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1. Turpentine and thinner exposed rats, during the last stage of pregnancy, delivered 59% and 20% of dead newborn, respectively. 2. Turpentine and thinner delayed foetal growth and caused no effects on neonates body size. 3. Cerebral cortex of newborn rats, prenatally exposed to organic solvents showed to histological alterations.
1. Within 24 hr of injection into plaice, cortisol, deoxycorticosterone, adrenalin or endotoxin cause an increase (P less than 0.001) in circulating C-reactive protein (CRP). Turpentine and soluble dexamethasone have no effect. 2. The increase in CRP with endotoxin is not enhanced with adrenalin or deoxycorticosterone, and in conjunction with cortisol the increase is additive. 3. Changes in CRP are independent of the amounts of serum amyloid P-component or total protein. 4. Turpentine, cortisol and adrenalin cause a rapid increase in circulating glucose. 5. It is concluded that some adrenal hormones stimulate the CRP acute phase response in plaice, without an apparent provoking agent.
OBJECTIVE: Some epidemiological studies have indicated that diseases resulting in prolonged and sustained fever, such as exanthemata, respiratory infections and otitis media in infantile period or childhood are likely to have a marked deleterious effect on enamel formation, but the relationship between fever and enamel defects is unknown. The purpose of the present study was to induce a persistent high fever and examine the effects on the developing tooth enamel. METHODS: Twenty male Wistar rats weighting 140+/-10 g were used in this study. For the experimental group, a dose of 2.3 ml/kg steam-distilled turpentine was subcutaneously injected into both hind limbs five times at 12h intervals. Control rats received 2.3 ml/kg of sterile saline into the same injection site. The rectal temperatures of animals were measured at the febrile period. After constant periods, the animals were sacrificed, and the mandibular incisors were examined by contact microradiography (CMR) and histological observation. RESULTS: The febrile state lasted for 57 h and the average temperature rose 1.51 degrees C higher than that of the control group. The ground sections, semi-thin and ultra-thin sections of mandibular incisors were prepared and the enamel was observed. The microradiographs showed a radiolucent line along with the incremental line in the enamel. Moreover, microscopic examination indicated disorientation of enamel prism and crystal-free area within this radiolucent lesion. CONCLUSIONS: Persistent high fever pattern was established firmly by the turpentine injections and the process of enamel formation was influenced by the febrile period.
A clinical technique for using rectified turpentine oil to soften and dissolve gutta-percha to facilitate retreatment is described. Turpentine oil should be heated to 160 degrees F (71 degrees C) to increase its reactivity before delivery to the canal space.
The effects of restricted food intake and acute inflammation on the small bowel were studied, Wistar rats (250 g) were given subcutaneous injections of turpentine (TR) and compared to two control groups, at 18, 42 and 66 h. One was fed ad libitum (C), the other was pair fed (PF) with TR. The TR and PF rats showed hypoplasia of the jejunal mucosa with decreased protein and DNA contents at 42 h and 66 h. The hypoplasia resulted in a reduced villus height that was significantly different from the controls at 66 h (C: 468 +/- 17, TR[66] : 376 +/- 20, PF[66] : 258 +/- 2.9 microm, P<0.001). This decrease in villus height was significantly greater in the PF rats than in the TR rats at 66 h. The crypt height/villus height (C/V) ratio in the PF rats was greater than in the TR group at all times. However, the protein and DNA contents in the TR group were significantly higher than in the PF group at 42 h and 66 h (TR/PF[42] : 29.5 +/- 1.9 vs 20.5 +/- 2.0, P< 0.001, [66]: 25.8 +/- 2.0 vs 16.6 +/- 1.3 mg/10 cm, P,< 0.001). Disaccharidase activities (sucrase and glucoamylase) per 10 cm jejunum at 66 h were significantly lower in the PF group than in the control and TR groups (sucrase mU/10cm[66] C : 3090 +/- 144, TR 2683 +/- 479, PF 1969 +/- 144, P,< 0.001; glucoamylase mU/10 cm[66] 237 +/- 25, TR 169 +/- 40, PF 123 +/- 5, P< 0.01). The N-aminopeptidase patterns in the TR and PF groups were similar. These data suggest that dietary restriction during acute inflammation is the main factor causing hypoplasia of the jejunal mucosa. However, acute inflammation has a trophic effect on the morphological and function of the mucosa. This effect is probably due to inflammatory mediators, whose synthesis is stimulated by turpentine.
