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PubMed1986

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↗
PubMed2006

[Allergic contact dermatitis from colophony and turpentine in resins of untreated pine wood].

Pine wood is one of the most used raw products in furniture manufacturing in Europe. High concentrations of colophony and turpentine can be extracted from pine resins. A 45-year-old woman developed a contact dermatitis of the face and hands due to a sensitization to colophony and turpentine after she had bought untreated pine chairs. The increased use of untreated pine in the furniture industry might result in an increase of colophony and turpentine-induced contact allergies. Therefore, the slogan "untreated=harmless" should be considered critically in such cases.

Administration, Topical↗
PubMed1986

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↗
PubMed1994

Acute inflammation in foetal and adult sheep: the response to subcutaneous injection of turpentine and carrageenan.

Because of the small number of inflammatory cells found in skin wounds, it has been considered that foetal sheep are incapable of an adequate inflammatory response. The present study shows that subcutaneous injection of turpentine or carrageenan into foetal sheep consistently excites a severe cellular inflammatory reaction. At 75 days gestation the inflammatory cells are all macrophages. As the foetus develops, polymorphs play an increasing role in the early response to turpentine. By 120 days inflammatory cells are almost all polymorphs as in adult sheep. However the response to carrageenan remains macrophage in type. At all stages of gestation the acute cellular response is followed by development of scar tissue, more pronounced with turpentine than carrageenan. Any proposed intrauterine surgery must allow for the pronounced and prolonged inflammatory response and scar tissue formation caused by persistent inflammatory stimuli in foetal animals.

Animals↗
PubMed1994

Turpentine poisoning: a case report.

The use of turpentine oil for suicidal and homicidal purposes has become quite infrequent with the increased availability of pesticides and toxic substances. Available literature exhibits few case reports of turpentine poisoning. Such a case is reported here which presented as status epilepticus, unresponsive to the usual line of treatment. Detailed clinical examination and inquiry into the case history revealed turpentine poisoning.

Adolescent↗
PubMed1994

Effect of temperature on rectified turpentine oil as a gutta-percha solvent.

The purpose of this study was to determine the effect of increasing the temperature on the ability of rectified turpentine oil to dissolve gutta-percha. Rectified turpentine oil was warmed to 158 degrees F and then exposed to gutta-percha. This resulted in a significant increase (p < 0.01) in the ability of rectified turpentine oil to dissolve gutta-percha.

Gutta-Percha↗
PubMed1997

The effect of topical turpentine on the functional properties of cutaneous afferents in the anaesthetized rat.

Turpentine was applied to the rat dorsal hindpaw over 1.5-3.5 h and afferent activity was recorded for 1.5-7 h after its removal. Increased spontaneous activity from both A- and C-fibres was observed. There was an increase in units with no response to natural stimuli and a reduction in the numbers of all types of afferent unit, with some recovery of the C- and A delta-classes during the recording period. Surviving C-polymodal nociceptor units had normal sensitivity to noxious heat, but higher mechanical thresholds. Thus turpentine application caused no nociceptor sensitization. Instead, the many insensitive units plus the generalized spontaneous firing may be signs of non-specific axonal damage. A general division of irritant chemicals into those that are predominately damaging, like turpentine, and those that generate specific nociceptor firing or sensitization, is proposed.

Administration, Topical↗
PubMed2001

Opposite nuclear level and binding activity of STAT5B and STAT3 proteins with rat haptoglobin gene under normal and turpentine induced acute phase conditions.

Transcription of the rat gene encoding haptoglobin (Hp) is highly induced during acute phase (AP) response which has been previously shown to be mediated by inducible STAT3 member of the Signal Transducer and Activators of Transcription (STATs) family proteins. In this study, we observed that under normal but not in the turpentine induced AP conditions, another member of the STAT family proteins, STAT5b is expressed and binds to the hormone regulatory element (HRE) of the rat Hp gene. We found that the nuclear amounts of constitutively active STAT5b in rat liver decreased significantly with time of turpentine treatment as opposed to that of cytosol STAT5b, suggesting possible export of constitutive STAT5b from the nucleus. Nuclear accumulation and binding of inducible STAT3 proteins to the rat Hp gene HRE following turpentine treatment implicated that STAT5b negatively regulates Hp gene expression during normal conditions.

Acute-Phase Reaction↗
PubMed2000

Cytochrome P450 inactivation by serum from humans with a viral infection and serum from rabbits with a turpentine-induced inflammation: the role of cytokines.

