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Estudo experimental do volume molar em excesso de soluções liquidas binarias contendo cloroformio e aminas a diferentes temperaturas e a pressão atmosferica; Experimental study of excess molar volume of binary liquid solutions containing chloroform and amines at different temperatures and at atmospheric pressure

Jucelio Gobi Magalhães
Fonte: Biblioteca Digital da Unicamp Publicador: Biblioteca Digital da Unicamp
Tipo: Dissertação de Mestrado Formato: application/pdf
Publicado em 26/02/2007 PT
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Este trabalho consiste em um estudo experimental do volume molar em excesso Vm de soluções líquidas binárias de clorofórmio + n-butilamina ou + s-butilamina; ou + dietilamina; ou + trietilamina a 288,15, 293,15, 298,15 e 303,15 K em função da composição e à pressão atmosférica, com o objetivo de estudar os possíveis efeitos físicos, químicos e estruturais nestes sistemas. Os dados experimentais foram ajustados a um polinômio do tipo Redlich-Kister e os resultados foram utilizados no cálculo de outras grandezas termodinâmicas, tais como, volume parcial molar, volume parcial molar em excesso, volume molar aparente, e volume molar aparente total. O Vm foi determinado indiretamente pela técnica de densitometria de oscilação mecãnica. Para os quatro sistemas estudados, e em todas as temperaturas os dados de Vm são negativos e tornam-se mais negativos com o aumento da temperatura. Os pontos de mínimo nos gráficos de Vm versus fração por mol de clorofórmio situam-se entre 0,35 e 0,50, dependendo do sistema. Os volumes parciais molares à diluição infinita do clorofórmio e das aminas são negativos em todas as temperaturas estudadas, e tornam-se mais negativos com o aumento da temperatura. Os resultados sugerem um pronunciado efeito estrutural (volume molar e volume livre) no valor de Vm ...

Membrane introduction mass spectrometry applied to the monitoring of chloroform degradation by hypochloride in acidic aqueous medium

Rocha,Lilian L. da; Rios,Rachel V. R. A.; Lago,Rochel M.; Augusti,Rodinei
Fonte: Sociedade Brasileira de Química Publicador: Sociedade Brasileira de Química
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/04/2005 EN
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Membrane Introduction Mass Spectrometry (MIMS) was used to investigate chloroform degradation in acidic aqueous medium by sodium hypochloride (NaClO). From the experimental results a reaction sequence for the complete degradation of CHCl3 to CO2 and HCl was suggested. Furthermore, it was also proposed the formation of phosgene (COCl2) as a transient species under these experimental conditions.

Chloroform formation by chlorination of aqueous algae suspensions: online monitoring via membrane introduction mass spectrometry

Borges,João T.; Sparrapan,Regina; Guimarães,José R.; Eberlin,Marcos N.; Augusti,Rodinei
Fonte: Sociedade Brasileira de Química Publicador: Sociedade Brasileira de Química
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/01/2008 EN
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Membrane introduction mass spectrometry (MIMS) was used to perform on-line monitoring of the chloroform formation via the chlorination of aqueous suspensions of several green and blue-green Brazilian algae (Microcystis panniformis, Selenastrum sp., Scenedesmus sp., Monoraphidium sp. (strain 354), Monoraphidium sp. (strain 960), and Staurastrum sp.). The influence of major parameters, such as temperature, pH, initial concentration of sodium hypochloride, filtration, and reaction time, on chloroform formation was evaluated. It was verified that the chloroform formation is strongly dependent on the alga type and is favored by high temperatures, pH, sodium hypochloride initial concentration and reaction time. Finally, filtered algae samples produce smaller amounts of chloroform in comparison to the rough suspension.

Chloroform degradation in methanogenic methanol enrichment cultures and by Methanosarcina barkeri 227.

