FINE-STRUCTURE OF THE ADRENOCORTICAL HOMOLOG IN THE NORTH-AMERICAN EEL AND MODIFICATIONS FOLLOWING SEAWATER ADAPTATION

The ultrastructure of the adrenocortical homologue (AH) of the north American eel (Anguilla rostrata) was studied from freshwater and long‐term (1.5 years) seawater (SW) adpated animals. The AH tissue situated in the wall of cardinal veins is surrounded by a thin layer of collagenous capsule; in the region away from the vein wall, parenchymal cells are separated by interstitial lacunae containing collagen bundles, capillaries, chromaffin cells and nerve fibers often applied closely to the surface of AH cells. The free surface of the cell near the vein wall, capillaries or interstitial space extends numerous slender microplicae. The cytoplasm is characterized by the presence of mitochondria with tubular cristae, a network of smooth endoplasmic reticulum, a few cisternae of rough surfaced endoplasmic reticulum, well developed Golgi apparatus, coated vesicles, centrioles, cilium, filaments, microtubules, dense bodies of variable nature and a scarcity of liposomes. The cell nuclei possess invaginated cytoplasmic pseudo‐inclusions. Electron histochemical reaction for free cholesterol revealed the occurrence of needle‐shaped crystals mainly associated with surface microplicae and smooth endoplasmic reticulum, which seems to be the major organelle for storage or synthesis of this steroid precursor. SW animals indicated ultrastructural signs of stimulated steroid synthesis and secretion, i.e., high degree of pseudo‐follicle formation, increased electron density of mitochondria, greater abundance of lysosomal dense bodies, hyperactivity of Golgi apparatus and dilation of smooth endoplasmic reticulum tubules. Some SW fishes showed extensive deposition of osmiophilic inclusions in the mitochondria and stacks of elongated cup‐shaped mitochondria. Chronic seawater acclimation enhances AH activity as judged by ultrastructural criteria with ultimate mitochondrial degeneration resulting possibly from prolonged cortisol hypersecretion; the latter may be linked with physiologic re‐adjustment of ionic transfer mechanism in hyperosmotic medium. Copyright © 1979 Wiley‐Liss, Inc.