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[Solvents for the removal of gutta-percha from root canals. 2. Side effects of chloroform, halothane and xylene].

High concentrations of organic solvents have adverse effects on the health of professional workers. In endodontics, halothane, chloroform and xylene are used to dissolve gutta-percha from root canals. It is therefore questioned whether the use of these solvents could affect the health of patients or of the dental team. It seems warranted to conclude that the amounts and concentrations of chloroform, xylene and halothane such as used in endodontic retreatment, are low and therefore are safe. However, the dentist should be aware of possible hypersensitivity induced by previous application of halothane as a narcotic.

Chloroform↗

[The biological levels of chloroform in the general population].

The paper reports the results of determination, via gas chromatography and mass spectrometry, of chloroform in expired air, blood and urine of a group of non-occupationally exposed blood donors. Chloroform concentrations were also measured for each subject in the air of the environment where samples were taken.

Adult↗

The hepatotoxic action of chloroform: short-time dynamics of biochemical alterations and dose-effect relationships.

Chloroform was administered ip to Balb/c mice as a single dose ranging from 1/8 to 1 of the approximate lethal dose. At different time periods after administration, mice were sacrificed. Serum glutamate-pyruvate transaminase (SGPT) and sorbitol dehydrogenase (SDH) as well as glutathione (GSH) and malondialdehyde (MDA) levels in the liver were determined. Increased SGPT and SDH levels were found for all doses exceeding 1/8 of the approximate lethal dose. The depletion of GSH level was kept within 40% for all doses. A 2-4 fold increase of hepatic MDA level was found. The depletion of hepatic GSH and, to some extent the increase of serum SGPT and SDH, occurred in biphasic fashion. Dose-effect functions for these biochemical alterations could only be constructed for the second, delayed phase of action. It is postulated that the hepatotoxicity of chloroform is mainly dependent on radical formation in the course of biotransformation.

Alanine Transaminase↗

[The first operations performed with chloroform in Spain. More facts and new contributions].

Although the issue of clinical introduction of chloroform in Spain was rather controversial, we can assure now with no doubt that first news of its discovery reached our country by the end of November and beginning of December of 1847. The cities first receiving those first news were Cádiz, Madrid, Barcelona, and Santiago de Compostela; in the latter two cities, during the first days of December, the new anesthetic agent was already available and the first experiments on dogs were conducted in 19th Sunday and first clinical assays in Barcelona and in Santiago de Compostela, the first experiments in Spain, were carried out in December 20th. Spanish scientific and daily press, particularly, press of Barcelona and Madrid promptly reflected the events and informed their readers about the discovery of chloroform as anesthetic. Our research deals with some of these aspects and we believe that will contribute to clarify not fully studied points to date.

Anesthesia, General↗

[Effect of carbon tetrachloride and chloroform on hematologic parameters in rats].

While the hepato- and nephrotoxicity of carbon tetrachloride (CCl4) in men and animals are well characterized, little is known about the haematological effects of CCl4 poisoning. Therefore some haematological parameters were investigated after oral administration of CCl4 and the CCl4-metabolite chloroform in rats. The haemoglobin concentration in the blood was significantly reduced 7 days after administration of CCl4. Chloroform produced a decrease of the relative reticulocyte count at the same time. All effects are moderate and reversible.

Animals↗

[Carcinogenicity of chloroform].

Carcinogenicity of chloroform for various dosage and route of administration was assessed in CBA X C57B1/6 mice in a chronic experiment (250 or 15 mg/kg body weight in vegetable oil, intra-esophageally via a probe; or 300; 30; 3; 0.3 or 0.03 mg/l in drinking water). Chloroform did not reveal its carcinogenic properties unless a dose of 250 mg/kg was given.

Administration, Oral↗

A double homicide as a result of chloroform poisoning.

Homicidal poisoning using chloroform has been reported infrequently. Presented is a case of a double homicide involving a 29-year-old male and his 23-year-old fiance. Gas chromatographic methodology and tissue concentrations of chloroform are presented. Evidence strongly suggests forced inhalation using an impregnated cloth.

Administration, Inhalation↗

Hepatic histochemistry after chloroform effects of pretreatment with an enzyme inducer.

Chloroform anesthesia induced some histochemical changes in hepatic lobules in the form of diminution in succinic dehydrogenase and acid phosphatase activities accompanied by an increase in alpha esterase activity. In this respect more manifest changes were observed as a result of the delayed effect of chloroform as well as after administration of the inducer.

Acid Phosphatase↗

Association between chloroform levels in finished drinking water supplies and various site-specific cancer mortality rates.