Bagley, D M; Gossett, J M
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /09/1995 EN
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The effects of methanol addition and consumption on chloroform degradation rate and product distribution in methanogenic methanol enrichment cultures and in cultures of Methanosarcina barkeri 227 were investigated. Degradation of chloroform with initial concentrations up to 27.3 microM in enrichment cultures and 4.8 microM in pure cultures was stimulated by the addition of methanol. However, methanol consumption was inhibited by as little as 2.5 microM chloroform in enrichment cultures and 0.8 microM chloroform in pure cultures, suggesting that the presence of methanol, not its exact concentration or consumption rate, was the most significant variable affecting chloroform degradation rate. Methanol addition also significantly increased the number of moles of dichloromethane produced per mole of chloroform consumed. In enrichment cultures, the number of moles of dichloromethane produced per mole of chloroform consumed ranged from 0.7 (methanol consumption essentially uninhibited) to 0.35 (methanol consumption significantly inhibited) to less than 0.2 (methanol not added to the culture). In pure cultures, the number of moles of dichloromethane produced per mole of chloroform consumed was 0.47 when methanol was added and 0.24 when no methanol was added. Studies with [14C]chloroform in both enrichment and pure cultures confirmed that methanol metabolism stimulated dichloromethane production compared with CO2 production. The results indicate that while the addition of methanol significantly stimulated chloroform degradation in both methanogenic methanol enrichment cultures and cultures of M. barkeri 227...

Inactivation of hepatitis B virus and non-A, non-B hepatitis by chloroform.

Feinstone, S M; Mihalik, K B; Kamimura, T; Alter, H J; London, W T; Purcell, R H
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /08/1983 EN
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To determine whether a non-A, non-B hepatitis agent contained essential lipids, we extracted with chloroform a dilution of human plasma that contained approximately 10(4) chimpanzee infectious doses of non-A, non-B hepatitis virus and then tested for infectivity in chimpanzees. In addition, we treated a serum containing hepatitis B virus in the same way. Both of these samples were also sham extracted as controls. Known chloroform-sensitive and chloroform-resistant viruses were added directly to the hepatitis-containing serum or plasma as internal controls or to fetal calf serum as external controls and were assayed for infectivity in vitro after chloroform extraction or sham extraction. All infectivity of the diluted plasma that contained at least 10(4) chimpanzee infective doses of non-A, non-B hepatitis agent and all infectivity of the serum that contained 10(3.5) chimpanzee infective doses of hepatitis B virus were destroyed by chloroform. The chloroform-sensitive control viruses were completely inactivated, but the chloroform-resistant control viruses lost less than 0.5 log10 of infectivity. Sham-extracted non-A, non-B hepatitis agent-containing plasma was shown to maintain its infectivity in chimpanzees that had initially been inoculated with the chloroform-extracted plasma. Thus...

The relationship between water concentrations and individual uptake of chloroform: a simulation study.

Whitaker, Heather J; Nieuwenhuijsen, Mark J; Best, Nicola G
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /05/2003 EN
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We simulated the relationship between water chloroform concentrations and chloroform uptake in pregnant women to assess the potential extent of exposure measurement error in epidemiologic studies of the health effects of exposure to water disinfection by-products. Data from the literature were used to assign statistical distributions to swimming pool chloroform concentrations, frequency and duration of swimming, showering and bathing, and average tap water consumption. Measured increases in blood chloroform concentrations after these activities were used to estimate average uptake per microgram per liter chloroform in the water, per minute spent in the activity or per liter consumed. Given average tap water chloroform concentrations from a U.K. epidemiologic study, an average daily uptake over 90 days was simulated for 300,000 mothers. The correlation between simulated uptakes and home tap chloroform concentration was 0.6. Mothers who swam regularly received far greater doses than did nonswimmers. Results suggest there will be considerable attenuation in risk estimates and/or power loss in epidemiologic studies if the putative agent is chloroform.

Enhancement of the hepatotoxicity of chloroform in B6C3F1 mice by corn oil: implications for chloroform carcinogenesis.

