A study was conducted to determine if exposure to elevated nitrate (NO 3 -)(3.76 AE 0.07 and 93.15 AE 2.79) during embryonic development influences the morphology of thyroid tissue in newly hatched Atlantic salmon, Salmo salar. Digital threedimensional imaging of thyroid follicles in S. salar showed that the thyroid tissue in newly hatched alevin consisted mainly of spherical follicles dispersed throughout the lower jaw in close proximity to the ventral aorta and other blood vessels. With these digital models, the number of follicles, average volume per follicle, and total luminal volume were calculated for alevin exposed to well water or 93.15 mg L À1 NO 3 -N during embryogenesis. There were no statistically significant differences in any of these parameters, suggesting that the normal thyroid development of S. salar could be relatively insensitive to excess environmental NO 3 -. These results are promising for the culture of Atlantic salmon embryos in recirculating aquaculture systems that naturally accumulate NO 3 -as a product of nitrification.
Embryo mortality of Atlantic salmon, Salmo salar, has been increasing for more than a decade in the State of Maine, a leading producer of this species in the United States. Increasing embryo mortality not only creates a financial bottleneck for farms but also prevents the sale of surplus eggs as an additional source of revenue. Blood and egg samples were collected at three Maine Atlantic salmon farms from female broodstock at the time of spawning over a 2‐year period. Correlative factors for reduced embryo survival were investigated by measuring egg and maternal plasma concentrations of 17β‐estradiol (E2), 11‐ketotestosterone (11‐KT), testosterone and calcium, as well as maternal hepatic ethoxyresorufin‐O‐deethylase (EROD) activity and fork length. Significant positive correlations were found between maternal plasma concentrations of E2 and 11‐KT and embryo survival. Interestingly, there was no correlation with egg concentrations of sex steroids and embryo survival, suggesting that embryo mortality does not likely rest with the maternal deposition of sex steroids into the egg, but with another hormone regulated process related to egg assembly, ovulation or post‐ovulatory ageing.
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