Turpentine. (Wood turpentine, gum spirits of turpentine, oil of turpentine).
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Dermatitis, Contact↗
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[Poisoning by spirits of turpentine or turpentine oil. Review of its treatment apropos of a personal case].
Authors deduce from their experience during 1979 that intoxication by spirit oil of turpentine is an accident with few repercussions in infancy, because the quantity ingested does not reach toxic levels, except for children over seven who try to commit suicide. Gastric lavage must not be practiced because removing turpentine can provoke its' aspiration with a consequent pulmonary disease in the majority of occasions. Only when ingestion is more than 1 ml./Kg., or symptoms suggest important disease, can gastric lavage, be done because secondary complications can aggravate the disease. Antibiotics are used if there is an obvious infection, remembering that turpentine intoxication itself can provoke fever. In their experience, corticoids don't modify the evolution.
Age Factors↗
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↗
Blockade of nitric oxide formation enhances thermal and behavioral responses in rats during turpentine abscess.
OBJECTIVE: The purpose of this study was to investigate the role of nitric oxide (NO) during the development of fever and other symptoms of sickness behavior (i.e. anorexia, cachexia) in response to localized tissue inflammation caused by injection of turpentine in freely moving biotelemetered rats. METHODS: To determine the role of NO in turpentine-induced fever, we injected the NO synthase (NOS) inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) intraperitoneally simultaneously or 5 h after turpentine injection. RESULTS: Rats responded with fever to intramuscular injection of 20 microl of turpentine that commenced 6 h after injection and reached peak values 11 h after injection. Although turpentine did not significantly alter food and water intake, it caused a drop in body weight. Rats injected with turpentine and treated with L-NAME responded with a substantial rise in fever, independently of the time of L-NAME injection. The rise in body temperature (T(b)) due to turpentine injection began slightly sooner and reached the maximal T(b) value faster in rats treated with L-NAME than in the ones treated with saline (control for L-NAME). The enhanced decrease in food and water intake in rats treated with a combination of L-NAME and turpentine was also observed. As a result, L-NAME-injected rats responded with a profound drop in body mass due to turpentine, independently of the time of L-NAME injection. L-NAME alone did not affect food and water intake, but slightly suppressed the gain of body mass. CONCLUSION: These results indirectly indicate that NO is involved in pyrogenic and behavioral responses in rats during turpentine abscess.
Animals↗
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↗
Increase in sensitization to oil of turpentine: recent data from a multicenter study on 45,005 patients from the German-Austrian Information Network of Departments of Dermatology (IVDK).
Contact allergy to oil of turpentine was reported to have become rare. However, the evaluation of standardized data of 45,005 patients tested 1992-1997 in 30 Dermatological Centers associated with the German-Austrian Information Network of Departments of Dermatology (IVDK) showed an increase in positive patch test reactions to turpentine from 0.5% during the years 1992-1995, up to 1.7% in 1996 and 3.1% in 1997. In particular, 17,347 patients tested in 1996-1997 were evaluated in detail by comparing 431 individuals with positive patch test reactions with the rest of the group found negative to turpentine. Using the so-called MOAHLFA index, the following characteristics were shown. Turpentine allergy (a) was found to be significantly less frequent in men and in patients with occupational dermatitis, (b) showed no difference in its association with atopic dermatitis, (c) patients with turpentine allergy had significantly less symptoms of the hands, more symptoms of the legs or in the face and (d) were significantly more often aged over 60 years. Also, patients sensitized to turpentine had increased rates of additional sensitizations. The definite reason for the increase in turpentine sensitization in the population tested here is not clear. Therefore, a detailed exposure analysis is necessary; the new increase in turpentine allergies may be due to popular topical remedies or household chemicals.
Adult↗
Transient re-emergence of oil of turpentine allergy in the pottery industry.
