Chronic, dietary polybrominated diphenyl ether exposure affects survival, growth, and development of Rana pipiens tadpoles.

Levels of polybrominated diphenyl ethers (PBDEs) in the environment have been increasing rapidly over the past two decades; however, the toxicology of these compounds to aquatic organisms is poorly understood. Because amphibians play a role in both aquatic and terrestrial food webs, and are currently undergoing worldwide population declines, it is of interest to determine how PBDEs may affect amphibian health. This is the first study that reports chronic, dietary effects of environmentally relevant levels (7-277 ng/g wet food) of PBDEs in amphibians throughout larval development. Beginning at the free-swimming stage (Gosner Stage [GS] 25), Rana pipiens tadpoles were orally exposed to a technical pentabromodiphenyl ether mixture (DE-71) through metamorphic climax (GS 42). On exposure day 43, a subset of tadpoles was removed for body residue analysis. Sum PBDEs in whole-body tissue correlated linearly to dietary concentrations with BDE-99 represented as the highest contributing congener in both diet and tissue. Survival among all treatments compared to the control was decreased by DE-71 exposure. Further, growth and development were delayed in all but the highest treatment, perhaps indicating greater PBDE tolerance among those individuals that survived the highest treatment. Time to metamorphic climax was delayed, on average, 22 to 36 d in DE-71-treated tadpoles compared to control tadpoles. Additionally, size at metamorphosis was smaller in the highest treatment, suggesting that individuals that survived and metamorphosed similarly to the controls did so with a trade-off in size. At environmentally relevant levels, PBDEs induced mortality as well as sublethal effects on developing tadpoles through dietary exposure.

Third prize: Effect of hydrocortisone on porcine ureteral contractility in vitro.

BACKGROUND AND PURPOSE: Corticosteroids have been commonly used in medical expulsive therapy for obstructing ureteral calculi. The exact mechanism of action responsible for facilitation of stone expulsion is unknown, but it is attributed to the anti-inflammatory properties of corticosteroids. Corticosteroids inhibit the production of phospholipase A2 and cyclooxygenase-2, both of which are involved in prostaglandin synthesis. We sought to determine if hydrocortisone inhibits ureteral contractility directly by assessing its action in an isolated in vitro contractility assay. METHODS: Porcine ureters were attached to force displacement transducers and suspended in organ tissue baths containing aerated Krebs buffer. Tissues were equilibrated for 1 hour, and a spontaneous contractility rate was established. After equilibration, tissues were incubated with a 10-fold concentration curve of hydrocortisone (1 nM-10 microM) for 90 minutes, and compared with indomethacin (1 microM) and dimethyl sulfoxide (DMSO) 0.1% as positive and negative controls of contraction, respectively. Contractility rates were recorded on a polygraph and analyzed for changes over exposure time during the course of the experiment. RESULTS: Hydrocortisone inhibited ureteral contractility in a concentration dependent trend. After 90 minutes of treatment, 100 nM, 1 microM, and 10 microM all produced a statistically significant decrease in ureteral contractility rates relative to DMSO controls. The average percent decrease was 43.7% by 100 nM, 66.9% by 1 microM, and 66% by 10 microM hydrocortisone. This decrease in ureteral contractility continued to be significant at 120 minutes. In addition, 10 microM and 1 microM hydrocortisone treatment caused a similar reduction in contractility to indomethacin at 120 minutes. CONCLUSION: Hydrocortiosone effectively inhibits stretch-induced ureteral contractility of porcine ureter in an isolated in vitro assay.