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PubMed1993

Involvement of the cervical sympathetic nervous system in the changes of calcium homeostasis during turpentine oil-induced stress in rats.

Hypocalcemia is a common finding during stress. The objective of this study was to examine: (a) the changes in circulating calcium, parathyroid hormone (PTH) and calcitonin (CT) concentration in rats stressed by being given a subcutaneous injection of turpentine oil, and (b) the involvement of the sympathetic cervical pathway in stress-induced changes of calcium homeostasis. Four hours after receiving turpentine oil or vehicle, rats were subjected either to hypocalcemia, by being given EDTA intraperitoneally, or to hypercalcemia, by being injected CaCl2 intraperitoneally. Significant changes in serum calcium (10% decrease), serum PTH (28% increase) and CT levels (40% decrease) were observed in stressed rats. EDTA administration brought about a significantly greater hypocalcemia, and a higher PTH secretory response in turpentine oil-stressed rats. During stress, the increase of serum calcium after CaCl2 was significantly smaller, and the rise of CT was greater than in controls. In the case of CT the changes were still observed in rats subjected to superior cervical ganglionectomy (SCGx) 14 days earlier. In the case of PTH, the increase found in stressed rats, but not the augmented response after EDTA, was blunted by SCGx. The potentiation of hypocalcemia brought about by turpentine oil was no longer observed in SCGx rats. In vehicle-treated controls, SCGx delayed PTH response to hypocalcemia, but did not affect the increased response of CT to CaCl2 challenge. The results indicate that a number of changes in calcium homeostasis arise during turpentine oil stress in rats. SCGx was effective to modify the set point for PTH release, but played a minor role in affecting the augmentation of CT release during stress.

Animals↗
PubMed1988

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↗
PubMed1996

Differential expression of cytokine genes in monocytes, peritoneal macrophages and liver following endotoxin- or turpentine-induced inflammation in rat.

Pro-inflammatory cytokines are produced after systemic or local inflammation by a wide variety of cell types including monocytes, macrophages, Kupffer and endothelial cells. Previous studies have shown that IL-6 gene expression does not occur in liver from rats undergoing an acute phase response after turpentine injection or controls. These data do not rule out the possibility that delivery of a pathogen to the liver via the portal circulation could directly activate the Kupffer cells. Rats were injected either intravenously or intraperitoneally with LPS, or subcutaneously with turpentine oil. The changes in IL-1 beta, IL-6, and TNF mRNA levels in monocytes (collected from portal vein or caval cein), peritoneal macrophages and liver over a 3-hour period post-treatment were examined. The kinetics of LPS-vs turpentine-induced cytokine mRNAs in these various cell types were compared by quantitative reverse transcription and polymerase chain reaction (RT-PCR). Our data demonstrate that an intrahepatic expression of cytokines in the non parenchymal cells was induced by an LPS challenge but not by a turpentine-induced inflammation. This process could act as a paracrine mechanism in the acute-phase response and play a role in the modulation of hepatic regeneration.

Animals↗
PubMed2005

Turpentine-induced inflammation reduces the hepatic expression of the multiple drug resistance gene, the plasma cholesterol concentration and the development of atherosclerosis in apolipoprotein E deficient mice.

We aimed to investigate the effect of turpentine-induced inflammation in an atherosclerosis-prone murine model. We have induced a chronic aseptic inflammation in apolipoprotein E-deficient mice, with or without a dietary supplement of aspirin (n = 10, each), by the injection of a mixture (1:1) of turpentine and olive oil in the hind limb twice weekly for a period of 12 weeks. Control animals were injected with olive oil alone (n = 10). The control mice did show any alteration neither in plasma nor at the site of injection. Turpentine-treated mice showed a significant increase in plasma TNF-alpha and SAA concentrations which indicated a systemic inflammatory response that was not substantially affected by aspirin. Also, turpentine injections significantly reduced the plasma cholesterol concentration, probably decreasing intestinal cholesterol re-absorption, and attenuated the size of atherosclerotic lesion. Both effects were minimally influenced by aspirin. The burden of atherosclerosis correlated with plasma lipid levels but not with plasma inflammatory markers. Finally, there was a concomitant decrease in the expression of the hepatic mdr1b gene that correlated with the decrease in plasma cholesterol concentration. Therefore, we conclude that mdr1 is an additional factor to consider in the complexity of alterations in cholesterol metabolism that occur in this model.

Animals↗
PubMed2004

Effect of turpentine oil on C-reactive protein (CRP) production in rainbow trout (Oncorhynchus mykiss).

