Experimental induction of jaw, gill and pectoral fin malformations in Japanese flounder, Paralichthys olivaceus, larvae

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The phenotypes of skeletal malformations induced in pharyngeal arches and pectoral fins of Japanese flounder larvae by retinoic acid (RA), disulfiram, 2,2′-dipyridyl and azetidine-2-carboxylic acid were characterized, RA controls gene expression essential for pharyngeal and pectoral fin development; disulfiram is an inhibitor of RA synthase, 2,2′-dipyridyl and azetidine-2-carboxylic acid are inhibitors of collagen synthesis. In larvae exposed to RA at shield stage for 1 h, the Meckel's cartilage did not form in mandible arch. Exposure to RA from hatching period shifted the growth direction of the pharyngeal cartilages posteriorly. Disulfiram did not affect the cartilage formation when given before hatching, even though it shortened the trunk. However, disulfiram exerted teratogenic effects when given after hatching time, inducing bending pharyngeal cartilages and S-shaped pectoral fin plate. 2,2′-Dipyridyl given from hatching also caused bending of pharyngeal cartilages and S-shaped pectoral fin plates. Azetidine-2-carboxylic acid reduced the size of cartilages, without causing remarkable malformation. Thus, it was demonstrated that both RA and inhibitor of its synthesis, and inhibitors of collagen synthesis exert specific teratogenic effects on both pharyngeal and pectoral skeletons of flounder larvae.