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PubMed1990

Effects of turpentine-induced inflammation on the hypoxic stimulation of intestinal Fe3+ absorption in mice.

Chronic subcutaneous turpentine administration (weekly for 6 weeks) induced a mild normocytic anaemia in mice. In-vitro and in-vivo intestinal Fe3+ absorption parameters were, however, not significantly altered from values in saline-treated or untreated mice. Normal mice, when exposed to 3 days hypoxia demonstrated a 2-3-fold increase in iron absorption in vivo, mainly due to changes in the amount of iron transferred from the mucosa to the plasma and thence to the carcass. A 2-3-fold increase in Vmax was also observed in in-vitro uptake experiments using isolated duodenal fragments. In contrast, turpentine-treated animals, though demonstrating an enhanced in-vitro maximal uptake capacity, failed to elicit an adaptive response in vivo following hypoxic exposure. These findings suggest that a circulating (humoral) factor may be responsible for the inhibition in absorption in vivo in this turpentine-induced inflammatory model.

Anemia↗
PubMed1985

The acute phase response of C3, C5, ceruloplasmin, and C-reactive protein induced by turpentine pleurisy in the rabbit.

Concentrations of five serum proteins, C3, C5, ceruloplasmin, C-reactive protein, and albumin, have been measured during the acute phase response in rabbits with turpentine-induced pleurisy. C-reactive protein concentrations in the circulation rose abruptly between 12 and 36 hours to a level greater than 50 times the pretreatment concentration, then returned to undetectable amounts by 96 hours. C3 and ceruloplasmin both showed some increase in concentration by 12 hours and reached their maximum concentrations of two to three times the baseline levels 48-72 hours after the turpentine treatment. Concentrations were still elevated at 120 hours, after which time they gradually returned to normal. C5 and albumin concentrations in the turpentine-treated rabbits did not differ from the baseline concentrations. The same five proteins were measured in the inflammatory exudate. C-reactive protein was not detectable at any of the time points. C3, C5, ceruloplasmin, and albumin were present in normal pleural fluid at roughly half their serum concentrations. The activities of C3, C5, and ceruloplasmin were low in the early exudate, but C3 and C5 activity rose relative to their concentrations in the later samples of pleural fluid. The specific activities of C3 and C5 were higher in the pleural fluid at 72 hours than in plasma, while that of ceruloplasmin remained less in the pleural fluid than in plasma throughout the experiment. The involvement of these proteins and their relation to the inflammatory response are discussed.

Acute-Phase Proteins↗
PubMedDate not supplied

[The influence in the rat of counter-irritation by turpentine on the leukocyte content of exudates induced by sponge implants].

In normal rats, PGE1, arachidonic acid, indomethacin and diclofenac did not modify the leucocyte content of sponge exudates withdrawn 4 hours after implantation while arachidonic acid increased the level in PGE2 and indomethacin reduced it. The leucocyte content of sponges exudates withdrawn 18 hours after implantation was not modified by PGE1 and TXB2, but diminished by indomethacin and NDGA and increased by arachidonic acid. As the chemotactic effect of arachidonic acid was slightly reduced by indomethacin and abolished by NDGA, it could depend on the formation of lipoxygenase derivatives. In normal rats, the leucocyte content of sponge exudates withdrawn 18 hours after implantation was increased slightly by normal serum and largely by serum from turpentine-treated rats. The blood leucocyte content was not modified in turpentine-treated rats. However in these rats, the leucocyte content of sponge exudates was low comparatively to the leucocyte content in normal rats. This low level was not affected by indomethacin, arachidonic acid and normal serum. The leucocytes of turpentine-treated rats seem to be desensitizated towards chemotactic factors. Similar desensitization was observed in rats treated by iota carrageenan.

Animals↗
PubMed1986

Turpentine-induced acute inflammatory response in Gallus gallus: oedema, vascular permeability and effects of non-steroidal anti-inflammatory drugs.

Turpentine-induced acute inflammatory responses in chicks were studied experimentally. Foot pad oedema was measured using a plethysmograph. Skin vascular permeability was evaluated using the Evans blue technique. Turpentine injury induced a typical biphasic response when the two parameters of the inflammatory reaction were studied. Some unexpected alterations of the turpentine-induced inflammatory response were seen when chicks received non-steroidal anti-inflammatory drugs. Pretreatment with promethazine, phenylbutazone, methysergide and indomethacin resulted in a decrease in foot oedema. An inhibitory effect upon vascular permeability was found when promethazine, phenylbutazone and indomethacin were used. Methysergide did not inhibit the increase in vascular permeability of the skin. Possible mechanisms are discussed.

