RESUMEN
Seasonal responses in estuarine metabolism (primary production, respiration, and net metabolism) were examined using two complementary approaches. Total ecosystem metabolism rates were calculated from dissolved oxygen time series using Odum's open water method. Water column rates were calculated from oxygen-based bottle experiments. The study was conducted over a spring-summer season in the Pensacola Bay estuary at a shallow seagrass-dominated site and a deeper bare-bottomed site. Water column integrated gross production rates more than doubled (58.7 to 130.9 mmol O2 m-2 d-1) from spring to summer, coinciding with a sharp increase in water column chlorophyll-a, and a decrease in surface salinity. As expected, ecosystem gross production rates were consistently higher than water column rates, but showed a different spring-summer pattern, decreasing at the shoal site from 197 to 168 mmol O2 m-2 d-1 and sharply increasing at the channel site from 93.4 to 197.4 mmol O2 m-2 d-1. The consistency among approaches was evaluated by calculating residual metabolism rates (ecosystem - water column). At the shoal site, residual gross production rates decreased from spring to summer from 176.8 to 99.1 mmol O2 m-2 d-1, but were generally consistent with expectations for seagrass environments, indicating that the open water method captured both water column and benthic processes. However, at the channel site, where benthic production was strongly light-limited, residual gross production varied from 15.7 mmol O2 m-2 d-1 in spring to 86.7 mmol O2 m-2 d-1 in summer. The summer rates were much higher than could be realistically attributed to benthic processes, and likely reflected a violation of the open water method due to water column stratification. While the use of sensors for estimating complex ecosystem processes holds promise for coastal monitoring programs, careful attention to the sampling design, and to the underlying assumptions of the methods, is critical for correctly interpreting the results. This study demonstrated how using a combination of approaches yielded a fuller understanding of the ecosystem response to hydrologic and seasonal variability.
RESUMEN
Imposex, the development of male sex characteristics by female gonochoristic snails, has been documented globally and is causally associated with exposure to the ubiquitous environmental contaminant tributyltin (TBT). Elevated testosterone levels in snails also are associated with TBT, and direct exposure to testosterone has been shown to cause imposex. We discovered previously that the mud snail (Ilyanassa obsoleta)biotransforms and retains excess testosterone primarily as fatty acid esters. The purpose of this study was to determine whether TBT interferes with the esterification of testosterone, resulting in the elevated free (unesterified) testosterone levels associated with imposex. Exposure of snails to environmentally relevant concentrations of TBT (> or = 1.0 ng/L as tin) significantly increased the incidence of imposex. Total (free + esterified) testosterone levels in snails were not altered by TBT; however, free testosterone levels increased with increasing exposure concentration of TBT. TBT-exposed snails were given [14C]]testosterone to measure the production of [14C]testosterone-fatty acid esters. The production of testosterone-fatty acid esters decreased with increasing exposure concentration of TBT. These results indicate that TBT elevates free testosterone levels in snails by decreasing the production or retention of testosterone-fatty acid esters. These findings were confirmed among field-sampled snails where individuals collected from a high-tin-affected site exhibited a greater incidence of imposex, higher free testosterone levels, and lower testosterone-fatty acid ester levels when compared with individuals sampled from a low-tin-affected site. Decreased testosterone-fatty acid esterification among TBT-treated snails was not caused by direct inhibition of the acyl coenzyme A:testosterone acyltransferase (ATAT) enzyme responsible for testosterone esterification, nor by suppressed ATAT protein expression. The target of TBT may be a co-contributor to the testosterone fatty esterification process or a factor in the enhanced hydrolysis of the testosterone-fatty acid pool.