Bull, R J; Brown, J M; Meierhenry, E A; Jorgenson, T A; Robinson, M; Stober, J A
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /11/1986 EN
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A recent study of the ability of chloroform in drinking water to produce cancer reported that male Osborne-Mendel rats developed renal tumors, but that female B6C3F1 mice failed to develop hepatocellular carcinomas. The results obtained in the male Osborne-Mendel rats were comparable to those observed in an earlier study sponsored by the National Cancer Institute (NCI). On the other hand, the lack of an increased incidence of hepatocellular carcinomas in female B6C3F1 mice was in sharp contrast to previously reported results. The doses of chloroform used were comparable to that which produced an 85% incidence in the NCI study. We have investigated the extent to which the vehicle might be responsible for the different results in these two studies by examining the differential effects of chloroform when it was administered by gavage using corn oil versus a 2% Emulphor suspension as the vehicle. Male and female B6C3F1 mice were administered chloroform at 60, 130, and 270 mg/kg per day for 90 days. At sacrifice, body and organ weights were measured, and blood was recovered to perform the following serum chemistry measurements (in order of priority): glutamate oxalacetate transaminase (SGOT), lactate dehydrogenase (LDH), blood urea nitrogen (BUN)...

Chloroform induction of ornithine decarboxylase activity in rats.

Savage, R E; Westrich, C; Guion, C; Pereira, M A
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /12/1982 EN
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Chloroform is a drinking water contaminant that has been demonstrated to be carcinogenic to mice and rats resulting in an increased incidence of liver and kidney tumors, respectively. The mechanism of chloroform carcinogenicity might be by tumor initiation and/or promotion. Since induction of ornithine decarboxylase (ODC) activity has been proposed as a molecular marker for tumor promoters, we have investigated the effect of chloroform on ODC activity in rats. Chloroform induced a dose-dependent increase of hepatic ODC with an apparent threshold at 100 mg/kg body weight. Female rats were two to four times more susceptible to to chloroform. Upon daily dosing of chloroform for 7 days the liver became less susceptible, with the last dose of chloroform resulting in only 10% of the activity observed after a single dose. Nuclear RNA polymerase I activity was also induced by chloroform. Chloroform, rather than increasing the activity of renal ODC, resulted in a 35% reduction. The induction by chloroform of hepatic ODC activity might be associated with regenerative hyperplasia while the renal carcinogenicity of chloroform could not be demonstrated to be associated with ODC induction.

Mechanistic considerations for carcinogenic risk estimation: chloroform.

Reitz, R H; Fox, T R; Quast, J F
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /12/1982 EN
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Chloroform has been reported to induce cancer in rodents after chronic administration of high doses by gavage. However, the interpretation of these findings is hampered by a lack of knowledge concerning the relative roles of genetic and nongenetic mechanisms in these bioassays. The present studies were carried out in male B6C3F1 mice in order to investigate the potential of chloroform to induce genetic damage and/or organ toxicity at the sites where tumors have been observed in the various bioassays. These studies revealed that carcinogenic doses of chloroform produced severe necrosis at the sites where tumors later developed. This was demonstrated by light microscopy as well as by determination of the cellular regeneration index following administration of 3H-thymidine. Noncarcinogenic doses of chloroform failed to induce these responses. In contrast, studies of DNA alkylation and DNA repair in vivo failed to give any indication that chloroform had produced the type of genetic alterations associated with known genotoxic chemicals. These data suggest that the primary mechanism of chloroform-induced carcinogenesis is nongenetic in nature. If the same mechanism predominates in man, there should be little to no carcinogenic risk associated with exposure to noncytotoxic levels of chloroform.

LIVER INJURY, LIVER PROTECTION, AND SULFUR METABOLISM : METHIONINE PROTECTS AGAINST CHLOROFORM LIVER INJURY EVEN WHEN GIVEN AFTER ANESTHESIA

