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).

The distribution of 35S-taurine in rat neonates and adults was investigated by wholy -body autoradiography. The neonates (4-day-old) were frozen in dry-ice hexane at 30 min, 1, 3 and 6 h after an intraperitoneal injection of 35S-taurine, whereas survival intervals for adult rats were 1 and 3 h. Whole-sagittal sections of the frozen rat, obtained by using a cryostat microtome were dried in situ and autoradiographed. In rat neonates and adults, 35S-taurine was mainly accumulated in the renal cortex, urine, feces, liver, eye (lens, vitreous fluid, retina), hypophysis, thymus, adrenal glands, nasal mucous membrane, salivary glands, gastric mucosa, small and large intestinal mucosa, choroid plexus, myocardium and sebaceous glands. In the rat neonate, such regions as the olfactory bulb, cerebrum, and cerebellum showed relatively high optical density.

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