Ultrastructural findings of Kupffer cells, particularly with relation to acid phosphatase (ACPase) activity and erythrophagocytosis, are described in mice with hereditary erythroblastic anemia which showed symptoms of severe anemia during the postnatal period.
At the 10th day after birth, the Kupffer cells of the anemic mice were swollen and intercalated the cytoplasmic process between the parenchymal cells. The lysosomes were more abundant than normal. In older mice, more progressed symptoms of erythroblastic anemia and more developed Kupffer cells were observed. At the 17th day, the secondary lysosomes and phagosomes with marked ACPase activity had dominated over the primary lysosomes. Some lysosomes release hydrolytic enzymes, including ACPase, into the cytoplasm of the Kupffer cell and the space of Disse and sinusoid.

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The localization of fibronectin (FN) and type I collagen in livers of normal rats and simular animals administered CCl₄ was investigated using immunoperoxidase techniques. Continuous observation of the respective specimens in these experiments were done on electron microscope.
Neither FN nor type I collagen was found in any hepatocytes and sinusoids of normal rat livers, except in a small amount in the central and portal areas. In CCl₄-induced hepatic fibrosis, FN was first distributed from plasma, followed by type I collagen distribution on the relevant FN deposits. These latter matrix proteins were found to exhibit a distribution pattern similar to that of FN.
From these results and other reports, primary changes in liver fibrosis due to the administration of CCl₄ are assumed to occur as follows:
FN is first deposited from plasma together with macrophages and fibroblasts, followed by the secretion of type I collagen in the FN deposits by infiltrated fibroblasts, and/or transported Ito cells.

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The lectin-binding activity in papillomas arising from the skin, oral cavity, nasal, paranasal, and pharyngeal mucosa was examined by the use of the horseradish peroxidase (HRP) -conjugated lectin method. Keratinized epithelia in the skin and hyperkeratinized papillomas showed a marked regional or zonal distribution in binding of the lectins used; on the contrary, non-keratinized epithelia such as pseudo-stratified columnar epithelia had no zonal lectin distribution. The hyperortho-keratinized layer gave negative binding for the various lectins; the hyperpara-keratinized layer, slightly positive the granular cell layer containing keratohyalin granules and the upper spinous layer, the most prominent binding; and the basal cell layer, mostly negative. These lectin-binding patterns in the homologous epithelium were similar to that of keratinized papillomas. Cytochemical localization of such lectin binding was limited to intercellular materials and cellular surface in keratinized squamous epithelium and pseudo-stratified columnar epithelium. PA Con A-HRP staining was positive in granular materials located in the spinous layer cells, corresponding to glycogen-positive cells. Malignant or dysplastic cells in papillomas lesions were reduced in lectin binding and irregular in their distribution pattern.

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In order to cytochemically demonstrate the NADPH dependent H₂O₂ generation system in the sinusoidal lining cells of the liver, the authors applied the modified method of Briggs et al. (5) to an isolated liver perfusion system devised by Sugano et al. (21) . The rat liver was perfused with the reaction medium containing 40mg NADPH, 40mg CeCl₃ 7H₂O and 2mg glucose in 100ml of 0.1M tris-maleate buffer solution (pH7.4), continuously supplied with a gas mixture (95%O₂ and 5%CO₂) . With respect to the specificity of the reaction, the in situ localization, and the amount of reaction products, adequate results were obtained with this system. Thus, the activity in the sinusoidal lining cells was compared between livers of the Jcl: Wistar-and the ICR/d-strain rats affected with spontaneously occurring cataracts and dermatitis.
Both Kupffer and endothelial cells showed conspicuous reactivity. A specific and significant reaction product was observed, adherent to the plasma membrane, on the external cell surface, including that of invaginated portions or coated pits. Furthermore, it was also noted on the internal surface of phagocytic vacuoles or coated vesicles. Comparing the two strains of rat, a much higher reactivity was shown in the liver of ICR/d-rat, suggesting that a defensive activity may be enhanced in the sinusoidal area to compensate for constitutional defects such as immunological disorders inherent in the ICR/d-strain.

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The affinity of estradiol (E₂) for eosinophils in the rat and mouse uteri during the estrous cycle was studied by light and electron microscope autoradiography (ARG) . In in vivo ARG, in which the prefixed uteri were incubated at each stage of estrous cycle with ³H-E₂ or its ligand 3H-moxestrol, the developed silver grains were localized on the specific granules of eosinophils. At the late estrus phase, eosinophils were frequently phagocytized by macrophage-like interstitial cells, whose phagosome included eosinophilic granules in various stage of degeneration covered with silver grains, and also showed positive reaction for acid phosphatase activity Grain accumulation was inhibited when the tissue was incubated in ³ H-E₂ with a 100-fold excess of nonradioactive E₂. When fresh frozen thin sections were incubated in 3H-E₂, we succeeded in demonstrating the binding ef E₂ to the eosinophils in spleen, small intestine, blood and bone marrow. However, in in vivo ARG using the fresh thaw-mounte technique, only the uterine eosinophils showed grain accumulation and eosinophils of other tissues did not bind ³H-E₂. Local eosinophilia was observed in the uterus of ovariectomized rats at one hr after E₂ injection into the uterine wall.
These results suggest that all eosinophils may have a strong affinity for E₂, and that they are directly induced into the uterus by estrogen. Specific granules of eosinophils, which contain strong peroxidase enzymatic activity, seem to destroy the excess amount of E₂ in the uterus at estrus, and then the eosinophils are phagocytized by the macrophage-like interstitial cell.

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