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PubMed1977

Evidence supporting the identity of beef heart mitochondrial chloroform-released adenosine triphosphatase (ATPase) with coupling factor I.

Highly purified mitochondrial chloroform-released beef heart ATPase had molecular weight 330 000, five bands (alpha, beta, gamma, delta, epsilon) in sodium dodecyl sulfate gel electrophoresis and could restore the oxidative-phosphorylation function of A particles. Maximal inhibition (90%) of the enzyme by N,N'-dicyclohexylcarbodiimide was achieved at a molar ratio of inhibitor to protein of 30 : 1. Chloroform introduced into an aqueous solution of beef heart coupling factor I protected it from cold inactivation.

Adenosine Triphosphatases↗
PubMed1988

Recovery of malondialdehyde in urine as a 2,4-dinitrophenylhydrazine derivative after exposure to chloroform or hydroquinone.

Malondialdehyde (MDA) excretion in urine as an index for toxicological effects of chloroform and hydroquinone was evaluated. In a first series of experiments three groups of rats were used: non-pretreated rats (group I), starved rats (group II) and starved plus phenobarbital pretreated rats (group III). Chloroform (0.15 or 0.30 ml/kg, p.o.) was given as a single dose. The MDA excretion was related to the pretreatment, and in group III to liver damage. In a second series of experiments control rats were administered hydroquinone (100 or 200 mg/kg, p.o.), which induced a dose-related MDA excretion. These data indicate that the MDA assay was a selective and accurate marker for toxicological effects induced by the tested compounds.

Alanine Transaminase↗
PubMed1984

Nephrotoxicity of chloroform: metabolism to phosgene by the mouse kidney.

In this investigation, we have attempted to determine whether chloroform (CHCl3)-induced nephrotoxicity might be due to its metabolism to phosgene (COCl2) in the kidney. We have found that kidney homogenates from DBA/2J male mice in the presence of glutathione metabolize CHCl3 to 2-oxothiazolidine-4-carboxylic acid (OTZ). This product appears to be formed by the initial trapping of COCl2 by two molecules of GSH to form diglutathionyl dithiocarbonate (GSCOSG). Kidney gamma-glutamyl transpeptidase can rapidly metabolize GSCOSG to N-(2-oxothiazolidine-4-carbonyl)-glycine which is then hydrolyzed, possibly by cysteinyl glycinase to OTZ. The finding that deuterium-labeled chloroform (CDCl3) was less nephrotoxic and depleted less renal GSH than did CHCl3 suggests that the metabolism of CHCl3 to COCl2 may also occur in the kidney in vivo and lead to nephrotoxicity.

Animals↗
PubMed1984

Effect of age on oxygen consumption, superoxide dismutase, catalase, glutathione, inorganic peroxides and chloroform-soluble antioxidants in the adult male housefly, Musca domestica.

The objective of this study was to determine whether aging in the housefly is associated with a general decline in the efficiency of the mechanisms protective against the intermediates of oxygen metabolism. The rate of oxygen consumption, activities of superoxide dismutase (total and cyanide-insensitive) and catalase, and levels of inorganic peroxides, glutathione (GSH and GSSG) and chloroform-soluble antioxidants were measured in adult male houseflies at different ages. Rate of oxygen consumption declined in flies approaching the average life span of the population. Activity of total and cyanide-insensitive superoxide dismutase decreased during the last trimester of life. Catalase activity steadily declined with age while the concentration of inorganic peroxides gradually increased during the later two-thirds of the average life span. Levels of total glutathione and GSH decreased during later half of life whereas the relative concentration of GSSG increased during this period. The concentration of chloroform-soluble antioxidants sharply declined during the first half of life. These results are interpreted to suggest that the enzymatic and non-enzymatic defenses against oxygen free radicals and hydroperoxides tend to deteriorate with age in the adult housefly.

Aging↗
PubMed1986

Conformations of gramicidin A and its 9,11,13,15-phenylalanyl analog in dimethyl sulfoxide and chloroform.

