SUMMARYEncysted embryos (cysts) of the brine shrimp Artemia undergo diapause, a state of profound dormancy and enhanced stress tolerance. Upon exposure to the appropriate physical stimulus diapause terminates and embryos resume development. The regulation of diapause termination and post-diapause development is poorly understood at the molecular level, prompting this study on the capacity of hydrogen peroxide (H 2 O 2 ) and nitric oxide (NO) to control these processes. Exposure to H 2 O 2 and NO, the latter generated by the use of three NO generators, promoted cyst development, emergence and hatching, effects nullified by catalase and the NO scavenger 2-phenyl-4,4,5,5,-tetramethylimidazoline-1-oxyl 3-oxide (PTIO). The maximal effect of NO and H 2 O 2 on cyst development was achieved by 4 h of exposure to either chemical. NO was effective at a lower concentration than H 2 O 2 but more cysts developed in response to H 2 O 2 . Promotion of development varied with incubation conditions, indicating for the first time a population of Artemia cysts potentially arrested in post-diapause and whose development was activated by either H 2 O 2 or NO. A second cyst sub-population, refractory to hatching after prolonged incubation, was considered to be in diapause, a condition broken by H 2 O 2 but not NO. These observations provide clues to the molecular mechanisms of diapause termination and development in Artemia, while enhancing the organism's value in aquaculture by affording a greater understanding of its growth and physiology.

In vivo effects of brown tide on the feeding function of the gill of the northern quahog Mercenaria mercenaria (Bivalvia: Veneridae) Robbins AbstractThe in vivo response of adult northern quahogs, Mercenaria mercenaria, to Aureococcus anophagefferens (brown tide) at the level of the gill was determined using video-endoscopy. Feeding activity, particle-approach velocities, and ventral-groove-transport velocities were documented after the quahogs were exposed to Isochryis galbana (baseline observations) supplemented with either toxic or nontoxic A. anophagefferens at two bloom concentrations (8 × 10 5 or 2 × 10 6 cells ml -1 ). Externally, there was no evidence of adverse effects of brown tide on feeding, as siphons remained extended and dilated. Toxic brown tide at both concentrations elicited gill muscular contractions, intermittent cessation of water flow, and decreased particle loading within the pallial cavity. The 8 × 10 5 cell ml -1 toxic treatment had no significant effect on approach velocities or ventral-groove-transport velocities after 2 h, although timeaveraging showed significant reduction of the latter during the last 30 min of exposure. The higher concentration of toxic brown tide caused a significant decrease in these velocities after only 1 h. Nontoxic brown tide produced none of these effects. Thus, A. anophagefferens compromised quahog feeding by stimulating contractions of the branchial musculature and interfering with lateral and ventral groove ciliary beating. These effects were both timeand concentrationdependent and could be caused by either a dopaminergic or a serotonergic toxic factor.