Animals↗
PubMed1981

Effects of turpentine-induced inflammation on the synthesis of dolichol-linked intermediates of N-glycosylation and the phosphorylation of dolichol by CTP-dependent dolichol kinase.

Inflammation was induced in rats by the subcutaneous injection of turpentine. Microsomes were prepared from the livers between 2 and 72 h after injection. Mannose and glucose incorporation into mannosyl and glucosyl dolichyl monophosphate was increased 2-fold over saline-injected controls 24 h after induction of inflammation. Synthesis of glycosylated dolichyl pyrophosphoryl oligosaccharides was also increased compared to controls. Extraction and assay of dolichol monophosphate from inflamed and control rat liver microsomes indicated that the endogenous levels of the lipid were elevated in the inflamed state. CTP-dependent phosphorylation of endogenous dolichol was also found to increase in microsomes from inflamed rats 24 h after injection of turpentine. When exogenous dolichol was added to the microsomal system an increase in phosphorylation was observed as early as 6 h after turpentine injection. Furthermore, the increase appeared to be biphasic, there being two peaks of elevated activity at 12 and 36-48 h after induction of inflammation. The earlier peak was the greater of the two. The results suggest that the increase in glycosylation of dolichol derivatives was due to greater amounts of endogenous dolichol monophosphate. The increase in dolichol monophosphate was itself due to greater availability of dolichol and an increase in the levels of CTP-dependent dolichol kinase.

Animals↗
PubMed1978

The effect of D-galactosamine on plasma protein synthesis by the perfused rat liver from turpentine-stimulated donors.

D-galactosamine (100 mg) was added to the reconstituted blood during 4h perfusion of livers isolated either from control rats or those injected with turpentine 20 h or 5 h earlier. This dose of galactosamine administered 30 min before [3H]lysine significantly inhibited the incorporation of the label into liver proteins, and even more into plasma proteins, but albumin and acute-phase reactants (fibrinogen, seromucoid fraction, Concanavalin A-adsorbed glycoproteins) were all similarly affected. When galactosamine was administered in vivo simultaneously with turpentine, and the liver was isolated 5 h later, trauma-induced fibrinogen synthesis was selectively inhibited. This can be explained either by a differential control of synthesis of various acute-phase reactants, or by augmentation of catabolism of fibrinogen in galactosamine-treated rats. Crossed immunoelectrophoresis of the full perfusate or Concanavalin A-adsorbed glycoproteins did not reveal any significant effect of galactosamine on the protein pattern obtained from control or turpentine-stimulated liver donors.

Animals↗
PubMed1994

The effect of prednisolone and a protein-deficient diet on plasma albumin and fibrinogen in a turpentine-induced acute-phase reaction in rats.

The acute-phase reaction (APR) that follows inflammation is characterized by profound metabolic changes such as hypoalbuminemia, which is frequently aggravated by malnutrition; and hyperfibrinogenemia. Because some of these changes are mediated by cytokines, corticosteroids that are known to suppress cytokine production might be expected to alleviate the course of the APR. In the present study, for 3 weeks rats were fed (1) a standard diet (25%) protein), (2) a protein-deficient diet (5% protein), or (3) a standard diet supplemented by treatment with intraperitoneal prednisolone (7.5 mg twice daily starting 3 days before and throughout the experiment). Changes in plasma albumin, fibrinogen, and total protein levels were measured 0, 1, 3, and 8 days after turpentine was injected subcutaneously. Albumin and fibrinogen were immunohistochemically stained in the liver 0, 3, and 8 days after injection. Plasma albumin decreased by roughly 50% in all three groups, and reached a nadir on day 3. Fibrinogen peaked by day 1 in all animals and fell gradually thereafter. The total protein concentration, which was higher with prednisolone, remained unchanged in all three groups. The level of immunostainable liver albumin was initially reduced in malnourished rats. If further diminished in the majority of hepatocytes after administration of turpentine in all groups. Although few hepatocytes stained positive for fibrinogen before the onset of inflammation, uniform increase in immunostaining occurred by day 3 in all rats regardless of treatment. Neither prednisolone nor malnutrition substantially altered the decrease in plasma albumin and the simultaneous increase in fibrinogen in a turpentine-induced APR.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute-Phase Reaction↗
PubMed2002

Characterization of uptake of 2-deoxy-2-[18F]fluoro-D-glucose by fungal-associated inflammation: the differential uptake ratio for blastomyces-associated lesions is as high as for lymphoma and higher than for turpentine abscesses in experimentally induced lesions in rats.