Serum from humans with an acute upper respiratory viral infection and from rabbits with turpentine-induced inflammation reduce the catalytic activity of hepatic cytochrome P450 (P450). The aim of this study was to identify the serum mediators responsible for the decrease in P450 activity. Rabbit and human sera were fractionated by size exclusion chromatography and the fractions tested for their ability to reduce the activity and amount of P450 after 4 h of incubation with hepatocytes from turpentine-treated rabbits (H(INF)). Rabbit and human sera decreased P450 activity by around 40% without any change in the amount of CYP1A1 and 1A2 apoproteins. In rabbit serum, the fraction containing proteins of M(r) 23-15 kDa decreased P450 content by 41%, but did not alter the amount of the apoproteins. Anti-IL-6 antibody added to the M(r) 23-15 kDa fraction restored P450 content to 97% of control values, while anti-IL-1beta, TNF-alpha and IFN-gamma antibodies had no effect. Supporting the role of IL-6, incubation of H(INF) in the presence of IL-6 for 4 h reduced P450 content by 40%. In human serum, the fraction containing proteins of M(r) >95 kDa lowered P450 content by 43% without modifying the amounts of CYP1A1/2. Neutralization experiments showed that IFN-gamma, IL-6, and IL-1beta contributed to the decrease in P450 content. In conclusion, the present results demonstrate that IL-6, and IFN-gamma, IL-6 and IL-1beta are the serum mediators released in vivo by a turpentine-induced inflammatory reaction in the rabbit and an upper respiratory viral infection in humans, respectively, inactivating hepatic P450.

Animals↗
PubMed1998

Production of mice deficient in genes for interleukin (IL)-1alpha, IL-1beta, IL-1alpha/beta, and IL-1 receptor antagonist shows that IL-1beta is crucial in turpentine-induced fever development and glucocorticoid secretion.

Interleukin (IL)-1 is a major mediator of inflammation and exerts pleiotropic effects on the neuro-immuno-endocrine system. To elucidate pathophysiological roles of IL-1, we have first produced IL-1alpha/beta doubly deficient (KO) mice together with mice deficient in either the IL-1alpha, IL-1beta, or IL-1 receptor antagonist (IL-1ra) genes. These mice were born healthy, and their growth was normal except for IL-1ra KO mice, which showed growth retardation after weaning. Fever development upon injection with turpentine was suppressed in IL-1beta as well as IL-1alpha/beta KO mice, but not in IL-1alpha KO mice, whereas IL-1ra KO mice showed an elevated response. At this time, expression of IL-1beta mRNA in the diencephalon decreased 1.5-fold in IL-1alpha KO mice, whereas expression of IL-1alpha mRNA decreased >30-fold in IL-1beta KO mice, suggesting mutual induction between IL-1alpha and IL-1beta. This mutual induction was also suggested in peritoneal macrophages stimulated with lipopolysaccharide in vitro. In IL-1beta KO mice treated with turpentine, the induction of cyclooxygenase-2 (EC 1.14.99.1) in the diencephalon was suppressed, whereas it was enhanced in IL-1ra KO mice. We also found that glucocorticoid induction 8 h after turpentine treatment was suppressed in IL-1beta but not IL-1alpha KO mice. These observations suggest that IL-1beta but not IL-1alpha is crucial in febrile and neuro-immuno-endocrine responses, and that this is because IL-1alpha expression in the brain is dependent on IL-1beta. The importance of IL-1ra both in normal physiology and under stress is also suggested.

Animals↗
PubMed2006

Turpentine oil inhalation leading to lung necrosis and empyema in a toddler.

Household poisons can cause serious damage to the health of children. Turpentine oil, used chiefly as a solvent in paints, varnishes, and waxes; is often placed within easy reach of children during polishing or painting work. It is capable of causing serious toxicity, whether ingested or inhaled. Pulmonary aspiration can lead to lung parenchymal damage and turpentine-associated pneumonia. We report a case of exploratory ingestion and inhalation of turpentine oil in an 18-month-old boy, leading to extensive lung parenchymal damage, formation of multiple abscess cavities, and necrosis treated with decortication and segmental resection.

Administration, Oral↗
PubMed1996

Clinical uses of rectified turpentine oil.

Rectified turpentine oil can be used to soften or dissolve gutta-percha in the root canal space to facilitate endodontic retreatment or preparation of space for a post. For endodontic retreatment, the turpentine oil can be heated to 71 degrees C which significantly increases its ability to dissolve gutta-percha. For removing only a portion of the gutta-percha while leaving the rest intact, as for the preparation of space for a post, the turpentine oil is delivered to the canal at body temperature (37 degrees C).

Gutta-Percha↗
PubMed1983

Turpentine: an attempt to explain sensitization to this allergen in Spain.

On turpentine being removed from the standard international series, and seeing that the % of positives in Spain were high, the Spanish group decided to study chromatographically the components of turpentine in order to know which of these components is present in the highest proportion. Various samples of turpentine are studied and the results are shown.

Allergens↗
PubMed1997

Sickness behavior in mice deficient in interleukin-6 during turpentine abscess and influenza pneumonitis.