The effect of turpentine oil on C-reactive protein (CRP) production was studied in rainbow trout (Oncorhynchus mykiss). Serum CRP concentration was estimated by sandwich enzyme-linked immunosorbent assay using anti-rainbow trout CRP monoclonal antibody (mAb) AC4 and polyclonal antibody. Intracellular CRP was demonstrated by flow cytometry using anti-trout CRP mAb. Hepatocytes, head kidney macrophages, spleen lymphocytes and peripheral blood lymphocytes showed reaction against AC4, but RTG-2 fibroblastic line cells, derived from rainbow trout gonad did not. This is the first report on the detection of intracellular CRP in fish. CRP levels decreased significantly 1 day after intramuscular injection of turpentine oil and remained low for 14 days. Significant decreases in the expression of CRP in hepatocytes, head kidney macrophages and spleen lymphocytes after injection of turpentine oil were found. The reduction of serum CRP concentration after turpentine oil injection may be attributed to decreases in intracellular CRP synthesis.

Acute-Phase Reaction↗
PubMed1980

Enhancement of hepatic drug biotransformation by a short-term intermittent turpentine exposure in the rat.

An inhalation exposure of male rats to 300 p.p.m. of a commercial turpentine 6 hrs daily 5 days a week for 8 weeks enhanced the activities of drug biotransformation enzymes of liver microsomes considerably. The activities of NADPH cytochrome c reductase and 7-ethoxycoumarin deethylase, and microsomal content of cytochrome P-450 were increased 35-60% during the first weeks of the experiment, but had a tendency to return towards the control values later on. A similar enhancement of activities was also found in liver microsomal epoxide hydratase and UDP glucuronosyltransferase, but these enzyme activities tended to adapt less during the experiment. The turpentine treatment increased the affinity of liver microsomal cytochrome P-450 to alpha-pinene (the main component of the turpentine). The present data suggests that exposure to turpentine is able to modify considerably the biotransformation of drugs.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1987

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↗
PubMed1993

Effects of turpentine oil pretreatment on beta-blocker pharmacokinetic parameters in rats.

Turpentine oil treatment (0.2 mL kg-1, s.c.) was used to increase the plasma concentration of alpha 1-acid glycoprotein (0.13 mg mL-1 in control rats) to 1.72 mg mL-1 after 2 days, and allow assessment of its effects on the pharmacokinetics and stereoselective binding of three beta-blockers. Racemates (5 mg kg-1) were administered intravenously to control and turpentine oil-pretreated rats and the plasma concentrations were determined up to 90 min. Stereoselective analysis showed the apparent distribution volume and the area under plasma concentration-time curves (AUC) of R-(+)-propranolol to be, respectively, one-quarter and twice those of the S-(-)-enantiomer and differences in pharmacokinetic parameters between the two were magnified by turpentine oil pretreatment. Pharmacokinetic parameters of oxprenolol enantiomers were essentially similar for the controls but after turpentine oil pretreatment, a higher affinity of the R-(+)-enantiomer for plasma was observed. Acebutolol enantiomers behaved non-stereospecifically throughout. These results were consistent with predictions from the in-vitro stereospecific binding properties of these agents to purified rat alpha 1-acid glycoprotein.

Acebutolol↗
PubMed1999

Regulation of Spi 2.1 and 2.2 gene expression after turpentine inflammation: discordant responses to IL-6.

The rat serine protease inhibitor (Spi) 2 gene family includes both positive (Spi 2.2) and negative (Spi 2.1) acute phase reactants, facilitating modeling of regulation of hepatic acute phase response (APR). To examine the role of signal transducer and activation of transcription (STAT) proteins in the divergent regulation of these model genes after induction of APR, we evaluated the proximal promoters of the genes, focusing on STAT binding sites contained in these promoter elements. Induction of APR by turpentine injection includes activation of a STAT3 complex that can bind to a gamma-activated sequence (GAS) in the Spi 2.2 gene promoter, although the Spi 2.2 GAS site can bind STAT1 or STAT5 as well. To create an in vitro model of APR, primary hepatocytes were treated with combinations of cytokines and hormones to mimic the hormonal milieu of the whole animal after APR induction. Incubation of primary rat hepatocytes with interleukin (IL)-6, a critical APR cytokine, leads to activation of STAT3 and a 28-fold induction of a chloramphenicol acetyltransferase reporter construct containing the -319 to +85 region of the Spi 2.2 promoter. This suggests the turpentine-induced increase of Spi 2.2 is mediated primarily by IL-6. In contrast, although turpentine treatment reduces Spi 2.1 mRNA in vivo and IL-6 does not increase Spi 2.1 mRNA in primary rat hepatocytes, treatment of hepatocytes with IL-6 results in a 5. 4-fold induction of Spi 2.1 promoter activity mediated through the paired GAS elements in this promoter. Differential regulation of Spi 2.1 and 2.2 genes is due in part to differences in the promoters of these genes at the GAS sites. IL-6 alone fails to reproduce the pattern of rat Spi 2 gene expression that results from turpentine-induced inflammation.

