A gelsolin-related protein was isolated from seminal vesicles of the annelid Lumbricus terrestris. Compared with the isoforms of the gelsolin-related protein previously found in the muscle of the annelid body wall, the isolated protein was assigned to the first isoform (EWAM-P1) because of its electrophoretic mobility, chromatographic elution behaviour, immunological cross-reactivity and identical nucleotide sequence of segments obtained by reverse transcription/polymerase chain reaction. Immunofluorescence studies with smear preparations of developing male germ cells revealed characteristic changes of the local distribution of actin and EWAM-P1 during spermatogenesis. These changes were correlated with the developmental transport processes and structural alterations. F-actin, as revealed by rhodamine-phalloidin staining, formed a toroid-shaped structure in cytoplasmic bridges connecting the germ cells to a central cytophore during the developmental stages. An actin antibody reacting with both G- and F-actin demonstrated that actin was concentrated at the proximal and distal parts of the spermatocytes. EWAM-P1 was also localized in these regions, with intense staining in the distal part of spermatocytes and young spermatids in which the Golgi complex and proacrosome resided. The anti-actin antibody further stained the periphery of the nucleus. This staining gradually reduced during sperm maturation and covered about half of the length of the nucleus in elongated spermatids. Co-localization of EWAM with actin implied a functional significance of this gelsolin-related protein for the rearrangement of the actin cytoskeleton during earthworm spermiogenesis.

This study was designed to investigate the in vitro effect of nitrogen dioxide on some immunofunctions of immune-competent cells. , and bovine alveolar macrophages (BAM) were exposed to synthetic air or to NO, (1.5 and 3.0 ppm) for 1 or 2 h. Under the special conditions of exposure, which allow the cells to be kept in direct contact with the gases during the whole incubation period, the cells stay alive in synthetic air for more than 4 h. After a lag phase of about 1 h, the exposure to NO, results in a decrease of the viability, which is dependent both on the time and on the concentration. The morphology of the cell surface structures is obviously changed, even under conditions in which a loss of viability cannot yet be observed. Simultaneously, the capability of the cells to generate superoxide anions in response to a stimulation with zymosan, but not with TPA, is markedly reduced and, in ' addition, the spontaneous release of superoxide anions from nonstimulated cells is also diminished after their exposure to NO,. Like the superoxide anion production, the tumor necrosis factor OL VNF-a) and the interleukin 8 (IL-8) releases by both types of cell in ~ response to a stimulation with lipopolysaccharide ILP5) are significantly suppressed after NO, exposure. But whereas the exposure to NO, increases the liberation of TNF-o( and IL-8 by nonstimulated HL60-M, the TNF-OL release of resting BAMs is drastically suppressed. The results indicate that NO, has some distinct effects on immunologically relevant functions of HL60-M and BAMs.The effects concern mainly the capability of the cells to respond to external stimuli and only in a minor extent the functions of resting cells. These findings can help to explain the reported higher susceptibility to infections of animafs that have been exposed to NO,.

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