Superoxide dismutase expression and oxidative damage in a case of myopathy in brown pelicans (Pelecanus occidentalis).
Four brown pelicans (Pelecanus occidentalis) housed at a rehabilitation facility were found dead after a 3-day history of muscle weakness and after being fed for about 2 weeks from a recent shipment of fish. The birds had pale streaking of the skeletal and heart muscles. Microscopically, the skeletal muscle, and to a lesser extent the cardiac muscle, had severe myocyte degeneration and necrosis characterized by microvacuolation with loss of cross-striations, condensation of cytoplasm, fragmentation, mineralization, and inflammatory cell infiltrates consisting of multinucleated cells, macrophages, and few heterophils. The findings were consistent with myopathy, and a nutritional myopathy caused by eating rancid fish was suspected. Immunohistochemical staining revealed abundant immunoreactive copper zinc superoxide dismutase and manganese superoxide dismutase either as diffuse homogeneous precipitates or granular aggregates in the cytoplasm of affected cells. Immunoreactivity was directly related to degree of cellular damage as estimated by light microscopic examination. We suggest that the lack of protection, despite upregulation of superoxide dismutase, is most likely attributable to supersaturation of oxidants beyond the capacity of superoxide dismutases to scavenge.[1]References
- Superoxide dismutase expression and oxidative damage in a case of myopathy in brown pelicans (Pelecanus occidentalis). Giri, D.K., Miller, D.L., Thompson, L.J., Mailler, L., Styer, E., Baldwin, C. J. Vet. Diagn. Invest. (2007) [Pubmed]
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