Allergy to oil of turpentine has diminished largely due to the use of cheaper substitutes in many occupations. However, 2 particular areas still reliant on real oil of turpentine are those of the perfume industry and ceramic decoration. We report 24 cases of hand dermatitis in pottery workers involved in ceramic decoration, paintresses, liners, gilders, enamellers and a fine china painter, seen in a 6-month period following a change from Portuguese to Indonesian turpentine, of whom 14 were sensitive to Indonesian turpentine, 8 to alpha-pinene, 4 to delta-3-carene and 2 positive to turpentine peroxides. Previous reports suggest that delta-3-carene is the main allergen and reports of sensitivity to alpha-pinene in the absence of sensitivity to turpentine peroxide, in particular to the hydroperoxide of delta-3-carene, are few. Turpentine allergy continues to be a problem in the pottery industry and is more common than allergy to the heavy metals of the colours used in ceramic decoration. alpha-Pinene, an unusual allergen, appears to be the most common in our area. Reversion to Portuguese turpentine seems to have alleviated the problem.
Allergens↗
The effect of turpentine-induced inflammation on rat liver glycosyltransferases and Golgi complex ultrastructure.
Turpentine-induced inflammation in the rat caused a 1.6--2.3-fold increase in liver homogenate sialyl-, galactosyl- and N-acetylglucosaminyltransferase total and specific enzyme activities. Peak transferase activities were achieved at about 40 h after turpentine injection; the rise and fall of these activities corresponded to a similar rise and fall in serum haptoglobin levels. Sialyl- and N-acetylglucosaminyltransferase activities were measured in both liver homogenates and Golgi-enriched membranes at 24 h after turpentine injection; both total and specific enzyme activities doubled in the homogenates following turpentine treatment but in the Golgi-enriched membranes only the total enzyme activities doubled while the specific enzyme activities increased only by about 20%. These findings suggest that turpentine injection results in an increase of Golgi complex protein relative to total cellular protein. This conclusion was supported by electron microscopic studies of rat liver at various times after turpentine injection. The increased glycosylation potential of the liver and the proliferation of liver Golgi complex may play an important role in the turpentine-induced secretion of acute-phase glycoproteins.
Animals↗
Evaluation of sensory irritation of delta3-carene and turpentine, and acceptable levels of monoterpenes in occupational and indoor environment.
The standard mouse bioassay was used for obtaining the RD50 (i.e., the concentration that causes a 50% decrease in respiratory frequency) and for estimating the irritation properties of d-delta3-carene (i.e., (+)-delta3-carene) and commercial turpentine. The chemicals studied possess mainly sensory irritation properties similar to the previously studied monoterpenes, pinenes. The irritation potency of d-delta3-carene (RD50 = 1345 ppm) was almost equal to that of d-pinenes. Thus, d-delta3-carene was about four times more potent as a sensory irritant than I-beta-pinene, whereas the difference with I-alpha-pinene was more marked; as a sensory irritant, I-alpha-pinene is almost inactive. Based on sensory irritation potency and physicochemical and structural properties of pinenes and delta3-carene, the potency of a closely related monoterpene, limonene, is discussed. For commercial turpentine, a mixture of monoterpenes (mainly d-delta3-carene, I-beta-pinene, alpha-pinenes, and limonenes), the RD50 (1173 ppm) was the same order of magnitude as those of d-pinenes and d-delta3-carene. Apparently, d-monoterpenes are responsible for the sensory irritation caused by turpentine. In the wood industry and in the indoor air of nonindustrial environments, monoterpenes are thought to be one of the causative agents for irritation symptoms. The occupational exposure limit (OEL) of turpentine (100 ppm in Finland and the United States) is also used for individual monoterpenes, excluding limonene. Using results from this and our previous study, proposed OELs and recommended indoor levels (RILs) for selected monoterpenes and turpentine were determined based on their RD50 values. According to our studies, the present OEL of turpentine (100 ppm; 560 mg/m3) in Finland and in the United States seems to be suitable only for I-pinenes. For d-monoterpenes and turpentine, an OEL about three times lower is suggested. Our results show that recommended indoor levels (RILs) for monoterpenes are high compared to the concentrations measured indoors in nonindustrial environments. Thus, it is very unlikely that monoterpenes alone can cause irritation symptoms in homes or offices under normal conditions.
Air↗
Induction of IL-1, in the testes of adult mice, following subcutaneous administration of turpentine.
