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Results for “Polyvinylpyridine N-Oxide”

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PubMedDate not supplied

[Effect of polyvinylpyridine N-oxide on lipid metabolism indices in healthy and silicotic rats].

In the early period of investigations (in 1 month) polyvinylpyridine-N-oxide (PNO) causes a fall in the content of lipid compounds (total lipids, phospholipids, choesterol) in the liver and an inhibition of the lipolytic activity in the tissue of intratracheally quartzdust laden rats. Introduction of PNO into the lungs of dust-laden rats over a period of 4 months produces an appreciable diminution in the quantity of all the lipid components against the background of an increased lipolytic activity, recuced under the effect of quartz dust. In healthy rats PNO depresses the lipolytic activity of the pulmonary tissue and intermittently brings down the lipid compounds therein and in the spleen. In the blood of healthy and silicotic rats receiging PNO the level of the total and free cholesterol goes up. Early after administration of PNO the content of total lipids and beta-lipoproteids in the blood serum of dust-laden rats augments, while later on the concentration of total lipids goes down, while the level of summary ketone bodies rises.

Animals↗
PubMed1977

Promotion of incidence of adenovirus type 12 transplantable tumors by carrageenan, a specific antimacrophage agent.

Carrageenan, a sulfated polygalactose with known macrophage-toxic properties, was used to ascertain the role of macrophages in resistance to adenovirus type 12 transplantable tumors. A single ip injection of 5 or 10 mg carrageenan led to increased incidence and more rapid growth of tumors in C3H mice. Carrageenan was most effective if given 1 day before tumor inoculation; the effectiveness decreased with increasing intervals before or after tumor cell injection. The macrophage stabilizer poly-2-vinylpyridine N-oxide injected sc (150 mg/kg) 1 day before carrageenan was given reduced the incidence of tumors. These data lend further support to the importance of macrophages in tumor immunity.

Adenoviridae↗
PubMed1976

Promotion of tumor growth in vivo by antimacrophage agents.

Various attempts were made to assess the role of the mononuclear phagocyte system in tumor resistance of rats in vivo. The growth of sc inoculated, weakly immunogenic, carcinogen-induced, syngeneic tumor cells was modestly reduced by ip injection and, more impressively, by local injection of peptone-induced, activated, nonimmune macrophages. A single iv injection of silica particles or carrageenan on the day of sc tumor cell inoculation greatly enhanced tumor growth. When these agents had been given a few days before or after tumor cell inoculation, the tumor-promoting efficiency was distintly diminished or even cancelled. The enhancing effects of silica and carrageenan on tumor growth were nulified by the macrophage-stabilizing agent, poly-2-vinylpyridine N-oxide, To assess the in vivo consequences of silica administration, various cellular, biochemical, and functional macrophage parameters were determined at different intervals. Results indicated the complexity of events elicited after the mononuclear phagoycte system was damaged, which made the interpretation of such results difficult.

Animals↗
PubMed1975

Involvement of macrophages in genetic resistance to bone marrow grafts. Studies with two specific antimacrophage agents, carrageenan and silica.

Carrageenans and silica, agents toxic for macrophages, were used in this study to examine the role of macrophages in resistance of irradiated mice to inbred parental and rat bone marrow grafts. Administration of 2.5 mg of carrageenans or 2.5-5 mg of silica particles intravenously to prospective graft recipients resulted in a prompt abrogation of hybrid and xenogeneic resistance. The macrophage stabilizer poly-2-vinylpyridine N-oxide (PVNO) injected subcutaneously in the dose of 150 mg/kg, 24 hr before silica prevented or reduced the suppression of resistance. PVNO, however, did not antagonize the suppression of resistance by carrageenen, horse anti-mouse thymocyte serum and cyclophosphamide. These results suggest that a) a subpopulation is involved in marrow graft rejection by irradiated mice; b) carrageenan and silica apparently act on macrophages by different mechanisms c) horse anti-mouse thymocyte serum and cyclophosphamide may act on cells other than macrophages or they act on macrophages by a different mechanism than silica, to resistance to bone marrow transplantation.

Animals↗
PubMed1978

Effects of Corynebacterium parvum on murine myeloid leukaemia.

The effects of C. parvum on RFM/UN myeloid leukaemia were studied. Mice inoculated with 7.0 mg but not 0.7 mg C. parvum i.p. survived significantly longer than untreated leukaemic mice (P less than 0.001). Administration of silica abrogated the effects of C. parvum, whilst polyvinyl pyridine-N-oxide prevented the inhibitory effects of silica. These studies demonstrate that a single large dose of C. parvum, either before or after leukaemic-cell passage, can significantly prolong the survival of RFM mice bearing myeloid leukaemia. The effects of silica and PVNO on C. parvum suggest a critical role for macrophages in C. parvum effects on myeloid leukaemia.

Animals↗
PubMed1975

In vitro action of quartz on alveolar macrophage lipid peroxides.

The in vitro effects of quartz particles on the lipid peroxide rate were measured on guinea pig pulmonary alveolar macrophages (PAMs). As controls, either PAMs alone or exposed to inert dust were used. The amount of lipid peroxide resulting after one-hour incubation was determined by means of the thiobarbituric acid test (TBA). The results showed that quartz induced a substantial increase of lipid peroxide in PAMs compared with both samples (dust-free or exposed to corundum). The influence of pretreatment of quartz by polyvinylpyridine-N-oxide (PVPNO) and by mineral water containing carbonate and chloride ions was also studied.

Adult↗
PubMed1979

Effect of SiO2-liberated macrophage factor on protein synthesis in connective tissue in vitro.