Acute-Phase Reaction↗
PubMed1997

Exacerbated febrile responses to LPS, but not turpentine, in TNF double receptor-knockout mice.

We examined the effects of injections of systemic [lipopolysaccharide (LPS), 2.5 mg/kg or 50 pg/kg ip] or local (turpentine, 100 microl sc) inflammatory stimuli on fever, motor activity, body weight, and food intake in tumor necrosis factor (TNF) double receptor (TNFR)-knockout mice. A high dose of LPS resulted in exacerbated fevers in TNFR-knockout mice compared with wild-type mice for the early phase of fever (3-15 h); the late phase of fever (16-24 h) and fevers to a low dose of LPS were similar in both groups. Motor activity, body weight, and food intake were similarly reduced in both groups of mice after LPS administration. In response to turpentine, TNFR-knockout and wild-type mice developed virtually identical responses to all variables monitored. These results suggest that 1) TNF modulates fevers to LPS dose dependently, 2) TNF does not modulate fevers to a subcutaneous injection of turpentine, and 3) knockout mice may develop cytokine redundancy in the regulation of the acute phase response to intraperitoneally injected LPS or subcutaneously injected turpentine.

Animals↗
PubMedDate not supplied

[Turpentine white emulsion baths in the rehabilation in patients with sexual dysfunctions].

100 patients with sexual dysfunction (SD) and 20 SD patients took turpentine white emulsion baths and sodium chloride baths, respectively. The turpentine baths were given with step-by-step rise in turpentine concentration from 20 to 50 ml per 200 l of water, temperature 36-37 degrees C, duration of the procedure 10-15 min. The course consisted of 10-12 procedures which were conducted daily or each other day. The turpentine baths were more effective than sodium chloride baths (85 vs 50%, respectively).

Balneology↗
PubMed1985

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↗
PubMedDate not supplied

The use of a constant infusion of [3H]phenylalanine to measure the effects of glutamine infusions on muscle protein synthesis in rats given turpentine.

Skeletal muscle protein fractional synthetic rate (MPFSR) was measured in rats with a constant infusion of [3H]phenylalanine to study the relationship between the rate of muscle protein synthesis in skeletal muscle and the intracellular glutamine concentration. The values for MPFSR (percentage per day) achieved in this study were in good agreement with those we have already reported with a flooding dose of [3H]phenylalanine to measure MPFSR. This was the case both for control rats and for those that had been injected with turpentine (constant infusion 12.82 +/- 0.43% in saline-injected rats, 6.58 +/- 0.34% in rats injected with turpentine; flooding dose 12.88 +/- 0.73% in saline-injected rats, 7.04 +/- 0.67% in rats injected with turpentine). Therefore, there was no evidence for a stimulating effect of a flooding dose of phenylalanine on MPFSR, an effect that could have invalidated the conclusions drawn in our previous investigation. In this study, turpentine reduced the MPFSR by a mean of 49% (p < 0.001). This reduction in MPFSR was associated with a 39% reduction in the mean intramuscular glutamine concentration (p < 0.001). This reduction in MPFSR was associated with a 39% reduction in the mean intramuscular glutamine concentration (p < 0.001). The reduction in intramuscular glutamine concentration was completely reversed by 5-h intravenous infusions of 0.22 M glutamine solutions, but there was no accompanying increase in the MPFSR. The results of this study therefore provide no evidence to support the proposal that an acute change in intramuscular glutamine concentration is a major factor in controlling the rate of protein synthesis in skeletal muscle.

Animals↗
PubMed1997

Acute intoxication and recovery following massive turpentine ingestion: clinical and toxicological data.

Reports of acute turpentine intoxication, particularly containing toxicological data, are poorly verified in the literature. This report regards the intentional massive ingestion of turpentine solution in an elderly woman who developed mainly central nervous system manifestations, then had an impressive and quick total recovery although the initial prognosis was very bad. Blood and urine levels of turpentine were monitored using gas chromatography and at the early toxicogenic stage were 28 micrograms/mL and 15 micrograms/mL respectively. Gastric fluid analysis on admission to the hospital revealed the presence of approximately 200 mL turpentine in the intestine. A review of earlier reports is given.

Administration, Oral↗
PubMedDate not supplied

[The use of white and yellow turpentine baths with diabetic patients].