In order to understand the difference in single channel behavior of gramicidin A as compared to that of gramicidin M- which is the mirror image of gramicidin M (all four tryptophanyl residues substituted by phenylalanine), conformational investigations were made under several experimental conditions. It is shown that, when examined under identical conditions, both molecules adopt the same conformations which could be identified in dimethyl sulfoxide (DMSO) and chloroform. In DMSO the conformation is based on a succession of beta-turns while in chloroform gramicidin A and M- can adopt a dimeric hybrid structure: a double helix terminated by two single-stranded helices involving the N- and C-terminal parts, respectively. It is therefore concluded that the difference in the energy profile between both gramicidins which was deduced from the ion transfer data has its origin in the nature of the aromatic side chains.

Chloroform↗
PubMed1983

Combined effects of fast-neutron irradiation and subcutaneously applied carbon tetrachloride or chloroform in C57Bl6 mice.

Male and female C57Bl6 mice received a single whole-body dose of irradiation with 170 rad or 330 rad of fast neutrons. Nine weeks later they were given a single subcutaneous injection of carbon tetrachloride or chloroform. Chloroform did not influence the occurrence of tumours, but carbon tetrachloride markedly increased the incidence of radiation-induced liver carcinomas.

Animals↗
PubMed1994

Hyperphosphorylation of p53 induced by benzene, toluene, and chloroform.

Phorbol 12-myristate, 13-acetate (PMA) is a known protein kinase C activator (PKC); benzene, chloroform, and toluene have also been reported to be PKC activators. We examined the effects of these three solvents on the phosphorylation of p53 in treated cells. Hyperphosphorylated p53 was found when p53 was immunoprecipitated from rat liver epithelial cell extracts treated with any of the solvents or PMA. The solvents also resulted in hyper-phosphorylation of human p53 produced by transfection of Saos-2 cells with a eucaryotic expression vector. Increased phosphorylation of p53 induced by the solvents was also observed through in vitro assays. Hyperphosphorylation of p53 may be involved in tumor promotion by benzene, toluene and chloroform.

Animals↗
PubMed1979

Ability of calf brain synaptic membranes to bind [35S]taurine to their triton X-100 and chloroform extracts.

A protein fraction containing reducing sugars was prepared from calf brain synaptic membranes with 0.5% Triton X-100, and another fraction containing bound phosphorus with a 2 : 1 chloroform--methanol mixture. Both protein fractions bound small amounts of [35S]taurine, the first fraction about 25 pmol/g protein and the second about 220 pmol/g protein. The Triton X-100 extract represented 13.8% of the membrane proteins, but the chloroform--methanol extract only 0.9%. The binding of taurine to the Trition X-100 extract was temperature sensitive, but was only slightly inhibited by hypotaurine and beta-alanine.

Alanine↗
PubMed1984

Choline uptake by lipid liposomes and its diffusion across chloroform are saturable and inhibited by hemicholinium-3.

Uptake of choline by lipid liposomes formed by cholate dialysis was saturable, inhibited by hemicholinium-3 and increased by preloading with unlabelled choline. Diffusion of choline between two aqueous phases separated by chloroform was also saturable, inhibited by high concentrations of hemicholinium-3, and increased by choline on the opposite side of the chloroform. These results indicate that choline diffusion may sometimes demonstrate properties qualitatively similar to those of low affinity carrier mediated transport systems.

Chemical Phenomena↗
PubMed1990

Increased methylation of chloroform extractable products in brain membrane preparations after propranolol injection to the rat.

