaks, 2'7' dichlorofluorescin fluorescence, reduced glutathione, intracellular free Ca2+, and mitochondrial membrane potential. DNA strand breaks in response to H2O2 were not evident immediately following exposure, but were increased 12h and 20h after exposure. Millimolar concentrations of H2O2 caused increases in the fluorescence of the oxidant-sensitive fluorescent dye, 2'7'-dichlorofluorescin. H2O2 treatment decreased reduced glutathione following 30 minutes of exposure using the fluorescent indicator, 5-chloromethylfluorescein diacetate, and increased intraneuronal free Ca2+ levels in a subpopulation of neurons. Mitochondrial membrane potential, measured by rhodamine 123 localization was unaffected by 25 microM H2O2, while higher concentrations of H2O2 (10 or 30 mM) depolarized mitochondria. These studies demonstrate that H2O2 is a potent and effective neurotoxin that produces oxidative stress, as well as apoptotic neuronal death.