Miller, L. L.; Whipple, G. H.
Fonte: The Rockefeller University Press Publicador: The Rockefeller University Press
Tipo: Artigo de Revista Científica
Publicado em 01/11/1942 EN
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Protein-depleted dogs are very susceptible to injurious agents—in particular, chloroform. Methionine given shortly before chloroform anesthesia will give complete protection against chloroform. Methionine (or cysteine plus choline) given 3 or 4 hours after chloroform anesthesia will give significant protection against the liver injury of chloroform anesthesia. Methionine given more than 4 hours after chloroform anesthesia gives no protection against liver injury. Choline alone given before chloroform gives no protection against liver injury. The protein-depleted dogs have livers which are deficient in both nitrogen and sulfur, but sulfur is depleted more than is the nitrogen. The N/S ratio therefore rises. Methionine or cystine feeding promptly makes up this liver sulfur deficit. Viable liver cells are necessary for this uptake of sulfur. Livers of fetuses in utero or of newborn pups tolerate a chloroform anesthesia which will cause fatal liver injury in adults. The nitrogen and sulfur values of these fetus or pup livers are within the high normal values for adults. Blood-forming cells are present in the fetus or pup livers during this period. When these blood islands are eliminated during the 3rd or 4th week of life, the liver then becomes normally susceptible to chloroform liver injury. Methionine or methionine-rich protein digests (e.g. casein) or various proteins by mouth or by vein should prove useful to protect the liver against certain types of injury and to aid in organ repair.

Mechanism of chloroform-induced renal toxicity: Non-involvement of hepatic cytochrome P450-dependent metabolism

Fang, Cheng; Behr, Melissa; Xie, Fang; Lu, Shijun; Doret, Meghan; Luo, Hongxiu; Yang, Weizhu; Aldous, Kenneth; Ding, Xinxin; Gu, Jun
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
EN
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Chloroform causes hepatic and renal toxicity in a number of species. In vitro studies have indicated that chloroform can be metabolized by P450 enzymes in the kidney to nephrotoxic intermediate, although direct in vivo evidence for the role of renal P450 in the nephrotoxicity has not been reported. This study was to determine whether chloroform renal toxicity persists in a mouse model with a liver-specific deletion of the P450 reductase (Cpr) gene (liver-Cpr-null). Chloroform-induced renal toxicity and chloroform tissue levels were compared between the liver-Cpr-null and wild-type mice at 24 h following differing doses of chloroform. At a chloroform dose of 150 mg/kg, the levels of blood urea nitrogen (BUN) were five times higher in the exposed group than in the vehicle-treated one for the liver-Cpr-null mice, but they were only slightly higher in the exposed group than in the vehicle-treated group for the wild-type mice. Severe lesions were found in the kidney of the liver-Cpr-null mice, while only mild lesions were found in the wild-type mice. At a chloroform dose of 300 mg/kg, severe kidney lesions were observed in both strains, yet the BUN levels were still higher in the liver-Cpr-null than in the wild-type mice. Higher chloroform levels were found in the tissues of the liver-Cpr-null mice. These findings indicated that loss of hepatic P450-dependent chloroform metabolism does not protect against chloroform-induced renal toxicity...

Solute-Solvent Complex Switching Dynamics of Chloroform between Acetone and Dimethylsulfoxide - 2D IR Chemical Exchange Spectroscopy

Kwak, Kyungwon; Rosenfeld, Daniel E.; Chung, Jean K.; Fayer, Michael D.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
EN
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Hydrogen bonds formed between C-H and various hydrogen bond acceptors play important roles in the structure of proteins and organic crystals, and the mechanisms of C-H bond cleavage reactions. Chloroform, a C-H hydrogen bond donor, can form weak hydrogen bonded complexes with acetone and with dimethylsulfoxide (DMSO). When chloroform is dissolved in a mixed solvent consisting of acetone and DMSO, both types of hydrogen bonded complexes exist. The two complexes, chloroform-acetone and chloroform-DMSO, are in equilibrium, and they rapidly interconvert by chloroform exchanging hydrogen bond acceptors. This fast hydrogen bond acceptor substitution reaction is probed using ultrafast two dimensional infrared (2D IR) vibrational echo chemical exchange spectroscopy. Deuterated chloroform is used in the experiments, and the 2D IR spectrum of the C-D stretching mode is measured. The chemical exchange of the chloroform hydrogen bonding partners is tracked by observing the time-dependent growth of off-diagonal peaks in the 2D IR spectra. The measured substitution rate is 1/30 ps for an acetone molecule to replace a DMSO molecule in a chloroform-DMSO complex and 1/45ps for a DMSO molecule to replace an acetone molecule in a chloroform-acetone complex. Free chloroform exists in the mixed solvent...

