The cellular content of carbon, nitrogen, amino acids, polysaccharides, phosphorus and adenosine trtphosphate (ATP) was determined at several stages during the life cycle of the dinoflagellate Scrippsiella trochoidea (Stein) Loeblich. Carbon per cell decreased slightly between exponential and stationary phase growth in vegetative cells whereas nitrogen per cell did not change. Both of these cellular components increased markedly on encystment and then decreased to vegetative cell levels during dormancy and germination. C/N ratios increased gradually during cyst dormancy and activation, reflecting a more rapid decrease in N than in C pools, even though both decreased through time. Amino acid composition was relatively constant during the vegetative cell stages; glutamic acid was the dominant component. Arginine was notably higher in cysts than in vegetative cells but decreased significantly during germination, suggesting a role in nitrogen storage. The ratio of neutral ammo acids to total ammo acids (NAA/TAA) decreased as cysts were formed and then gradually increased during storage and germination. The ratio of basic ammo acids to total ammo acids (BAA/TAA) changed in the opposite direction of NAA/TAA, whereas the ratio of acidic acids to total amino adds (AAA/TAA) was generally invariant. Ammo acid pools were not static during the resting slate in the cysts: there was degradation or biosynthesis of certain, but not all, classes of these compounds. The monosacchande composition of cold and hot water extracted polysaccharides was quite different between cells and cysts. A high percentage of glucose in cysts suggests that the storage carbohydrate is probably in the form of glucan. Total cellular phosphorus was higher in all cyst stages than in vegetative cells. However, ATP‐cell−1 decreased as vegetative cells entered stationary phase and encysted, and continued to decrease in cysts during dark cold storage. ATP increased only as the cysts were activated at warm temperatures in the light and began to germinate. The above data demonstrate that dormancy and quiescence are not periods of inactive metabolism but instead are times when numerous biochemical transformations are occurring that permit prolonged survival in a resting state.

Histological and histochemical alterations on gill primary lamellae of the teleost, young yellowtail (Seriola quinqueradiata), affected by the sea bloom (Chattonella antiqua) were studied and causative factors responsible for fish death were considered in the present work.A significant loss of mucous goblet cells on the afferent ridges occurred within about one hr. Among the remainder, mucous cells located on the afferent ridge of the basal part of the gill primary lamellae were markedly impaired (64% decrease in number). For TEM preparation, hyaline degenerations of the mucous cell membrane were observed.Histochemically, these mucous goblet cells contained neutral and acid glycoproteins.The cell layer on both ridges exposed to sea bloom appeared to be thinner than that of the control.The cell body of the internal multilayered mass was shrunk and intercellular spaces were markedly expanded. These edematous gill lamellae might be caused by the disappearance of the mucous coat, leading to locally impaired osmoregulations. As a result, gas exchange on the gill lamellae might be disturbed.The sea bloom often appearing on the Seto Inland Sea during the summer causes great damage to the fish farms, especially to young yellowtails. The species of plankton causing the sea bloom depend on the time, place, and year. The effects of these organisms on the fish are thought to concern oxygen deficiency (7,11,14). However, the mechanisms leading to fish death are still unknown. In the previous work, the effects of sea bloom (Gymnodinium) on gill primary lamellae of the teleost, young yellowtail (Seriola quinqueradiata) were investigated from the morphological and histochemical point of view (1, 12). As a result, it was found that the mucous coat on the gill and most of the mucous goblet cells located on the afferent ridge disappeared, though they were intact on the efferent ridge. Scanning electronmicroscopically, pavement cells were swollen also on the afferent ridge, while they were intact on the efferent ridge. Chloride and mucous goblet cells with many cellular extensions appeared in the epithelia of the afferent ridge of the primary lamellae. These observations suggest that the causative factors responsible for fish death might be locally impaired osmoregulations on the gill lamellae, leading to the respiratory disorders (oxygen deficiency).

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