Abstract
Perfluorooctane sulfonate (PFOS) is a widely distributed industrial compound that has been detected in the eggs of various wild avian species. Laboratory studies have indicated that PFOS is embryotoxic to domestic chickens ( Gallus gallus domesticus), but the mechanisms of toxicity in the developing avian embryo remain unknown. We recently demonstrated that PFOS acts as a peroxisome proliferator by causing increased expression of peroxisome proliferator activated receptor alpha (PPARα)-regulated genes in cultured primary chicken embryo hepatocytes. The present study examined whether PPARα-regulated genes were dose-dependently affected in chicken embryos exposed in ovo to PFOS. White leghorn chicken eggs were injected with 0.1, 5.0 or 100.0 μg PFOS/g egg into the air cell prior to incubation. Embryos were incubated until pipping, after which the expression of PPARα-regulated genes was measured in the liver tissue of surviving embryos using real-time reverse transcription polymerase chain reaction. A dose-dependent decrease in embryo pippability was observed with an LD50 of 93 μg/g (3.54 μg/g–672,910 μg/g, 95% confidence interval). Hepatic PFOS concentrations increased concomitantly with dose. The PPARα-regulated genes measured were peroxisomal acyl CoA oxidase, bifunctional enzyme, liver fatty acid binding protein and peroxisomal 3-ketoacyl thiolase. PFOS exposure via egg injection prior to incubation did not affect the transcriptional activity of any of the assayed PPARα-regulated genes at any of the doses examined in day 21 chicken embryos.
Published Version
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