Acute Chloroform Ingestion Successfully Treated with Intravenously Administered N-acetylcysteine

Dell’Aglio, Damon M.; Sutter, Mark E.; Schwartz, Michael D.; Koch, David D.; Algren, D. A.; Morgan, Brent W.
Fonte: Springer-Verlag Publicador: Springer-Verlag
Tipo: Artigo de Revista Científica
EN
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Chloroform, a halogenated hydrocarbon, causes central nervous system depression, cardiac arrhythmias, and hepatotoxicity. We describe a case of chloroform ingestion with a confirmatory serum level and resultant hepatotoxicity successfully treated with intravenously administered N-acetylcysteine (NAC). A 19-year-old man attempting suicide ingested approximately 75 mL of chloroform. He was unresponsive and intubated upon arrival. Intravenously administered NAC was started after initial stabilization was complete. His vital signs were normal. Admission laboratory values revealed normal serum electrolytes, AST, ALT, PT, BUN, creatinine, and bilirubin. Serum ethanol level was 15 mg/dL, and aspirin and acetaminophen were undetectable. The patient was extubated but developed liver function abnormalities with a peak AST of 224 IU/L, ALT of 583 IU/L, and bilirubin level reaching 16.3 mg/dL. NAC was continued through hospital day 6. Serum chloroform level obtained on admission was 91 μg/mL. The patient was discharged to psychiatry without known sequelae and normal liver function tests. The average serum chloroform level in fatal cases of inhalational chloroform poisoning was 64 μg/mL, significantly lower than our patient. The toxicity is believed to be similar in both inhalation and ingestion routes of exposure...

Evaluation of the inhibitory effects of chloroform on ortho-chlorophenol- and chloroethene-dechlorinating Desulfitobacterium strains

Futagami, Taiki; Fukaki, Yuko; Fujihara, Hidehiko; Takegawa, Kaoru; Goto, Masatoshi; Furukawa, Kensuke
Fonte: Springer Publicador: Springer
Tipo: Artigo de Revista Científica
Publicado em 27/05/2013 EN
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Organohalide-respiring Desulfitobacterium strains are believed to play an important role in the bioremediation and natural attenuation of chlorinated aliphatic and aromatic hydrocarbons. However, several studies have reported that chloroform significantly inhibits microbial reductive dechlorination of chloroethene. In this study, we examined the effect of chloroform on several Desulfitobacterium strains, including ortho-chlorophenol-dechlorinating Desulfitobacterium dehalogenans JW/IU-1 and Desulfitobacterium hafniense DCB-2, and also the chloroethene-dechlorinating strain D. hafniense TCE1. In medium containing 3-chloro-4-hydroxyphenylacetate as an electron acceptor, chloroform inhibited the growth of strains JW/IU-1 and DCB-2. Although chloroform did not directly inhibit dechlorination of 3-chloro-4-hydroxyphenylacetate by resting cells, cells cultivated with chloroform showed decreased dechlorination activity. Moreover, transcription of the gene encoding the reductive dehalogenase CprA decreased significantly in cells cultivated with chloroform. These results indicate that chloroform inhibits the growth and dechlorination activity of strains JW/IU-1 and DCB-2 via inhibition of cprA transcription. In contrast, cultivation of strain TCE1 in the presence of chloroform gave rise to a PceA reductive dehalogenase gene-deletion variant of strain TCE1; a similar phenomenon was observed in our previous study of chloroethene-dechlorinating D. hafniense strain Y51. Our results suggest that chloroform extensively inhibits the dechlorination activity of Desulfitobacterium strains...

Chronic toxicity of chloroform to Japanese medaka fish.

