Abstract

The decline of the Western population of the Alaskan Steller sea lion is of serious concern and has no apparent explanation. The fact that the decline is limited to the western and Asian populations, while the eastern stock continues to grow, suggests that there may be an environmental factor involved. Contaminants, such as metals, may be one such factor playing a role in the decline. We are examining the toxicity of numerous metals to cell lines established from major organ systems of the Steller sea lion. Currently, we have established primary cell lines from skin, testes, kidney, liver and lung. Our initial metal toxicity experiments indicate that hexavalent chromium Cr(VI) is variably cytotoxic to Steller sea lions, depending on the organ involved. For example, 2.5, 5, 10 and 25 uM sodium chromate induced 87, 46, 49, and 3 percent relative survival respectively in skin fibroblasts, but 38, 18, 3 and 0 percent relative survival in lung fibroblasts and no survival at any of these concentrations in liver fibroblasts. Thus, skin is more resistant to Cr(VI) than lung cells, and liver cells are the most sensitive of the three. In addition, we have found that 2.5, 5, 10 and 25 uM arsenic induced 84, 72, 40, and 3 percent relative survival in lung cells. Thus, lung cells are more sensitive to Cr(VI) than arsenic. Further testing is underway to determine the toxicity of additional metals such as cadmium, nickel, vanadium, and copper in the lung, skin, kidney, liver, and reproductive organs of the Steller sea lion.

Acknowledgements

This work was supported by a grant from National Oceanic and Atmospheric Administration, NA16FX1412. The authors would like to thank Jen Burns, Tom Gellatt, Denise Grieg, Millie Gray, Kendall Mashburn, Jo-Ann Mellish, Natalie Noll, Lorrie Rea, Julie Richmond, Carol Stephens, Pam Tuomi, and Jason Waite for help in tissue collection.