In rat liver stimulated by partial hepatectomy a significant expression of Egr-1 and to less extent c-jun genes was observed within 15-30 min after the surgery. The induction is transient and vanishes within one hour. Egr-1 and c-jun were also induced in liver after subcutaneous injection of turpentine, a strong inducer of acute phase response. A maximum activation of these genes was observed within 4-9 hours after administration of turpentine. Both Egr-1 and c-jun extend the list of "immediate early" genes involved in proliferative response and constitute a group of genes inducible at the beginning of acute phase response.
A 52-year-old comatose white male was admitted to the hospital with what was later learned to be severe poisoning by a turpentine solution of dicrotophos, an organophosphorous insecticide he had ingested while drunk. The patient was treated effectively with atropine and pralidoxime chloride and required the largest doses of both agents reported to data. The case was complicated by difficulty in evaluating the response to therapy because of the effects of alcohol and turpentine. The patient was discharged from the hospital on the thirty-third day with no apparent sequelae.
After a dental operation a former laboratory technician was referred to our clinic because of swelling of his tongue, lips, and gingival mucosa. Patch testing with the ICDRG standard test battery gave positive reactions to colophony, balsam of Peru, and turpentine peroxides. Further patch testing revealed hypersensitivity to peppermint oil (an ingredient of several dental preparations) due to the sensitizing properties of three ingredients: alpha-pinene, limonene, and phellandrene. These compounds also occur in turpentine oil, a substance used in the patient's laboratory.
Oil of turpentine has become an infrequent allergen because of its replacement by the petroleum product white spirit, its deliberate exclusion from industrial products, and because the balsam oils used nowadays do not contain the sensitiser delta 3-carene. On the basis of the generally low incidence of sensitisation being currently recorded, the International Contact Dermatitis Group recommend that oil of turpentine be removed from standard patch test series.
Oil of turpentine is still a common allergen in Portugal although it does not contain delta 3-carene, as ascertained by gas chromatography. Patch tests with 6 terpenes on 22 patients revealed that 17 were allergic to alpha-pinene and 15 to dipentene; 12 were allergic to both. 4 patients were sensitive to delta 3-carene, 3 to alpha-terpineol and 2 to beta-pinene. These results explain the incidence of allergy to oil of turpentine in Portugal.
Hamster cheek pouches were painted thrice weekly with 50% v/v turpentine in liquid paraffin over periods ranging from 1 day to 16 weeks. Pouch mucosa was examined histologically for changes and measurements of epithelial thickness were made with a calibrated eyepiece micrometer. An increase in epithelial thickness was first observed 48 hrs. after a single painting and was accompanied by inflammatory changes in both epithelium and connective tissue. Maximal epithelial thickening occurred after 9 weeks of thrice weekly painting. Cheek pouches of animals left without further treatment for up to 1 year following 9 weeks painting were indistinguishable from controls. The epithelial response to treatment with turpentine is that of a reversible benign epithelial hyperplasia with hyperkeratosis.
When turpentine was instilled into the right pleural cavity in rabbits a pleural effusion developed in half of the animals, with a low pH, low glucose concentration, high lactic dehydrogenase activity and the constant presence of rheumatoid arthritis cells in the affected pleural cavity. The biochemical values in the pleural fluid were significantly different from the values for normal pleural fluid obtained by a special microtechnique. These changes resulting from the experimentally induced, simple, irritative turpentine pleuritis are similar to the findings in the pleural effusion in human rheumatoid pleuritis; this implies that such changes are probably non-specific and without evidence of an immunological background.
Turpentine was injected into the right pleural cavity of nude immune-incompetent mice, causing a temporary irritative exudative pleuritis. A transient occurrence of so-called rheumatoid arthritis cells was observed in the pleural fluid together with parallel characteristic biochemical changes. In similar experiments in nude mice, however, immunization followed by intrapleural application of bovine fibrin showed irritative "dry" pleuritis without the presence of rheumatoid arthritis cells. This is in contrast with previous results from similar experiments done using normal mice. The conclusion from the present experiments is that in nude immune-incompetent mice only the non-immunological, turpentine-induced pleuritis will generate cellular and biochemical changes typical of the rheumatoid disease in patients, while the fibrin-induced pleuritis fails to show similar changes. This suggests that the rheumatoid-like pleural changes described in the present experiments in nude mice have a non-immunological basis.