In patients with insulin-dependent diabetes mellitus while and yellow turpentine baths produced a positive effect on carbohydrate metabolism. White baths were more effective in respect to lipid metabolism, blood viscosity, produced a good effect on plasmic hemocoagulation factors. Both while and yellow turpentine baths were beneficial for capillary blood flow: initially high distal blood flow in patients with prevailing distal polyneuropathy decreased while in patients with macroangiopathy initially subnormal blood flow increased. Both white and yellow turpentine baths promoted better pulse blood filling of the lower limbs and weaker peripheral resistance of large vessels. In patients with non-insulin-dependent diabetes mellitus white and yellow turpentine baths contributed to normalization of carbohydrate metabolism. Yellow baths were more effective in lowering lipids. White baths induced inhibition of platelet aggregation but had no effect on coagulation, yellow baths promoted a reduction of fibrinogen but had no effect on platelet aggregation. Yellow baths produced more pronounced effect than white ones on blood viscosity and microcirculation. Both yellow and white baths stimulated pulse blood filling, corrected peripheral resistance of large and small vessels of the lower limbs.

Adult↗
PubMed2001

alpha-Terpineol from hydration of crude sulfate turpentine oil.

Hydration of alpha-pinene under various conditions was studied and compared with the literature. Optimal reaction conditions have been established for the hydration of alpha-pinene and crude turpentine oil in the absence of catalyst and using a low volume of acetone. A detailed reaction product analysis is reported. The main hydration product, alpha-terpineol, was obtained at a yield of 67 wt % of the initial alpha-pinene by reacting with 15% aqueous sulfuric acid and an excess of acetone in an oil bath heated to 80-85 degrees C over the course of 4 h. A progressive transformation of alpha-terpineol to 4-(2-hydroxypropyl)-1-methylcyclohexanol (1,8-terpine) takes place as the hydration time exceeds 4 h. A crude turpentine oil sample was also hydrated under conditions similar to those of alpha-pinene. The alpha-terpineol yield was 77 wt % of the initial alpha-pinene in the crude turpentine oil. The chemical analysis of the crude turpentine oil before and after hydration was carried out, and the distribution of the products was discussed.

Acetone↗
PubMed2000

Effect of alpha(1)-acid glycoprotein on the pharmacokinetics of tamsulosin in rats treated with turpentine oil.

The pharmacokinetics of tamsulosin (TAM) was investigated using male Sprague-Dawley rats in which plasma alpha(1)-acid glycoprotein (alpha(1)-AGP) levels were elevated by the subcutaneous injection of 0.2 mL/kg of turpentine oil. alpha(1)-AGP levels increased about eight times after turpentine oil treatment, causing a threefold decrease in plasma unbound fraction (f(u)) of TAM. When 0.3 mg/kg of TAM was dosed intravenously, total and nonrenal clearances (CL(tot) and CL(nr)) in turpentine-treated rats were 47% and 44% lower than those in nontreated controls, respectively. The area under the concentration-time curve of plasma unbound TAM (AUC(inf,u)) was lower than that in the control. When 1 mg/kg of TAM was dosed orally, oral clearance (CL(oral)) in alpha1-AGP-induced rats was 65% lower than in the control. The AUC(inf,u) and unbound oral clearance (CL(oral,u)) were nearly equal in both groups. Moreover, a positive correlation was observed between fu and CL(oral) of TAM (r(2) = 0.603, P < 0.01), whereas no correlation was observed between f(u) and CL(oral,u). The absolute bioavailability (BA) increased from 19.2% to 46.9% by induction of alpha(1)-AGP. These results suggest that decreased f(u) caused by the elevation of plasma alpha(1)-AGP level affects the pharmacokinetics of TAM, but does not affect the CL(oral,u,) which represents the hepatic metabolism of TAM.

Animals↗
PubMed1984

The mechanism of the anti-inflammatory effect of turpentine in the rat.

The influence of counter irritation by turpentine on carrageenan-oedema, leucocyte count, plasma kininogen stores and composition of sponge-induced exudates has been investigated in the rat. Counter irritation reduced the carrageenan-oedema in normal as well as in adrenalectomized rats. It induced leucopenia with lymphopenia but did not modify the plasma kininogen stores. In turpentine-pretreated rats, the exudates induced by sponge implantation 18 h previously had a lower content in leucocytes. Their levels in beta-glucuronidase and beta-galactosidase were slightly reduced, their content in PGE2 was not modified and their level in malonaldehyde was increased. The exudates induced by sponge implantation 4 h previously had a lower content in leucocytes and PGE2 while their level in kinins was not modified. The mechanism of the anti-inflammatory effect of counter irritation by turpentine is discussed. We suggest that the main factor involved is a decrease in leucocyte accumulation into the exudates.

Adrenalectomy↗