Turpentine. (Wood turpentine, gum spirits of turpentine, oil of turpentine).
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Dermatitis, Contact↗
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Properties of turpentine relative to the effects on fowl plasma in vitro. II. The separation of peroxide components of turpentine by thin-layer chromatography.
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Chromatography, Thin Layer↗
Intestinal iron absorption during turpentine sterile inflammation in the rat. Influences of isoproterenol and propranolol.
59Fe was incorporated in vivo into intestinal sacs prepared in control rats as well as in animals with turpentine sterile abscesses and 59Fe counts were detected in the intestinal wall, in blood, in liver, in spleen and in femur of animals, at different time intervals (20, 40 and 120 min) following i.v. injection of isoproterenol (10 micrograms/kg, body weight) or of (-)-propranolol (2 mg/kg, body weight). In rats without inflammation isoproterenol alone enhanced significantly iron counts in blood, spleen, liver and femur, but not in intestinal cells, whereas propranolol evoked opposite actions, the influence being more marked after 40 min, reaching maximal values at 120 min. In animals with sterile turpentine abscesses explored 40 min after injections, iron intestinal counts in turpentine, in turpentine plus isoproterenol and in turpentine plus propranolol groups were significantly lower than in normal saline injected controls (p less than 0.001) and the opposite was the case at 120 min. In blood, iron counts at 20 and 40 min were higher in saline controls (p less than 0.05) than in the turpentine group, whereas at 120 min, values in the turpentine plus isoproterenol group were higher than (p less than 0.01) in saline injected controls or in the group with turpentine alone. Also, at all time intervals explored, iron counts in blood in the propranolol plus turpentine group were smaller (p less than 0.01) than in saline injected controls or in the group with turpentine alone.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effects of human recombinant interleukin-1 beta on protein synthesis in rat tissues compared with a classical acute-phase reaction induced by turpentine. Rapid response of muscle to interleukin-1 beta.
The early time course (1, 3, 9, 24 h) of changes in rates of protein synthesis (ks) in liver and three different muscles (gastrocnemius, soleus and heart) was investigated after injection of saline, interleukin-1 beta (IL-1) or turpentine in rats. IL-1 injection induced a consistent increase in body temperature of about 3 degrees C between 3 and 5 h, but thereafter a hypothermic response occurred. With turpentine, a delayed fever response with a peak value by 9 h was observed. Both IL-1 and turpentine had no effect on protein synthesis in the small intestine, but produced a significant increase in ks in the liver at 9 h. By 24 h in IL-1-treated animals, liver ks had returned back to control values, whereas the turpentine-treated group showed a progressive rise in ks. Gastrocnemius and soleus muscles exhibited a significant fall in ks at 9 h after IL-1 and turpentine injection compared with the control. In contrast, the ks of heart muscle increased at 3-9 h after IL-1 injection, but there was no effect of turpentine. Thus for the first time a marked decrease of protein synthesis in skeletal muscle in response to IL-1 could be demonstrated.
Acute-Phase Proteins↗
Evidence against benefit from replacement doses of thyroid hormones in nonthyroidal illness (NTI): studies using turpentine oil-injected rat.
Sprague-Dawley rats were treated with saline or turpentine oil (5 mu 1/g bw sc at 3-day intervals x3) with or without replacement doses of T4 (0.8 g/100 g bw/day ip) or T3(0.3 microgram/100 g bw/day ip). Injection of turpentine oil to the rat consistently caused a significant reduction in serum total T4, total T3, free T4 index and TSH. Despite marked changes in thyroidal economy in experimental rat, iodothyronine 5'-monodeiodinating activity (MA) in the liver, the kidney and the hearth and the hepatic alpha-glycerophosphate dehydrogenase activity were decreased inconsistently and when decreased, the various enzyme activities were not influenced appreciably by treatment with replacement doses of T4 or T3. Cerebral cortical T4 5-MA was normal or increased in the turpentine oil-injected rat. Dermal T4 5-MA was decreased in the turpentine oil-injected rat and replacement doses of thyroid hormones did not normalize it. Urinary excretion of urea nitrogen was normal in the turpentine oil-injected rat and did not change appreciably after treatment with thyroid hormones. Our data suggest that replacement doses of thyroid hormones are not beneficial to a host with altered thyroid economy during a systemic illness.
Analysis of Variance↗
The acute-phase response to turpentine-induced abscesses in malnourished rats at different environmental temperatures.