Toussaint, M W; Rosencrance, A B; Brennan, L M; Beaman, J R; Wolfe, M J; Hoffmann, F J; Gardner, H S
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /01/2001 EN
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Japanese medaka (Oryzias latipes) were continually exposed in a flow-through diluter system for 9 months to measured chloroform concentrations of 0.017, 0.151, or 1.463 mg/L. Parameters evaluated were hepatocarcinogenicity, hepatocellular proliferation, hematology, and intrahepatic chloroform concentration. Histopathology was evaluated at 6 and 9 months. Chloroform was not hepatocarcinogenic to the medaka at the concentrations tested. Chronic toxicity was evidenced at these time points by statistically significant ([alpha] = 0.05) levels of gallbladder lesions and bile duct abnormalities in medaka treated with 1.463 mg/L chloroform. We assessed hepatocellular proliferation by exposing test fish to 5-bromo-2'-deoxyuridine in the aquarium water for 72 hr after 4 and 20 days of chloroform exposure; we then quantified area-labeling indices of the livers using computer-assisted image analysis. We observed no treatment-related increases in cellular proliferation. We analyzed cells in circulating blood in medaka after 6 months of chloroform exposure. Hematocrit, leukocrit, cell viability, and cell counts of treated fish were not significantly different from those of control fish. Using gas chromatography (GC), we evaluated intrahepatic concentrations of chloroform in fish after 9 months of exposure. Livers from the 0.151 and 1.463 mg/L chloroform-treated fish had detectable amounts of chloroform...

Evaluation of dermal and respiratory chloroform exposure in humans.

Lévesque, B; Ayotte, P; LeBlanc, A; Dewailly, E; Prud'Homme, D; Lavoie, R; Allaire, S; Levallois, P
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /12/1994 EN
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Chloroform is a known contaminant of chlorinated drinking water and of swimming pool water disinfected with chlorine or one of its derivatives. Few data exist regarding the importance of dermal and inhalation exposure routes to the chloroform body burden resulting from domestic and recreational use of chlorinated water. In our experimental study involving 11 male swimmers, we quantified the body burden resulting from exposure to various concentrations of chloroform in water and air of an indoor swimming pool, during a daily 55-min exercise period. From the first to the sixth exercise period, CHCl3 mean concentration in water was increased from 159 micrograms/l to 553 micrograms/l. Corresponding mean air CHCl3 level ranged from 597 ppb to 1630 ppb. To dissociate the dermal exposure route from that of inhalation, swimmers used scuba tanks during an additional exercise period. Chloroform concentrations were measured in alveolar air before and after each exercise period, as well as after 35 min of physical activity. Chloroform levels in water and air were measured every 10 min. We examined the relationship between alveolar air concentration (a measure of body burden) at 35 and 55 min and environmental chloroform concentrations by using multiple regression models. The natural logarithm of alveolar air concentration was strongly correlated with aqueous chloroform concentration both at 35 (p2 < 0.001...

PREGNANCY AND CHLOROFORM ANESTHESIA : A STUDY OF THE MATERNAL, PLACENTAL, AND FETAL TISSUES.

Whipple, G. H.
Fonte: The Rockefeller University Press Publicador: The Rockefeller University Press
Tipo: Artigo de Revista Científica
Publicado em 01/03/1912 EN
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Pregnant dogs are susceptible to chloroform administered shortly before delivery or during labor, and show the same degree of liver injury as normal dogs, or even a somewhat greater one. Chloroform anesthesia may cause more or less hyaline necrosis in the border zone between the maternal and fetal parts of the placenta that may lead to hemorrhage, placental separation, and premature delivery. Chloroform anesthesia causes no injury to the liver of the fetus nor to any other fetal organ, in spite of the fact that it can be demonstrated to be present in these tissues. These experiments raise objections to the use of chloroform in pregnant women where an anesthetic must be continued for half an hour or longer. Chloroform anesthesia may be admissible for the few minutes at the end of the delivery, but when operative measures are necessary, before or after delivery, it is a dangerous anesthetic and surely capable of producing injury to the liver in the manner recognized in the case of normal persons. Objections may be raised to the application of conclusions derived from experiments on dogs to human cases; but the similarity of the effects of chloroform in man and dog surely affords a sound basis of comparison. Two fundamental facts would seem to be now established: (1) Normal human adults may be fatally poisoned (late chloroform poisoning) by chloroform anesthesia of one half to one hour's duration. (2) Normal and pregnant dogs are equally susceptible to late chloroform poisoning...