This paper discusses some of the statistical and biological problems that are likely to be encountered when an indirect or ecological approach is used to assess the possible public health impact of general population exposures to environmental agents. For purposes of illustration, the potential association between various site-specific cancer mortality rates and chloroform levels in public drinking water supplies was considered. The analyses that were performed demonstrated that, for the data sets under consideration, there were some definite associations between chloroform levels and cancer mortality for specific sites such as the rectum-intestine and bladder. However, the marked extent to which these results were dependent on (1) the weighting scheme adopted in the analysis, (2) the presumed appropriateness of the data, and (3) the characteristics of the statistical model was also clearly illustrated. Because of these dependencies the quantitative, causal interpretation of results generated from an indirect study would appear to be a very tenuous and questionable practice in most instances.

Chloroform↗

Whole-body autoradiography and allied tracer techniques in distribution and elimination studies of some organic solvents: benzene, toluene, xylene, styrene, methylene chloride, chloroform, carbon tetrachloride and trichloroethylene.

Whole-body autoradiography has been used to study the distribution and fate of 14C-labeled benzene, toluene, xylene, styrene, methylene chloride, chloroform, carbon tetrachloride and trichloroethylene in mice after inhalational exposure. Total radioactivity, including the volatile part of the solvents were registered by autoradiography of dried, evaporated tape-fastened sections. In addition, dried, evaporated tape-fastened sections were extracted with water, trichloroacetic acid and a series of organic solvents and autoradiographed to register organs where metabolites were firmly bound. In another facet of the study, the quantitative elimination of the solvents and their metabolites via various routes was investigated. The expiration of unchanged solvents was subject to mathematical and computerized compartmental pharmacokinetic analysis. All solvents were rapidly taken up in fatty and nervous tissues where they were retained for different periods of time largely dependent on their fat solubility. Unexpectedly long retention times were noted for the chlorinated solvents, particularly for chloroforn, which showed a specific long-term retention in the cerebellum, meninges and spinal nerves, indicating interactions with specific nervous tissue receptors. Solvent metabolites appeared rapidly in several organs, mainly the liver and kidney, and were excreted both via urine and bile. Toluene and xylene metabolites were completely extractable whereas firmly bound metabolites were registered after inhalation of benzene, styrene and all chlorinated solvents, notably in the liver and kidney but also in the bronchi of the lung. Three-compartment pharmacokinetics were observed for the majority of the solvents selected for study although a two-compartment model was found to fit the elimination rate curves for styrene, methylene chloride and chloroform in the exhaled air. The fat solubility of the solvents was found to influence their pharmacokinetics since lower rate constants were generally obtained for the expiration of more fat soluble solvents.

Adipose Tissue↗

[The Braun apparatus for mixed ether-chloroform anesthesia. A contribution to the early history of combination anesthesia].

The Braun ether-chloroform vaporiser was very frequently used during the first fifty years of the 20th century, mainly in the German speaking region. This primacy was principally involved by the simple management, the universal possibilities of application and the "expedient" combination of ether and chloroform: this term means the differential employment of these two substances for conducting individual anaesthesia. Heinrich Braun had published his method after extensive experimental studies, here briefly referred to; further reasons for the considerable success of the apparatus are discussed.

Anesthesia, Inhalation↗

[Chloroform sniffing: a new variant of substance abuse].

The nearly fatal outcome of a case of chloroform sniffing is described. After a brief review of the organ toxicity of chloroform, a potential therapeutic approach is discussed. Inhalation anesthetics should be considered in the differential diagnosis of coma of unknown etiology in the adolescent.

Adolescent↗

Effects of alterations in drug metabolism on chloroform-induced cardiac arrhythmias in rabbits.

Control rabbits or those treated with phenobarbital to induce drug metabolism or SKF 525A or Lilly 18947 to inhibit were exposed by inhalation to 10,500 ppm chloroform for one hour. Phenobarbital treatment decreased blood levels only prior to reaching equilibrium and did not alter the response to epinephrine-induced cardiac arrhythmias. The inhibitors, despite causing higher blood levels of chloroform, did not alter its cardiotoxicity.

Animals↗

Reduction of nitro-BT by some components of the chloroform-methanol extract of the grey matter of the rat brain after reserpine.