PURPOSE: The objective of this investigation was to determine the biologic basis and the significance of uptake of 2-deoxy-2-[18F]fluoro-D-glucose (FDG) using experimentally created fungal lesions in rats. PROCEDURES: Uptake of FDG by experimentally induced Blastomyces granulomas was compared with uptake by turpentine abscesses (Group 1) and by lymphomas (Group 2) using the differential uptake ratio (DUR) measured one hour after administration of 2 mCi FDG intravenously. Frozen tissue sections of Blastomyces lesions and turpentine abscesses were placed in contact with radiographic film for macroautoradiography. RESULTS: In rats in Group 1, the median (range) DUR for the Blastomyces granulomas was 1.9 (1.1-2.6) and was significantly higher than the DUR for turpentine abscesses 0.9 (0.6-1.4) and muscle 0.2 (0.1-0.5; P < 0.001). In Group 2, the median (range) DUR for the Blastomyces granulomas, lymphomas, and muscle from the rats in Group 2 were 1.8 (1.2-3.4), 1.9 (1.0-4.0), and 0.2 (0.1-0.3), respectively. There was no significant difference between the DUR of Blastomyces granulomas and lymphomas. Macroautoradiographs of the Blastomyces granulomas revealed intense uptake of FDG in the region occupied by the yeast organisms and the granulomatous inflammation. CONCLUSIONS: Blastomyces granulomas typically have high uptake of FDG associated with the region composed of the granulomatous inflammatory reaction and Blastomyces yeast organisms.

Journal Article↗
PubMed2001

Isolation, characterization, and cDNA cloning of chicken turpentine-induced protein, a new member of the scavenger receptor cysteine-rich (SRCR) family of proteins.

Acute-phase serum proteins were induced by administrating a chicken with turpentine oil. One of these proteins was a new protein that appeared in front of albumin in polyacrylamide disc gel electrophoresis using a 4.5-16% gel. To purify this protein, turpentine-administrated chicken serum was fractionated by ammonium sulfate precipitation at 50% saturation, and the supernatant fraction was chromatographed on a DEAE-Toyopearl 650S column. The purified protein is a mannose-glycoprotein, and its N-terminal sequence, determined by the Edoman method, is not homologous from that of other reported acute-phase proteins. An analysis of physiological function with two different test systems, chemiluminescence measurement and electron spin resonance spectroscopy, showed that the purified protein has antioxidant activity and inhibits superoxide (O(2)) mediated by activation of the receptor. In support of these results, the complete amino acid sequence of 18-B is homologous to the scavenger receptor cysteine-rich (SRCR) family of proteins that participate in the regulation of leukocyte function. 18-B is composed of four SRCR domains, which is different from the previously characterized SRCR family of proteins such as Spalpha, CD6, and CD163. These findings indicate that turpentine-induced 18-B, a new member of scavenger receptor cysteine-rich family, may be implicated in regulation of cell function in a manner of inhibition of the overproduction of the reactive oxygen species.

Amino Acid Sequence↗
PubMed1978

Early colonisation of a local inflammatory lesion and its relationship to changes in systemic leucocyte availability: a study of turpentine-induced lesions in the rat.

The changes in both peripheral blood leucocyte counts and lesion inflammatory cells have been measured at intervals up to 24 hr following the subcutaneous injection of turpentine in rats. The lesion PMNL changes were characterised by a sharp rise between 0 and 6 hr and a less-rapid fall between 6 and 24 hr. The half-life of lesion PMNL's, as determined by tritiated thymidine labelling between 12 and 24 hr after turpentine injections, was 13 hr and there was a significant correlation between blood and lesion PMNL counts throughout the experimental period. A dependence of the lesion PMNL population on the availability of these cells is thus suggested. Mononuclear cells, which were predominantly monocyte-derived, showed a sharp rise between 6 and 12 hr, plateauing thereafter. These changes were not associated with significant alterations in blood monocyte counts. Although significant changes in blood lymphocyte counts were observed, these were not reflected in the local inflammatory lesion.

Animals↗
PubMed1998

Interleukin 6, but not ciliary neurotrophic factor or leukaemia inhibitory factor, is responsible for the acute phase response to turpentine-induced myositis.