1. One and four hours after acute or chronic (8 days) intraperitoneal injection of propranolol to rat at doses up to 25 mg/kg, a beta-adrenergic receptor blockage occurred in brain homogenates, as monitored by [3H]dihydroalprenolol binding. 2. A dose-dependent increased methylation of chloroform extractable products was observed (acute treatment: 18% increase, chronic treatment: 136% increase for the dose of 25 mg/kg). 3. The implication of beta-adrenergic receptors in this effect was studied and this revealed that: (a) acute intraperitoneal injection of the less active propranolol stereoisomer (+) did not produce any effect; (b) the chronic intraperitoneal injection of salbutamol, a beta-adrenergic receptor agonist, induced a decreased methylation of chloroform extractable products (62% decrease for the dose of 2.5 mg/kg). 4. It is concluded that injection of beta-adrenergic antagonist to the rat increases basal methyltransferase activity in the brain. This induces a decreased sensitivity of the enzyme activity to noradrenaline.

Albuterol↗
PubMed1990

Selective extraction of outer-membrane proteins from membrane complexes of Pseudomonas maltophila by chloroform-methanol.

An organic phase partitioning method is described for the selective purification of outer-membrane proteins (OMPs) from the total membrane complex of the opportunistic human and sheep pathogen, Pseudomonas maltophila. SDS-PAGE analysis confirmed that OMPs purified by chloroform-methanol treatment of the total membrane complex were not only identical to OMPs extracted from outer-membrane vesicles separated by sucrose gradient density centrifugation, but also possessed little or non-detectable levels of inner-membrane contaminants. Further analysis by enzyme linked immunosorbent assay (ELISA) and immunoblotting established that OMPs extracted by organic phase partitioning with chloroform-methanol retained antigenicity and serological activity indistinguishable from OMPs that were present in outer-membrane vesicles resolved by isopycnic sucrose density centrifugation of sarkosyl-treated membrane complexes.

Animals↗
PubMed1984

Mechanisms in 2-hexanone potentiation of chloroform hepatotoxicity.

2-Hexanone (2-Hx) is known to potentiate chloroform (CHCl3) hepatotoxicity in part by increasing the bioactivation of CHCl3 to phosgene (COCl2). Treatment of rats with 2-Hx + CHCl3 in vivo did not initiate peroxidation of hepatic fatty acids as determined by formation of conjugated dienes or depletion of unsaturated fatty acids, or as determined by production of malondialdehyde (MDA) in vitro. A 5-fold decrease in the specific activity of succinate-dependent cytochrome c reductase in liver from rats treated in vivo with corn oil (vehicle) + CHCl3 and in rats treated with 2-Hx + CHCl3 indicated that a mechanism independent of CHCl3 bioactivation may add to the hepatotoxic effects which result from the metabolism of chloroform to phosgene.

Animals↗
PubMed2004

Spectroscopic studies on the photoeffects on some metallocenes in the presence of chloroform molecules confined in poly(methyl methacrylate) thin films.

The changes in the electronic absorption spectra (UV-Vis) (after photoexcitation) of poly(methyl methacrylate) (PMMA) thin films doped with a metallocene and containing chloroform molecules as impurities, have been studied as a function of photoexcitation wavelength (210-750 nm), photoexcitation time (duration), amount of metallocene in the film and amount of chloroform molecules present in the film. Photoeffects on the metallocenes have been observed, which depend significantly on the nature of the central metal atom of the metallocene and the results have been discussed on the basis of the electronic configuration of the metallocenes, which is under study.

Chloroform↗
PubMed1995

The effect of environment on the stability of an integral membrane helix: molecular dynamics simulations of surfactant protein C in chloroform, methanol and water.

A series of three molecular dynamics simulations at 300 K in explicit solvent environments of chloroform, methanol and water has been performed on the pulmonary surfactant lipoprotein, SP-C, comprising several consecutive valine residues in order to investigate the stability of the alpha-helical conformation. Two additional simulations were performed on truncated SP-C with a five-residue N-terminal deletion at 300 K and 500 K in water, the high temperature run in order to increase the rate of peptide denaturation. Indications of destabilization appear in chloroform during 1 ns while the SP-C alpha-helix is remarkably stable during 1 ns in methanol and water. In particular the polyvalyl part comprising residues Val15 to Val21 remains intact even at elevated temperature, and the valines do not disrupt the alpha-helical conformation. The valyl-rotamer sampling is partly restricted. Unfolding takes place successively along the primary sequence starting from the C-terminal end. Factors affecting polypeptide stability in molecular dynamics simulations are addressed. The intrinsic helix-forming tendency of valine residues and its dependence on the sequence context, and the role of the solvent environment in stabilizing or destabilizing an alpha-helical fold, are discussed.