Investigations have been performed with the chloroform-methanol extract obtained from the grey matter of the rat brain, to find out if some of the fractions interfere with catecholamines in the reduction of Nitro-BT. The experiments were conducted on white Wistar rats, which were reserpinized with a dose of 10 mg/kg of body weight through 24 hrs. The fractions which were prepared from the chloroform-methanol extract of the grey matter of the rat brain after reserpinisation were compared with fraction of the control animals. The spectrophotometric measurements of the reduced Nitro-BT to formazan have shown, that one of the fractions, namely the water fraction of the reserpinized rats had the extinction curve significantly decreased as compared with the water fraction of the control animals. This observation favours the view, that there can exist an interference of catecholamines with the substances present in the water fraction.

Animals↗

Chlorinated aliphatic hydrocarbons used in the foods industry: the comparative pharmacokinetics of methylene chloride, 1,2 dichloroethane, chloroform and trichloroethylene after I.V. administration in the rat.

the pharmacokinetics of methylene chloride, CH2Cl2, 1,2-dichloroethane, CH2ClCH2Cl, chloroform, CHCl3 and trichloroethylene, CHCl.CCl2 were determined, after i.v. administration to male Wistar rats, at five dose levels ranging from 3 to 15 mg/kg. The elimination of chloroform followed a three compartment model at all dose levels. The remaining compounds gave data that fitted a two compartment model at low doses which changed to a three compartment model at higher dose levels. All data were fitted to a two and three compartment model and the model that gave the best fit was selected on the basis of the smallest residual mean squared error. Very few differences, apart from the change in the nature of the pharmacokinetic model, were seen in the rate coefficients over the dose range tested. At the highest dose level, the rates of uptake and elimination for the major tissues were similar to those observed for the blood but were much slower for the perirenal fat.

Animals↗

The diurnal rhythm of hepatotoxic action of chloroform.

Mice were administered with chloroform at 10 a.m., 2 p.m. and 6 p.m. and the signs of hepatotoxicity were measured 18 or 24 hrs later. The levels of alanine aminotransferase (ALT) in serum, and malondialdehyde (MDA) in the liver were higher after the evening administration compared to the morning one. The decrements of reduced glutathione (GSH) levels in the liver followed a similar pattern. It is concluded that the susceptibility of mice to the toxic effect of chloroform follows a circadian rhythm.

Alanine Transaminase↗

[Effects of chloroform, chlorobenzene and polychlorinated biphenyls on erythrocyte lipid peroxidation and membrane fluidity in poisoned rabbits].

Effects of three chlorinated compounds, i.e., chloroform, chlorobenzene and Aroclor 1254 (PCBs), on lipid peroxidation and membrane fluidity of erythrocytes in poisoned rabbits were studied. Results revealed daily intraperitoneal injection of peanut oil containing chlorinated compounds into rabbits showed nonenzymic promotion effects on its erythrocyte lipid peroxidation in varying degrees, but different effects on erythrocyte membrane fluidity, promoting by chloroform and inhibiting by Aroclor 1254. It suggested the constitutional characteristics of toxicant molecules also had effects on membrane fluidity. In addition, it was found there existed potential relationship between maintenance of cell morphology and membrane fluidity.

Animals↗

The identity of immunosuppressive components of the ethyl acetate extract and chloroform methanol extract (T2) of Tripterygium wilfordii Hook. F.

A variety of preparations of Tripterygium wilfordii Hook.F (TWHF) have been reported to be effective in the treatment of autoimmune diseases, including a chloroform methanol extract termed T2 and an ethyl acetate (EA) extract. The immunosuppressive activity of the EA extract was analyzed and the components accounting for this effect determined and compared to those of T2. More than 0.25 microgram/ml of the EA extract inhibited antigen- and mitogen-stimulated human T cell proliferation. The inhibitory effect of the EA extract on T cell proliferation resulted largely from suppression of interleukin-2 production. At concentrations that inhibited T cell function, the EA extract also profoundly suppressed [3H]-thymidine incorporation by mitogen-stimulated B cells, but it did not inhibit antigen presentation by monocytes and only modestly affected interleukin-6 production by lipopolysaccharide-stimulated monocytes. The profile of inhibition was comparable to that previously reported for the chloroform-methanol extract of Tripterygium wilfordii Hook.F, T2. To delineate the components of these extracts that might account for their immunosuppressive effect, we analyzed the composition of diterpenoid compounds. Both extracts contained triptolide and tripdiolide as the major immunosuppressive diterpenoids, but at different concentrations. Comparison of the composition of these extracts and the inhibitory capacity of the purified components indicated that the triptolide concentration of the EA extract can account for its immunosuppressive activity, although the combination of both triptolide and tripdiolide or other unknown components may be necessary to explain the inhibitory effects of T2.

Acetates↗