Pleural effusions were made by intrapleural turpentine installation in mice. The fine structure of inflammatory cells from the effusions was normal except for lipid inclusions. The same type of inclusion was previously found in neutrophils from pleural effusions in patients with tuberculous infection, rheumatoid disease, or carcinomatosis. The lipid inclusions observed in neutrophils from an irritative turpentine-induced pleurisy should be considered as "fatty change", and are structurally similar to the rheumatoid arthritis cells seen in patients with different diseases.
Inflammatory reactions reduce the activity of cytochrome P450 isoforms. The aim of the study was to determine the mechanisms underlying the decrease in CYP1A2 and CYP3A6 catalytic activities produced by serum from rabbits with a turpentine-induced inflammatory reaction (S(TIIR)) and interleukin 6 (IL-6). S(TIIR) and IL-6 were incubated with cultured primary hepatocytes from control rabbits (H(CONT)), and from rabbits with a turpentine-induced inflammatory reaction (H(TIIR)) in the absence or presence of pyrrolidine dithiocarbamate (PDTC), an antioxidant and inhibitor of nuclear factor kappaB transcription; 2'-amino-3'-methoxyflavone (PD98059), an inhibitor of extracellular signal-related kinase (Erk1/2); 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole (SB203580), an inhibitor of p38MAPK; Nomega-nitro-L-arginine methyl ester, an inhibitor of nitric-oxide synthase 2 (NOS2); the combination of PDTC, PD98059, and SB203580; and genistein, an inhibitor of Janus-associated protein tyrosine kinase (JAK). After 4 and 24 h of incubation of H(CONT) with S(TIIR) and IL-6, CYP1A2 activity was reduced without changes in expression; the reduction in activity was partially prevented by the inhibition of JAK, Erk1/2, and NOS2. In H(CONT), S(TIIR) and IL-6 did not affect CYP3A6 activity; however, PDTC reduced CYP3A6 activity by 40 and 80% after 4 and 24 h of incubation. In H(TIIR), S(TIIR) and IL-6 reduced both CYP1A2 and CYP3A6 activities; this decrease is partially prevented by inhibitors of protein tyrosine kinases, Erk1/2, and NOS2. In H(TIIR), SB203580 increased CYP3A6 activity in a dose-dependent manner without changes in protein expression. These results show that the signal transduction pathways mediating the decrease in CYP1A2 and 3A6 activity, produced by S(TIIR) and IL-6, involve JAK, Erk1/2, and NOS2.
An acute inflammatory reaction was induced in chickens by intraperitoneal injection of turpentine. The birds were then killed at various intervals and the peritoneal exudate sampled. The antihistamine mepyramine maleate was administered to another group of birds and the procedure repeated. Following turpentine injections there was a biphasic increase in vascular permeability, the early phase apparently mediated by histamine.
Subcutaneous injections of turpentine induced discrete aseptic abscesses in rats without detectable injury to other tissues. Hypoalbuminemia and high circulating concentrations of alpha 2-macroglobulin were present after 48 h. Liver size, protein content, and protein fractional synthetic rate (FSR) were all increased, whereas loss of muscle protein occurred together with similar (45-50%) reductions in both intramuscular glutamine concentrations ([Gln]i, mmol/l intracellular water) and FSR. The rats became anorexic, but pair feeding (50% ad libitum for 48 h) produced a 22% increase in muscle [Gln]i and only an 18% reduction in muscle FSR. Dietary restriction therefore did not demonstrate the positive relationship between muscle [Gln]i and FSR, which has been observed in animal trauma studies. It is concluded that subcutaneous injections of turpentine produce many of the features of the acute-phase response to injury, and therefore this technique is recommended as a convenient laboratory model for studying various aspects of the protein metabolic response to injury.
This study examined the role of the interleukin-1 (IL-1) type I receptor (IL-1RtI) in the acute phase response (APR) to inflammation in mice. Turpentine (100 microliters/mouse) injected subcutaneously induced fever, lethargy, body weight loss, and anorexia in IL-1RtI wild-type mice. Knockout mice lacking the IL-1RtI were resistant to these effects of turpentine, supporting a role for this receptor in the APR to local inflammation. The intraperitoneal injection of a low (50 micrograms/kg) or high (2.5 mg/kg) dose of lipopolysaccharide (LPS) induced similar APRs in IL-1RtI wild-type and knockout mice. IL-1RtI knockout mice were resistant to the APR induced by peripherally injected murine IL-1 beta, suggesting that it is not the interaction of endogenous IL-1 beta with IL-1RtII that induces an APR to LPS in these mice. We speculate that the absence of IL-1RtI in these knockout mice results in the sensitization of other cytokine pathways to mediate the APR to LPS.