Interleukin-6 (IL-6), among other cytokines, is thought to be involved in the regulation of sickness behavior (e.g., anorexia, cachexia, fever, and lethargy) induced by infections bacterial and viral origin) and sterile tissue necrosis (burns and surgical traumas). Mice deficient in IL-6 (IL-6 KO) were generated by gene targeting. Homozygous IL-6 KO male and female mice and their appropriate controls were implanted with biotelemeters to monitor body temperature (Tb) and motor activity (Act). Normal circadian rhythms in Tb and Act as well as rates of food intake and weight gain did not differ significantly between sex-matched IL-6 KO and control groups at 30 degrees C in a 12:12-h light-dark cycle. Sterile tissue damage was induced in mice by subcutaneous injection of turpentine (0.1 ml, left hindlimb). Influenza pneumonitis was induced by intranasal inoculation of mouse-adapted influenza A virus (17.5 plaque-forming units). Lack of IL-6 completely prevented fever, anorexia, and cachexia because of turpentine abscess in both sexes. It did not prevent lethargy, although IL-6 KO mice recovered to normal Act significantly sooner than wild-type mice. Symptoms of sickness were only slightly modified during influenza virus infection in IL-6 KO mice. Attenuation of sickness behavior was more pronounced in IL-6 KO female than in male mice. We conclude that, although IL-6 is induced during both turpentine abscess and influenza infection, this cytokine appears to be more critical in induction of the symptoms of sickness behavior during sterile tissue abscess than during influenza infection.

Abscess↗
PubMedDate not supplied

Down-regulation of albumin synthesis in the rat by human recombinant interleukin-1 beta or turpentine and the response to nutrients.

BACKGROUND: Inflammatory stimuli and provision of nutrients are important factors regulating both total liver protein synthesis and albumin synthesis. METHODS: The influence of interleukin-1 beta or turpentine injection and a 2-hour infusion of a hypocaloric mixture of glucose and amino acids on the synthesis of total liver protein and albumin was investigated in rats. Total liver protein synthesis was measured by an i.v. flooding dose of L-[2,6(3)H]phenylalanine and albumin synthesis was determined from the labeling of immunoprecipitated albumin and expressed both as a fraction of total liver protein synthesis and as an absolute rate. RESULTS: Interleukin-1 beta or turpentine injection stimulated total liver protein synthesis compared with controls, whereas albumin synthesis, both as a fraction of total liver protein synthesis and as an absolute synthesis rate, decreased. In control animals, the 2-hour i.v. infusion with glucose and amino acids resulted in a significant increase of total liver protein synthesis. Albumin synthesis as a fraction of total liver protein synthesis was not altered, but increased when expressed as an absolute rate in control animals. However, interleukin-1 beta or turpentine injection abolished this response of albumin synthesis to nutrient supply. CONCLUSIONS: Total liver protein synthesis increases under inflammatory conditions and remains responsive to nutrient supply. In contrast, albumin synthesis decreases under the same conditions and does not seem to be responsive to short-term i.v. nutrients.

Acute-Phase Proteins↗
PubMed2002

Modified immunoglobulin G glycosylation pattern during turpentine-induced acute inflammation in rats.

Alterations in the pattern of protein glycosylation have been described during inflammation. In chronic parasitic and tumoral diseases we have reported an increase in the proportion of serum Immunoglobulin G (IgG) molecules possessing an altered Fab glycosylation pattern designated asymmetric antibodies. The alteration results in augmented concanavalin A affinity and functional univalence of the antibody. In addition, Fc agalactosylation has been described as occurring in chronically autoimmune diseases. Therefore, the aim of this paper was to evaluate by analyzing sera whether during an acute inflammatory response in rats produced by subcutaneous inoculation of turpentine oil, there was an alteration in the synthesis and glycosylation of IgG (as revealed by concanavalin A binding). We found that during acute inflammation there was a decrease in the synthesis of IgG which was not affected by prior oral administration of dexamethasone; however, the turpentine-induced increase in IgG binding to concanavalin A was found to be inhibited upon prior administration of the anti-inflammatory agent. As with turpentine, the corticoid used induced an increase in the interleukin-6 levels detected in sera by ELISA. Although we have described an improvement in asymmetric antibody synthesis by low dose of interleukin-6 previously, here we found no correlation between the observed glycosylation pattern of IgG and interleukin-6 concentration assessed in sera of treated rats, probably due to a different dexamethasone mediated pathway.

Acute Disease↗
PubMed2003

Turpentine-induced chemical pneumonitis with broncho-pleural fistula.

Turpentine is a volatile hydrocarbon used in polishes, solvents, paints and textile industry. When hydrocarbons are aspirated into the lung, they cause chemical pneumonitis, acute respiratory distress syndrome (ARDS), and rarely pneumatoceles and pneumothorax. We report a 20-year old boy with turpentine-induced chemical pneumonitis that evolved into a bronchopleural fistula. He was treated with oxygen, steroids and intercostal tube drainage. This is the first reported case of turpentine-associated bronchopleural fistula.

Adult↗
PubMed1991

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↗