The effect of chloroform on mitochondrial energy transduction.

Chien, L F; Brand, M D
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em 15/12/1996 EN
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The effect of chloroform on mitochondrial respiration with succinate was investigated by applying the method of Brand, Chien and Diolez [(1994) Biochem. J. 297, 27-29] to examine whether chloroform causes redox slip (fewer protons pumped per electron transferred) during mitochondrial electron transport. N,N,N',N'-Tetramethyl-p-phenylenediamine (TMPD), which lowers H+/O (the number of protons pumped to the external medium by the electron transport complexes per oxygen atom consumed) by altering the electron flow pathway, was investigated for comparison. Non-phosphorylating mitochondria that had been treated with 350 microM TMPD or 30 mM chloroform were titrated with malonate in the presence of submaximal concentrations of the uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP). Linear relations between CCCP-induced extra respiration and protonmotive force were obtained. These results showed that there was no measurable protonmotive force-dependent or rate-dependent slip in mitochondria treated with either TMPD or chloroform. However, both TMPD and chloroform seemed to decrease H+/O in a manner independent of protonmotive force and rate. The relationship between non-phosphorylating respiration and protonmotive force was simulated in mitochondria of which 25% of the total population were assumed to have been broken. The simulation showed that the apparent decrease in H+/O on the addition of TMPD or chloroform to mitochondria could be in principle accounted for by breakage. Assays of mitochondrial breakage (ATP hydrolysis in the presence of atractyloside and oxidation of exogenous NADH) showed that chloroform broke mitochondria but TMPD did not. We conclude that chloroform changes the measured H+/O as an artifact by causing mitochondrial breakage and does not cause measurable redox slip...

Effect of beta-cyclodextrin on the extraction of isoxazolines from aqueous ethanol into chloroform

Easton, Christopher; Hughes, Colin; Lincoln, Stephen F; Simpson, Gregory Wayne; Vuckovic, George
Fonte: ARKAT Foundation Publicador: ARKAT Foundation
Tipo: Artigo de Revista Científica
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Regioisomeric pairs of isoxazolines were prepared through reaction of nitrile oxides with ethyl trans-cinnamate. The effect of β -cyclodextrin on the solubility of these compounds in aqueous ethanol and their extraction into chloroform has been examined.

Chloroform fumigation-extraction labile C pool (microbial biomass C "plus") shows high correlation to microbial biomass C in Argentinian and Brazilian soils

De-Polli,Helvécio; Costantini,Alejandro; Romaniuk,Romina; Sampaio Pimentel,Márcio
Fonte: Ciencia del suelo Publicador: Ciencia del suelo
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/07/2007 EN
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363.4519%
Chloroform fumigation-incubation and chloroform fumigation-extraction approaches have significantly contributed to assess soil microbial biomass. Some controversy is found in the literature about the suggestion to calculate microbial biomass carbon (MBC) without the subtraction of the un-fumigated control, in opposition to the originally proposed method that requires such subtraction. Some authors consider the non-subtraction proceeding as a more robust method. Nevertheless, values obtained without subtraction of a control include other labile organic fractions of soil carbon besides microbial biomass. Therefore, due to the usefulness of this measurement we consider more appropriate to call it as chloroform-fumigation labile C pool or microbial biomass carbon "plus" (MBC PLUS). We used a vast series of data from soils of Argentina and Brazil under different management situations to verify whether MBC correlates to MBC PLUS. There was a significant statistical correlation between values of MBC obtained by fumigation-extraction method and the corresponding MBC PLUS. The MBC PLUS performed as well as MBC as an indicator to differentiate soil managements and their impact on soil quality.