PROBLEM: Interleukin-1 family is present in the testicular homogenates and its cellular compartments. It has been suggested that IL-1 is involved in physiological and pathological functions of the testicular tissues. In the present study we examined the effect of acute mostly localized inflammation, using turpentine, on the expression levels of testicular IL-1 system. METHODS OF STUDY: Mice were subcutaneously injected with steam-distilled turpentine or saline (control). Three hours to 10 days following the injection, mice were killed and testis and spleen were homogenized and examined for interleukin (IL)-1alpha, IL-1beta, and IL-1 receptor antagonist (IL-1ra) levels by enzyme-linked immunosorbent assay and polymerase chain reaction. RESULTS: Subcutaneous injection of turpentine induced mice systemic inflammation, as indicated by significant increase in serum IL-1beta levels, and IL-1alpha, IL-1beta and IL-1ra in spleen homogenates. The levels of IL-1alpha, IL-1beta and IL-1ra were significantly induced in testicular homogenates of adult mice following subcutaneous injection of turpentine. The significant induction of testicular IL-1alpha was detected after 3-24 hr of turpentine injection and decreased later (after 3-10 days) to levels similar to the control. However, significant induction of testicular IL-1beta was detected only after 3-10 days of turpentine injection, and for testicular IL-1ra levels was detected after 3 hr to 6 days of turpentine injection, and after 10 days the levels were similar to the control. These results were also confirmed by mRNA expression of these factors. CONCLUSION: Our results demonstrate for the first time the distant effect of acute localized inflammation on testicular IL-1 levels. Thus, transient inflammatory response to infectious/inflammatory agents at non-testicular sites that elicit systemic IL-1 response should be considered during clinical treatment as a possible factor of male infertility.
Animals↗
Short term inhalation exposure to turpentine: toxicokinetics and acute effects in men.
OBJECTIVES: This study describes the toxicokinetics, pulmonary function, and subjective ratings of discomfort in volunteers experimentally exposed to turpentine vapour (a mixture of monoterpenes). The results were compared with similar exposure to single monoterpenes to look in the toxicokinetics and acute effects for signs of interactions between the monoterpenes. METHODS: Eight male volunteers were exposed to 450 mg/m3 turpentine by inhalation (2 h, 50 W) in an exposure chamber. RESULTS: The mean relative uptakes of alpha-pinene, beta-pinene, and 3-carene were 62%, 66%, and 68% respectively, of the amount supplied. Between 2% and 5% of the net uptake was excreted unchanged in the expired air after the end of exposure. The mean blood clearance 21 hours after exposure (CL21h) of alpha-pinene, beta-pinene and 3-carene, were 0.8, 0.5, and 0.4 l.kg-1.h-1, respectively. The mean half lives (t1/2) of the last phase of alpha-pinene, beta-pinene, and 3-carene averaged 32, 25, and 42 hours, respectively. The t1/2s agreed with previously calculated half lives from single exposures. The total blood clearance CL21h of 3-carene found in this turpentine study was lower, and CL4h of 3-carene was significantly lower than the values obtained from similar exposure to pure 3-carene. The subjects attending both exposure to turpentine and to pure alpha-pinene at 450 mg/m3 had lower CL4h during the exposure to turpentine, when they experienced more discomfort of the throat or the airways (F = 5.7, P = 0.048) than during exposure to control concentrations. After experimental exposure to turpentine an increase in airway resistance was found that differed significantly from results of exposure to 3-carene at 10 mg/m3 (P = 0.021) or 450 mg/m3 (P = 0.047). CONCLUSIONS: Toxicokinetics and acute effects show small, if any, interactions between alpha-pinene, beta-pinene, and 3-carene. The subjects experienced discomfort in the throat and airways during exposure to turpentine and airway resistance was increased after the end of exposure.
Administration, Inhalation↗
The influence of increased plasma protein binding on the disposition of quinidine in turpentine-treated rats.
