title: Oxidative stress among SOD-1 genotypes in rainbow trout (Oncorhynchus mykiss).
abstract: Natural variation in the antioxidant-enzyme SOD-1 (superoxide dismutase) is known to alter the impacts of oxidative damage at both the cellular and organismal levels. Using three homozygous clonal lines of rainbow trout [Hot Creek (n=30), Arlee (n=21), and Swanson (n=10)], which differ for single nucleotide polymorphisms (SNPs) and amino acid substitutions at the SOD-1 locus, we investigated the functional effects of this variation on SOD-1 activity during ozone stress and subsequent levels of oxidative damage to DNA and cell membranes. Fish from each line were subjected to either control conditions or 24h of ozone stress, after which tissues were analyzed for antioxidant status and oxidative damage. Liver SOD-1 activity was lower in ozonated vs. control fish in the Hot Creek line, and among ozonated fish, Hot Creek was lower than Arlee. Total erythrocyte SOD activity was not significantly impacted by ozonation; however significant differences in total erythrocyte SOD activity were measured among clonal lines, driven primarily by lower activity in the Hot Creek line. Ozone had a significant treatment effect in all oxidative damage parameters assessed: it increased DNA lesions in erythrocytes and levels of lipid peroxidation in gill tissue and plasma. Among lines, Swanson showed higher lipid peroxidation levels in gill tissue after ozonation than Arlee or Hot Creek. Conversely, Swanson control and treatment fish had significantly lower plasma lipid peroxidation levels than did fish from the other lines. Overall, the among-line differences in SOD and SOD-1 activity and oxidative damage provide evidence that SOD-1 genotypes differ functionally under both oxidative stress and control conditions; however, other genetic differences among lines should be investigated in order to further explain the phenotypic differences in SOD enzyme activity and oxidative damage described here.
authors.affiliation: School of Biological Sciences, Washington State University, Pullman, WA 99164-4236, USA. Electronic address: anna.heink@cchmc.org.
authors.forename: Anna E
authors.initials: AE
authors.lastname: Heink
authors.forename: Amber N
authors.initials: AN
authors.lastname: Parrish
authors.forename: Gary H
authors.initials: GH
authors.lastname: Thorgaard
authors.forename: Patrick A
authors.initials: PA
authors.lastname: Carter
mesh_terms: D000818:Animals; D004249:DNA Damage / Q000187:drug effects; D004912:Erythrocytes / Q000187:drug effects / Q000201:enzymology; D005838:Genotype; D005880:Gills / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000201:enzymology; D017686:Oncorhynchus mykiss / Q000235:genetics* / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects* / Q000235:genetics; D010126:Ozone / Q000633:toxicity*; D013482:Superoxide Dismutase / Q000235:genetics* / Q000378:metabolism*; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
chemical_list: D017392:Thiobarbituric Acid Reactive Substances; D010126:Ozone; D013482:Superoxide Dismutase
keywords: Oncorhynchus mykiss; Oxidative damage; Oxidative stress; SOD