HEPATIC CHOLESTASIS DURING THE POSTEMBRYONIC DEVELOPMENT OF FISH LARVAE

Citation
Jp. Diaz et al., HEPATIC CHOLESTASIS DURING THE POSTEMBRYONIC DEVELOPMENT OF FISH LARVAE, The Journal of experimental zoology, 280(4), 1998, pp. 277-287
Citations number
59
Categorie Soggetti
Zoology
ISSN journal
0022104X
Volume
280
Issue
4
Year of publication
1998
Pages
277 - 287
Database
ISI
SICI code
0022-104X(1998)280:4<277:HCDTPD>2.0.ZU;2-1
Abstract
The ultrastructural mechanisms of hepatic cholestasis were studied for the first time in fish during the early post-embryonic development of three teleostean species: sea bass, Dicentrarchus labrax, sea bream, Sparus aurata; and pike-perch Stizostedion lucioperca. The larvae were submitted to different diets (live prey, synthetic feed, or seawater with added glucose) and fasting. They displayed drastic modifications in liver structure leading to hepatocyte degeneration. Anomalies in th e biliary system were observed in all the larvae. Golgi activity and p ericanalicular vesicle production were very marked and frequently asso ciated with multilamellar bodies, leading to the formation of autophag ous vacuoles. Synthesis of biliary lipids was marked with the fed larv ae, whereas the secretion of particulate lipids failed in the fasting larvae. Lipid droplets formed at the hepatocyte sinusoidal pole in all the larvae. The hepatocytes resorbed their glycogen and displayed con siderable mitochondrial changes. Hypertrophied and pleomorphic mitocho ndria were associated with multilamellar bodies arising form the endop lasmic reticular membranes. These multilamellar bodies are released bo th into the bile canaliculi, and, mainly, into the sinusoids. The sinu soids, the perisinusoidal spaces, and the bile tract were strongly dil ated. The bile canaliculi are hypertrophied and deformed and, in the n on-fed larvae, contained multilamellar bodies. The relationship betwee n hepatic changes and metabolism is discussed. It is suggested that th e fish responded to lack of food or an unsuitable diet by biliary dysf unction that induced the anomalies mentioned. (C) 1998 Wiley-Liss, Inc .