Fish oil-induced yellow fat disease in rats. II. Enzyme histochemistry of adipose tissue

Adipose tissue in various stages of fish oil-induced yellow fat disease in the rat had the same acid phosphatase and 5-nucleotidase activity pattern as similar stages of the disorder in mink and pig. A weak acid phosphatase and 5-nucleotidase activity was seen in interstitial lipofuscin-laden macrophages in "stage M" yellow fat disease without fat cell degeneration. Activity of these macrophagic enzymes increased when there was fat cell degeneration ("stage S" and "stage E" yellow fat disease). This different phosphatase activity in the same cell type may result from phagocytosis of substrates with variable digestibility. Macrophages directly surrounding affected fat cells in steatitis areas ("stage S" and "stage E") had strong acid phosphatase and 5-nucleotidase activity. As in the pig, increased 5-nucleotidase activity was found in affected fat cells, which probably indicates plasma membrane damage. Increased nonspecific esterase activity occurred around affected fat cells. Only a small part of this esterase activity originated from inflammatory cells. This indicates that an increase of esterase activity in degenerating adipose tissue may be an endogeneous process in this tissue.     

Enzyme activity in cell cultures infected with herpesvirus suis]

The activity of succinate dehydrogenase (SDH) and lactage dehydrogenase (LDH) was studied in chick-embryo fibroblast cultures after inoculation of the virulent strain "A2" and the avirulent strain "MK" of herpesvirus suum. Strain "A2" reduced SDH activity, and so did strain MK, but here the decrease of enzyme activity was slower, and it did not become evident until the 24th hour. LDH activity fluctuated after "A2" infection but was generally increased, while there was no change in LDH activity, compared with uninfected control cells, after "MK" infection. When interaction of cell and virus took place in the presence of 5-iodo-2-desoxyuridine (IUDR), strain "A2" produced little change in the enzymes, but "MK" infection was accompanied by a definite fall in SDH and a slight increase in LDH. The presence of IUDR inhibited the proliferation of the virulent strain but had no apparent effect on proliferation of the attenuated strain "MK". Investigation of the enzyme activity of cells infected with Aujeszky's disease virus has revealed new biological properties of the virus, which might serve to distinguish between different strains of the virus.     

The effects of ultraviolet-B (UV-B: 290–320 nm) radiation on blister blight disease of tea (Camellia sinensis)

Sunlight is known to reduce the incidence of blister blight disease of tea, caused by Exobasidium vexans . The effects of the ultraviolet-B (UV-B: 290–320 nm) component of solar radiation on the disease and the development of E. vexans were studied in the field in Sri Lanka using UV-screening filter materials held over a commercial crop. Exclusion of UV-B radiation by Polyester, which reduces fluxes in the UV-B region by approximately 75–85%, increased both the number of translucent spots (immature sites of infection) and number of sporulating blisters (mature sites of infection), but it had little or no effect on the sporulation of the pathogen. When basidiospores were artificially inoculated on leaves, and were exposed to full or filtered solar radiation, their survival and germination increased when UV-B wavelengths were removed; significant differences were found 62 h after inoculation. However, UV-B did not affect the extension of germ tubes. This study indicates that the UV-B component of solar radiation plays an important role in the natural regulation of blister blight disease in the field.