The acute phase response to inflammation is mediated in part by the endogenous production of pro-inflammatory cytokines. Interleukin 6 (IL-6) and members of its superfamily, including ciliary neurotrophic factor (CNTF) and leukaemia inhibitory factor (LIF) have been implicated as primary mediators of the hepatic acute phase response. In the present report, mice suffering a turpentine-induced myositis were passively immunized with antibodies against either IL-6, CNTF or LIF. Passive immunization against IL-6 attenuated the anorexia and completely prevented the hypoalbuminaemia, and increases in the serum concentration of the acute phase reactants, amyloid P, amyloid A and seromucoid. In contrast, passive immunization against either CNTF or LIF failed to modulate the anorexia, weight loss or hepatic acute phase protein responses. The findings suggest that IL-6, but not other members of its superfamily, is primarily responsible for the hepatic acute phase response, and contributes to the anorexia, associated with turpentine-induced myositis.

Acute-Phase Reaction↗
PubMed1994

Elevation of circulating monitor peptide/pancreatic secretory trypsin inhibitor-I (PSTI-61) after turpentine-induced inflammation in rats: hepatocytes produce it as an acute phase reactant.

Monitor peptide (MP) is a trypsin-sensitive cholecystokinin (CCK)-releasing peptide purified from rat pancreatic juice on the basis of its stimulatory activity toward pancreatic enzyme secretion and has been reported to exhibit cell growth-stimulating activity. Pancreatic secretory trypsin inhibitor (PSTI) prevents premature activation of trypsinogen in the pancreatic duct. There are two PSTIs (PSTI-61 and -56) purified from rat pancreatic juice on the basis of trypsin inhibitory activity as reported previously. Fushiki et al. (1989, FASEB J. 3, 121) showed that MP is structurally the same peptide as PSTI-61. We measured the serial changes of circulating MP/PSTI-61 in rat and those in the level of PSTI-61 mRNA in the rat liver to investigate another novel role of this peptide in the turpentine-induced acute inflammation model. The elevation of serum MP/PSTI-61 as well as the alpha 2-globulin fraction, which is known to include several acute phase reactants such as alpha 2-macroglobulin and haptoglobin, was observed after induction of the turpentine inflammation. The serum alpha 2-globulin fraction had increased approximately 3-fold over the initial level at 48 hr after the injection. In contrast, serum MP/PSTI-61 had increased approximately 17-fold over the initial level at 48 hr after the injection. The elevation of circulating MP/PSTI-61 was significantly related with that of the alpha 2-globulin fraction (r = 0.91, P < 0.01). Immunoreactive MP/PSTI-61 was detected in the liver after induction of the inflammation (152.5 +/- 16.5 ng/g wet weight), but in the normal rat liver there was no immunoreactive MP/PSTI-61.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute-Phase Proteins↗
PubMed1995

Hemorrhagic shock abolishes the myelopoietic response to turpentine-induced soft tissue injury.

Hemorrhagic shock has been shown to alter bone marrow (BM) myelopoiesis. Isolated hemorrhagic shock is uncommon after trauma and the combined effect of tissue injury and shock on myelopoiesis is unknown. We studied the growth of BM granulocyte-macrophage colony forming units (CFU-GM) following shock and soft tissue injury. Rats were anesthetized and allocated into one of four groups: CONTROL, sham neck dissection; SHOCK, rats were bled to a mean BP of 45 mmHG for 45 min and resuscitated with shed blood and saline; TURP, soft tissue injury was induced by turpentine 0.5 ml/100 g SQ into the hindquarter; SHOCK + TURP, rats received TURP just before SHOCK as described above. Groups (n = 6) were sacrificed 1, 3, and 5 days after treatment. BM cells plated for CFU-GM and splenic macrophages were cultured for IL-1 production. Unstimulated splenic macrophage production of IL-1 alpha was not different for any group except Day 5 turpentine animals. TURP induced a significant increase in CFU-GM on Day 1 compared to that in control (47 +/- 22 vs 21 +/- 11; P < 0.05). SHOCK completely abolished this response to TURP. Both the SHOCK and TURP alone increased CFU-GM on Day 5 compared to that in CONTROL but there was no additive effect in the SHOCK + TURP group. These data show that the BM response to combined soft tissue injury and shock (TURP + SHOCK) appears similar to that of SHOCK alone and that hemorrhagic shock appears to be a significant immunosuppressive factor in the regulation of myelopoiesis following injury.

