Utilization of dissolved organic phosphorus by the two toxic dinoflagellates, Alexandrium tamarense and Gymnodinium catenatum (Dinophyceae)

ABSTRACT: The utilization of dissolved organic phosphorus (DOP) by the two toxic dinoflagellates Alexandrium tamarense (Lebour) Balech and Gymnodinium catenatum Grahamm which were isolated from Hiroshima Bay, Japan, was studied. Alexandrium tamarense grew poorly on fructose-6-phophate, glucose-1-phosphate, glycerophosphate, and ribose-5-phosphate with a phosphomonoester bond, although it grew well on the nucleotides adenosine-5-diphosphate (ADP) and adenosine triphosphate (ATP), as well as on dissolved inorganic phosphorus (DIP; as metaphosphate, pyrophosphate, tripolyposphate and orthophosphate). The results imply that A. tamarense was able to utilize DOP and DIP from ambient water using nucleotidase, pyrophosphatase and poly-phosphatase, which hydrolyze phosphodiesters. In contrast, G. catenatum was able to utilize DOP compounds of various molecular weights and structures as well as DIP. In time-course experiments, alkaline phosphatase activity (APA) was induced at orthophosphate concentrations of 0.43 mmol/L and 3.3 mmol/L for A. tamarense and G. catenatum , respectively, and APA increased with orthophosphate depletion. The experiments also demonstrated that APA was maximum at the optimum temperatures for the growth of A. tamarense and G. catenatum ; that is, 15°C and 25°C, respectively. These results suggest that the DIP-depleted conditions in Hiroshima Bay might have led to the outbreaks of noxious dinoflagellates in recent years.     

Failure to gulp surface air induces swim bladder adenomas in Japanese medaka (Oryzias latipes)

In order to elucidate the effects of swim bladder inflation failure on swim bladder carcinogenesis, we investigated the sequential histopathological changes of swim bladders at 13, 24, 35, and 53 days post-hatch (dph) in medakas with an uninflated swim bladder, which was experimentally induced by denying access to the air–water interface between 0 and 6 dph. The reactive oxygen species (ROS) levels were measured at 24 dph. An uninflated swim bladder was induced in 47.3% of the fish denied access to the air–water interface (the denied group). The total incidence of swim bladder adenoma was 54.1% in the denied group; however, these tumors were observed in all fish with an uninflated swim bladder. In fact, these tumors were observed from 13 dph and onwards. The TBARS levels of the juveniles showed a 2.6-fold increase in fish with an uninflated swim bladder in the denied group compared to that in the control group. It is speculated that swim bladder inflation failure has some effects on the gas gland to produce ROS, leading to DNA damage in the gas glandular epithelium, which develops into swim bladder adenomas. Consequently, it is concluded that denying access to the air-water interface between 0 and 6 dph in medaka is an easy method of inducing swim bladder tumors in a short-term period, and is a useful method for producing tumor-bearing fish.