An assessment was made of the independent effect environmental temperature (13, 21, and 30 degrees C) and either protein deficiency or energy deficiency on the metabolic response of rats that had aseptic abscesses induced by subcutaneous injections of turpentine. Measurements of food intake, alpha 2-macroglobulin (alpha 2-M; a major acute-phase protein in the rat), albumin, and various circulating metabolites were made 48 hours after turpentine injection in animals acclimatized at 13, 21, and 30 degrees C and compared with pair-fed controls. Despite differences in basal circulating albumin concentrations between controls and protein deficient rats (P less than .001), turpentine produced a similar reduction in all groups of animals (approximately 10 g/L), independent of environmental temperature. The alpha 2-M response to turpentine was attenuated in all protein-deficient animals and also in the energy-restricted animals at 13 degrees C. The increase in circulating 3-hydroxybutyrate (BOH) and nonesterified fatty acid (NEFA) concentrations, which normally occur with reduced dietary intake, was reduced in the turpentine-injected animals to an extent that depended on prior dietary intake. It is concluded that the metabolic response, particularly the acute-phase protein response, to a standard form of "injury" is affected by protein deficiency and possibly by energy restriction under adverse environmental temperature.
Abscess↗
Liver damage induced by intrabiliary turpentine in rats.
Inflammation of the rat bile duct induced by administration of turpentine into it has been used to study the influence of the impaired duct on liver function. Turpentine was dissolved in olive oil 1:1000 and 1:500. A 2 h ligation of the bile duct was used to promote a local effect. Contemporary groups of intact, sham-operated, control rats (given 0.9% NaCl by intrabiliary injection) and animals with total chronic obstruction were compared to assess the significance of changes. Serum concentrations of total and conjugated bilirubin, cholesterol and creatinine, activities of S-alanine-aminotransferase, S-aspartate aminotransferase and alkaline phosphatase, mortality of rats, and also total body weight compared with the weight of the liver, were investigated on days 1, 4, 8, 12, 16, 32 and 64 after surgery and turpentine, or following ligation of the bile duct. An increase in bilirubin and cholesterol, an augmentation of enzymatic activity and the histological changes were indicative of hepatotoxicity or cholestasis. The turpentine concentration--effect, manifested in body-weight change, suggests some specificity of the effect. There were no changes in serum creatinine arterial blood pressure, heart rate or portal blood pressure, when turpentine was administered by the intrabiliary route. These results suggest primary liver damage.
Alanine Transaminase↗
Alterations in thyroidal economy in a systemic illness induced by turpentine oil injection to the rat.
Injection of turpentine oil (5 microliter/g, sc) to Sprague Dawley rats was associated with a significant reduction in serum concentration of T4, T3 and TSH that lasted throughout 48 h of study. Dialyzable fraction of T4 and resin uptake of T3 did not change for 10 h after turpentine oil injection, but were increased significantly at 24 h and 48 h. Serum rT3 concentration was decreased significantly at 24 h and 48 h. The pituitary content of TSH in the experimental rat was significantly increased at 24 h after turpentine oil injection, but the TSH-beta subunit content was decreased significantly. Serum TSH response to TRH did not change in experimental rats. Thyroidal radioiodine uptake, serum T4, and serum T3 in experimental rats demonstrated little or no increase in response to exogenous bovine TSH. A thyroid hormone binding inhibitor (THBI) was detected in serum and iodothyronine 5'-monodeiodinating activity was decreased significantly in liver, kidney and heart of rats injected repeatedly with turpentine oil. Oxygen consumption of experimental rats did not change appreciably. Our data suggest that administration of turpentine oil to the rat leads, within a few hours of the injection, to a systemic illness associated with marked changes in thyroidal economy.
Animals↗
In-vitro biotransformation of antipyrine, lignocaine and propranolol in the liver of rats with turpentine-induced inflammation.
In rats with inflammation induced by turpentine injection, changes in drug disposition occur in-vivo and in the perfused isolated liver. Therefore the biotransformation of a low extraction drug, antipyrine, and of two high extraction drugs, lignocaine and propranolol, has been evaluated in the 9000g supernatant fraction of the liver of turpentine-treated rats. Aminopyrine N-demethylase activity and cytochrome P450 content were also measured. Turpentine treatment significantly reduced the in-vitro breakdown of the three drugs; aminopyrine N-demethylase activity and cytochrome P450 content were also decreased. Similar results were found in the proadifen-treated rats, except that in those, the cytochrome P450 content was slightly increased. The changes in drug disposition seen after turpentine-induced inflammation, could therefore be due in part to a change in hepatic enzymatic activity.
Aminopyrine N-Demethylase↗
Effect of serum proteins from normal and turpentine-treated rats on prostaglandin synthesis by peritoneal cells.