The effect of the increased plasma protein binding of quinidine on its disposition was investigated in turpentine-treated rats, since turpentine treatment is known to increase the plasma concentration of alpha 1-acid glycoprotein which preferentially binds basic drugs. The plasma free fraction of quinidine 16 and 48 h after turpentine treatment was decreased by 30 and 76%, respectively, compared to the control value. The treatment did not cause liver injury nor alter the hepatic blood flow. The disappearance of quinidine in plasma after an intravenous injection (3.0, 7.0, 12.5 mg/kg) was analyzed by a two-compartment open model in both control and turpentine-treated rats. The blood total body clearance (CLb) of quinidine at 48 h after the treatment was decreased by 30 to 65% in a dose-dependent manner, compared to that in control rats. The distribution volume (Vdss) of quinidine (12.5 mg/kg) at 16 and 48 h after turpentine treatment was decreased by 30 and 79%, respectively. Hepatic extraction ratio (HER) of quinidine, which was determined at steady state blood concentrations from 0.5 to 2.3 micrograms/ml, was decreased from 0.8 to 0.35 with an increase in the quinidine concentration in control rats. The HER value 48 h after turpentine treatment was consistently reduced by 15 to 40% in a concentration-dependent manner compared to the corresponding control value. These findings indicate that the increased plasma binding of quinidine caused a reduction of HER of the drug, and the reduced HER resulted in the decrease in CLb in turpentine-treated rats.(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↗
The effects of an intrathecal NMDA antagonist (AP5) on the behavioral changes induced by colorectal inflammation with turpentine in rats.
Visceral pain, especially that associated with inflammation of visceral organs, is poorly understood and difficult to treat clinically. The purpose of this study was to investigate the effects of intrathecal 2-amino-5-phosphonovaleric acid (AP5, a competitive NMDA antagonist) upon a visceromotor response to distension of colonic tissue inflamed by exposure to turpentine. All experiments were conducted under pentobarbital anesthesia. Animals were prepared with a laminectomy from T12 to L1 to facilitate intrathecal drug administration. Colonic distension thresholds for a visceromotor response were determined in the presence and absence of AP5. Animals were divided into two groups. The NS group received 50 microl of saline intrathecally and the AP5 group 10 mM of AP5 in 50 microl saline. After baseline measurements, intrathecal drugs were administered. Five minutes later, the effects of intrathecal drugs were measured, then 1 ml of 25% turpentine was administered anorectally. Subsequent measurements were made every 5 minutes for the next 90 minutes. Visceromotor thresholds to colorectal distension (CRD) were significantly decreased 50 min after turpentine administration in the NS group. There was no threshold change in the AP5 group. This study suggests that the administration of the competitive NMDA receptor antagonist AP5 in this model blocks the effect of turpentine sensitization on visceromotor response to CRD. The absence of AP5 effects in animals not sensitized by turpentine suggests that NMDA systems may be involved in the sensitization.
2-Amino-5-phosphonovalerate↗
Responses of tissue protein synthesis to nutrient intake in rats exposed to interleukin-1 beta or turpentine.
1. The influence of an acute-phase reaction on the ability of protein synthesis rates in liver and three different muscles (gastrocnemius, soleus and heart) to respond to a short intravenous infusion of nutrients (glucose plus amino acids) was investigated during experimental inflammation induced by injection of human recombinant interleukin-1 beta or turpentine in young male rats. 2. Interleukin-1 beta induced a consistent increase of 3 degrees C in body temperature between 3 and 5 h after injection, whereas turpentine induced a delayed fever, peaking by 13 h. 3. Interleukin-1 beta and turpentine stimulated fractional rates of protein synthesis in liver. The synthesis rate was inhibited by interleukin-1 beta in gastrocnemius and soleus muscle, but an elevation was seen in heart muscle. In this study there was no significant response of muscle to turpentine injection. 4. Two hours of parenteral nutrition increased fractional synthesis rates in all tissues when compared with Ringer's lactate. Somewhat larger responses to feeding were observed as a result of either interleukin-1 beta or turpentine injection in all tissues, but these improvements were not significant. 5. We conclude that the response of protein synthesis rates in liver and skeletal muscle to parenteral nutrition is not inhibited, and may be somewhat enhanced, during acute inflammatory conditions in the growing rat.
Acute-Phase Proteins↗
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↗