Assessment of the phototoxicity of weathered Alaska North Slope crude oil to juvenile pink salmon.

Petroleum products are known to have greater toxicity to the translucent embryos and larvae of aquatic organisms in the presence of ultraviolet radiation (UV) compared to toxicity determined in tests performed under standard laboratory lighting with minimal UV. This study assessed the acute phototoxicity of the water accommodated fractions of weathered Alaska North Slope crude oil (ANS) to juvenile pink salmon, which are a heavily pigmented life stage. Fish in the highest ANS treatments exhibited melanosis, less mobility, reduced startle response, erratic swimming, and loss of equilibrium. Gills from fish exposed to ANS had elevated levels of hydroperoxides in oil-only, UV-only, and oil+UV treatments compared to control fish, which was indicative of increased lipid peroxidation in gill tissue. Under the test conditions of moderate salinity, low UV and high short-term oil exposure there were no indications of photoenhanced toxicity as assessed by elevation of mortality, behavioral impairment, or gill lipid peroxidation in oil+UV treatments. The results of this study suggest that pink salmon may be at less risk from photoenhanced toxicity compared to the translucent early-life stages of several other Alaska species.

Differential susceptibility of fish and rat liver cells to oxidative stress and cytotoxicity upon exposure to prooxidants.

Species differences in the ability to cope with pollutant-mediated oxidative stress can provide insight into the mechanisms behind both the mode of toxicity of a specific chemical as well as the different ways in which an organism may deal with such stressors. In this study, the effects of exposure to model prooxidants on parameters of oxidative stress were investigated in liver cells from both fish (PLHC-1) and rat (H4IIE). The goals of this study were to compare the oxidative stress response of these cell lines and to assess the relative utility of several different measures of oxidative stress as signals preceding cytotoxicity. Cellular response to two model prooxidants, copper and Fenton reagents (ferrous sulfate plus hydrogen peroxide), was assessed by measuring cytotoxicity, lipid peroxidation, total glutathione (GSHT), and percent glutathione disulfide (%GSSG). Additionally, transcriptional activation of an antioxidant response element (ARE) reporter gene was measured using the chloramphenicol acetyltransferase (CAT) assay in response to these chemicals. In general, the fish cells were more sensitive than rat cells to prooxidants, and the assays for lipid peroxidation and ARE reporter gene activation were more sensitive for measuring oxidative stress than GSH or %GSSG. Fish cells were significantly (P < 0.0001) more sensitive to copper sulfate and Fenton reagent induced oxidative stress, as measured through lipid peroxidation and ARE reporter gene transcriptional activation. Copper sulfate and Fenton reagents caused a two-fold increase in %GSSG in both cell lines. Basal levels of GSHT were higher in the HII4E cells than the PLHC-1 cells, and Fenton reagents significantly reduced GSHT in fish cells but showed no effect on the rat cells. Significant differences were also observed in the cytotoxicity of the test chemicals to both cell lines, with the fish cells demonstrating a higher level of cell death. Lipid peroxidation and ARE transcriptional activation appeared to better reflect subsequent cytotoxicity than a change in GSHT or %GSSG. These results suggest that HII4E (rat) cells are more protected from oxidative stress than PLHC-1 (fish) cells. Additional studies are addressing oxidative stress-mediated signal transduction pathways that may play a role in the differential responses of these cells lines.