The influence of serum from normal and turpentine-treated rats on prostaglandin synthesis by peritoneal cells has been investigated. Both types of serum had the same inhibitory effect on the formation of myostimulating prostaglandin-like substances and of 14C-PGE2 by rat peritoneal cells in the presence of 82 or 100 mumol of arachidonic acid. On guinea-pig peritoneal cells, the serum from turpentine-treated rats had a smaller inhibitory effect than normal serum on 14C-PGE2 and 14C-HETE formation from 2 mumol of arachidonic acid. Thus the acute inflammatory reaction produced by turpentine did not increase the inhibitory effect of rat serum on prostaglandin synthesis. It is suggested that the anti-inflammatory effect of counter irritation by turpentine does not depend on prostaglandin synthesis inhibition but has to be attributed to some other mechanisms.
Animals↗
Further studies of the mechanism of counter irritation by turpentine.
The influence of counter irritation by turpentine (0.2 ml) on zymosan- and carrageenan-oedemas was investigated in the rat. Zymosan-oedema was inhibited by mepyramine and methysergide and by leucopenia. It was not modified by captopril and developed normally in kininogendeficient Brown Norway rats. Leucocytes and mast cell amines but not kinins are thus involved in zymosan-oedema. The last phase of this reaction was inhibited by counter irritation alone, but the odema was largely depressed by counter irritation in rats pretreated with mepyramine and methysergide. Carrageenan-oedema was increased by kininase inhibitors and inhibited by leucopenia in normal rats. This inflammatory reaction had a small developement and was not increased by kininase inhibitors in kininogen-deficient BN rats. Leucocytes and kinins participate in the developement of this inflammatory reaction in normal rats while kinins are lacking in deficient rats. Counter irritation depressed carrageenan-oedema in deficient Brown Norway rats and suppressed the potentiating effect of kininase inhibitors in normal rats. Carrageenan oedema was nearly abolished in turpentine-treated leucopenic rats. These results suggest that the anti-inflammatory effect of counter irritation by turpentine could depend on a reduction of leucocyte accumulation into zymosan-oedema and on a reduction of both kinin formation and of leucocyte accumulation into carrageenan-oedema. The significance of T-kininogen as acute phase reactant is discussed.
Animals↗
Changes in the rate of epithelial proliferation of rat oral mucosa in response to acute inflammation induced by turpentine.
Inflammatory lesions were produced in the buccal mucosa by a subepithelial injection of turpentine; animals were killed 24 h later, 1 h after an intravenous injection of tritiated thymidine ( [3H]-Tdr). Control rats were given [3H]-Tdr but no turpentine. Lesions comprised a turpentine pool surrounded by a dense layer of inflammatory cells, beyond which the tissues were more diffusely inflamed. The labelling index (L.I.) for mitotic activity in overlying epithelium was determined in a region (C) close to the layer of dense infiltration and in a region (D) more distant. The L.I. in region D was over four times greater than in region C, and nearly four times greater than that of the contralateral, uninjected cheek. The L.I. in the uninjected cheek was significantly lower than that in controls, which may indicate a systemic depression of proliferative activity in the experimental animals, probably due to stress. Thus mild inflammatory injury stimulates epithelial proliferation, whereas more severe inflammation depresses it, perhaps due to more extensive progenitor-cell damage.
Acute Disease↗
Glucocorticoid status affects the response of rat striatal dopamine D2 receptors to hyperthermia and turpentine treatment.
The influence of glucocorticoid status of the rats (absence of glucocorticoid hormones achieved by adrenalectomy and substitution by dexamethasone 5 mg/kg b.w.) on the response of striatal dopamine-D2 receptors to environmentally induced hyperthermia and treatment with a local inflammatory agent turpentine (1 ml/kg b.w.) was studied. Both stress situations affected the density of D2 receptors in opposite directions. While hyperthermia led to an increase, turpentine treatment reduced Bmax value. The changes in the D2 receptor binding affinity were expressed as a certain decrement, which was statistically significant in sham-adrenalectomized hyperthermic animals and in both turpentine treated groups (sham-operated and adrenalectomized) administered dexamethasone. The absence of glucocorticoids in the circulation caused an elevation of Kd values in the control and both stressed groups and dexamethasone attenuated these changes. Dexamethasone also attenuated stress-related alterations of Bmax, as well as Kd increase upon adrenalectomy in control and hyperthermic animals. These results corroborate the evidence on the role of D2 receptors in thermoregulation and stress and demonstrate the significance of glucocorticoid hormones in the control of these processes.
Adrenalectomy↗
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↗
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↗
[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↗
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↗
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↗