1. To elucidate the role of macrophages in fibrosis the effect of the SiO2-liberated macrophage factor was assessed on protein synthesis in granulation-tissue slices. SiO2 could be replaced by chrysotile asbestos. The active factor is found in the 45/55% sucrose interface of macrophage homogenate. 2. There is no evidence of the involvement of collagenase. 3. The SiO2 effect is not influenced by the addition of yeast RNA to the incubation medium. 4. At a small concentration of polyvinylpyridine-N-oxide (PVNO) protein synthesis in the granulation tissue slices is stimulated, but at higher concentrations PVNO prevented the liberation of the fibrogenic factor from macrophages by SiO2. 5. Phospholipase C and trypsin inhibited the effect of SiO2, which was partially abolished also by heating, and by repeated freezing and thawing. 6. The macrophage RNAse, its inhibitors and fibroblast mRNA are suggested as key factors in the development of fibrosis.

Animals↗
PubMed1976

Counteraction of poly(4-vinylpyridine-n-oxide) on the depression of viral interferon induction by coal dust.

The depressive activity of coal dust on interferon induction by influenza was markedly subverted when either coal dust or LLC-MK2 cell monolayers were pretreated with poly (4-vinylpyridine-N-oside). The polymer alone neither induced interferon synthesis, inhibited viral induction of interferon, influenced viral multiplication, nor affected cellular-induced resistance by interferon. Absorption of the polymer to coal dust not only occurred at a more rapid rate than to cell monolayers, but also less polymer was required to pretreat coal dust than cell monolayers to achieve comparable amelioration of interferon production. The polymer effectively negated the adverse activity of coal dust particles, irrespective of the latter's size (is less than 2.0 to 74.0 mum). Virus multiplication in the presence of coal dust=treated cell monolayers attained a level that was twofol higher than that noted with either polymer-pretreated coal dust or polymer-pretreated cell monolayers. Interferon production was almost completely inhibited in the presence of coal dust; pretreating coal dust or cells with the polymer abrogated this inhibitory activity of coal dust. It is tentatively suggested that coal dust particles per se directly interact with cell membranes to subvert interferon induction and that the formation of an absorbed polymerlayer on these complexes prevents their interaction.

Coal↗
PubMed1979

Effect of silica on the innate resistance of inbred mice to Salmonella typhimurium infection.

The role of macrophages in the innate immunity of (CBA/N female X DBA/2N male)F1 female mice to Salmonella typhimurium was assessed with silica, an agent which has been reported to selectively inactivate macrophages. Silica, administered intravenously to mice, markedly decreased the phagocytic capacity of splenic macrophages but had no effect on splenic responsiveness to the B-cell mitogen lipopolysaccharidide or the T-cell mitogen phytohemagglutinin, nor did it affect the frequency of surface immunoglobulin-positive cells (B cells). Silica given to mice 1 day before intraperitoneal challenge decreased the 50% lethal dose of S. typhimurium 100-fold. The incidence of survival of mice given silica up to 14 days before infection with a sublethal dose of organisms was also decreased. This susceptibility could also be demonstrated when silica was given 10 days, but not 20 days, after S. typhimurium infection. Poly-2-vinylpyridine-N-oxide, a lysosomal stabilizing agent, abrogated the silica effect. Deaths among silica-treated mice followed uncontrolled multiplication of the organism in the spleen. These results provide direct evidence that macrophages play an essential role in natural immunity to murine typhoid and demonstrate the efficacy of silica as a tool to analyze macrophage function.

Animals↗
PubMed1975

Adsorption of syndiotactic and isotactic poly(2-vinylpyridine 1-oxide) on quartz surface.

Poly(2-vinylpyridine 1-oxide) inhibits the cytotoxic effects of quartz in cell cultures but the syndiotactic polymer behaves differently from the isotactic and atactic polymers. In each case approximately 1-0 mg/m2 of the polymer represents the adsorption maximum. No difference has been found between the adsorption isotherms of the stereoisomeric polymers or the stability of the adsorbed layers. The layers are not removed by repeated washing. The observations do not support the theory that the poly(2-vinylpyridine 1-oxide) is active because it coats the quartz surface.

Adsorption↗
PubMed1976

[Morphofunctional state of pulmonary macrophages and their biological protection during phagocytosis of toxic elements].

Studies of a morphofunctional state of macrophages of the lungs of rats in phagocytosis of quartz (size of particles 1-2 mum) and against the background of prophylactic administration of polyvinylridine-N-oxyde (PVNO) were carried out using the method of quantitative cytochemistry (interference microscopy and cytometry) and electron-microscopy techniques (raster and transmissive). It was established that administration of PVNO led to intensification of the phagocytic activity of macrophages, increase in the content of RNA and dry weight (total proteins) therein, enlargement of the sizes of cells. The electron-microscopy investigation showed a good preservation of organelles of macrophages.

Animals↗
PubMedDate not supplied

The biological effects of mineral fibres, especially asbestos, as seen from in vitro and in vivo studies.

Two in vitro models have been extensively used to compare the biological action of different types of asbestos fibres: the haemolytic effect and the cytotoxic one on macrophages grown in cell culture. The use of both techniques as led towards a better understanding of the chemical reactions which occur between fibres and the biological membranes of cells or intracellular organelles. Studies on the prevention of haemolysis and cytotoxicity have also been of use in explaining how asbestos acts a the cellular and molecular levels. Regarding in vivo studies, useful comparisons have been made of the fibrogenic and carcinogenic effects of different types of fibres in man and experimental animals. Both the in vitro and the in vivo aspects of the problem are discussed in some detail and an attemps is made to provide a reasonably unified concept for both.

Animals↗