Animals↗
PubMed1999

Down-regulation of liver RNA breakdown by turpentine administration in the starved rat: autophagy and relevant factors.

OBJECTIVE AND DESIGN: To determine whether the inhibition of RNA breakdown observed in ad libitum fed rats 24 h after turpentine administration still occurs in inflamed rats fasted for 24 h and to examine the mechanism and factors involved. METHODS: RNA breakdown was measured during cyclic in situ perfusion of livers by the accumulation of [14C] cytidine after in vivo RNA labelling. Autophagic activity was determined by the morphometric analysis of lysosomal structures. RESULTS: The decrease in RNA breakdown (53%) observed in the inflamed rats was accompanied by a 38% drop in the fractional cytoplasmic volume of initial and digestive autophagic vacuoles. Among amino acids, only the portal levels of glutamate were significantly enhanced by 83%. In vivo suppression of glucocorticoid activity using RU 38486 in inflamed rats did not affect the inhibition of RNA breakdown. CONCLUSIONS: The results show that turpentine-induced inflammation in fasted rats inhibits RNA degradation as well as autophagy and that glucocorticoids do not seem to be involved.

Acute Disease↗
PubMed1985

Effect of ethanol on turpentine-induced acute phase response in rats.

Turpentine-induced acute-phase response and its modulation by ethanol in rats at 48 hr has been studied. There was more than 2.3-5.1 fold increase in fibrinogen and seromucoids concentrations in plasma, accompanied by 28% decline in albumin concentration in turpentine-stimulated rats. The fractional synthesis rate of these two acute-phase proteins was increased by 4.1-6.4 fold, while that of albumin (non acute-phase protein) was reduced by 32.6%. Ethanol inhibited this induction of acute-phase protein synthesis at 48 hr. The inhibition of acute-phase response by ethanol was significantly more pronounced for seromucoids than for fibrinogen and appeared to be dependent on the carbohydrate content of the acute-phase glycoprotein.

Acute Disease↗
PubMed1978

Effects of long-term turpentine inhalation on rat brain protein metabolism.

Chronic exposure of adult male rats to commercial turpentine resulted in an accumulation of the solvent in perinephric fat and brain. The body solvent content remained virtually stable during 8 weeks. Brain RNA content was below the control range initially and it increased to the control level at the 4th week of exposure. Serum non-specific cholinesterase activity was somewhat below the control range at the first and second week of exposure and it returned to the control level thereafter. The present data are in agreement with the small effects of turpentine exposure on human central nervous system in clinical follow-up studies.

Aerosols↗
PubMed1994

Lack of expression of T-kininogen gene in the hearts of untreated and turpentine-injected rats.

Cystatins, inhibitors of cysteine proteinases, are present in rat heart. However, the controls of genes coding for various cystatins in the heart, and the cellular sites of expression of these genes are not known. With a sensitive reverse transcriptase--polymerase chain reaction T-kininogen mRNA was readily detected in the submandibular glands and livers, but not in the hearts, of control or turpentine-injected rats. Immunocytochemical observations employing a monoclonal antibody to bradykinin, which reacts with kininogens in general, revealed no specific staining in cardiac structures, but a weak staining was apparent in blood vessels and on the surface of endothelial cells of both control and turpentine-injected rats. The monoclonal antibody revealed the presence of kininogens in the acinar cells of the submandibular gland, and, in acute inflammation, in the hepatocytes. These findings suggest that the T-kininogen gene is not expressed in the heart, and the T-kininogen demonstrable in heart extracts derives from the blood. Circulating kininogens are likely bound to endothelial cells, and may be a local source of kinins. In addition, kininogens, as potent inhibitors of cysteine proteinases, may play a role in pathologic conditions of the heart by controlling the deleterious effects of cathepsins released from lysosomes or secreted by macrophages.

Animals↗
PubMed1983

Prostaglandin biosynthesis is not affected by the anti-inflammatory effect of turpentine.

In turpentine-pretreated rats, the development of carrageenan induced oedema is reduced, while dextran and PGE2-induced oedemas are not influenced. In these pretreated rats, carrageenan oedema is potentiated by arachidonic acid, the hypotensive effect of arachidonic acid is not decreased and the production of malonaldehyde by platelets is not inhibited. Thus, the reduction of carrageenan oedema in turpentine treated-rats does not appear to depend on an endogenous PG synthesis inhibition, while plasma level of acute phase reactants is greatly increased.

Animals↗