Meeting Abstract
Elasmobranchs utilize a unique osmoregulatory strategy based on urea as the main osmolyte. Because this strategy is energetically expensive, perturbations to homeostasis, such as that presented by legacy polychlorinated biphenyl (PCB) exposure, may be detectable in osmoregulatory biomarkers. Multiple tissues were obtained from pregnant Round Stingrays (Urobatis halleri) and associated embryos over the course of a gestational cycle from two locations where both environmental concentrations and physiological response to PCB exposure differs between sites. Solutes (urea, TMAO, proteins) were quantified in matched pairs of maternal plasma and histotroph and activities of enzymes indirectly and directly related to urea synthesis were measured in maternal and embryonic liver tissue. Pregnant females from the reference site maintained stable plasma urea concentrations, whereas plasma urea declined over the course of pregnancy in females from the contaminated site. In addition, muscle protein content significantly declined in contaminant-exposed, but not reference, females, indicating a potential loss of substrate for urea formation. Embryonic enzymes involved in the urea cycle and protein processing were functional, in contrast to the hypothesis that internal gestation (matrotrophic histotrophy), would delay the developmental onset of embryonic osmoregulation. While embryos were able to maintain urea and TMAO concentrations comparable to reference embryos, their liver protein content also significantly decreased over development, suggesting that osmoregulatory costs were higher. Increased costs for osmoregulation join other physiological measures adversely affected by legacy PCB contamination in these stingrays.