Amino Acid Sequence↗
PubMed2001

Inhibiting effects of chloroform on anaerobic microbial consortia as monitored by the Rantox biosensor.

The Rantox biosensor was designed for anaerobic wastewater treatment process control, and detects modifications of the feed based on the response of the acetoclastic methanogens contained in the sensor to periodic pulses of a concentrated organic substrate. The biosensor was tested under various operating conditions at the laboratory scale, in parallel with a digester under control fed on the same substrate. The aim was to evaluate the response of the biosensor in the presence of an incoming organic toxic compound (CHCl3). The experimental set-up, i.e. the biosensor and the digester, was connected to an automated control system developed under LabVIEW environment for data acquisition and operational sequence programming (the Rantox Virtual Instrument). Biomasses with different activities were used as inocula, and inhibition was induced by dosing chloroform according to two different procedures. The results showed good sensitivity and rapid response of the biosensor to feed intoxication. The presence of chloroform was detected by the Rantox with a rapid and visible response, and well in advance with respect to the digester.

Anaerobiosis↗
PubMed1993

Thermafil retreatment with and without chloroform solvent.

A previous study reported that retreatment of Thermafil-obturated canals resulted in significantly more remaining gutta-percha than retreatment of those obturated with laterally condensed gutta-percha. The purpose of this study was to evaluate two retreatment methods in Thermafil-obturated canals. Thirty canals were cleaned and shaped. They were obturated with Thermafil and sealer. One-half were retreated using chloroform to aid in gutta-percha removal (group 1). The others were retreated without chloroform (group 2). The ease or difficulty of removing the metal carrier was assessed during each retreatment. The teeth were split longitudinally; the canal area and remaining gutta-percha area were measured in the coronal, middle, and apical thirds. The results were analyzed by analysis of variance. In each group, seven Thermafil devices were easy to remove and eight were difficult. No significant differences were found in comparing the two groups. However, when the factor of ease of removal was added there were significant differences. Group 2 had significantly less gutta-percha in the apical third (5.9%) when the device was easily removed than when it was hard to remove (54.2%). Group 2 canals were significantly cleaner in the apical third than group 1 canals whether the device was difficult (38.3%) or easy to remove (42.5%). Adequacy of Thermafil retreatment may be related more to the ability to easily remove the carrier than to the technique of gutta-percha removal.

Analysis of Variance↗
PubMed1989

Endodontic retreatment: ultrasonics and chloroform as the final step in reinstrumentation.

Forty extracted teeth were instrumented using a step-back flare technique and obturated with gutta-percha and either AH26 or Roth's 801 sealer. After 3 months the canals were retreated by removing gutta-percha and sealer with hot instruments followed by chloroform and files. As a final step, the teeth were instrumented using ultrasonics with either chloroform or with NaOCl. Most teeth were well cleaned. No significant differences were found between sealer groups or between the two irrigants as to the ability to remove gutta-percha/sealer.

Chloroform↗
PubMed2003

Late administration of COX-2 inhibitors minimize hepatic necrosis in chloroform induced liver injury.

Our previous studies have described the protective effects of hepatoprotective agents against liver injury elicited by chloroform even when given 24 h after the toxicant, at a time when the liver injury is taking place and rapidly developing. However, the mechanisms involved in this protection remain unknown. The cytoprotective mechanism of these hepatoprotectants such as DMSO, may be due to a dramatic shift in the production of prostaglandins that are responsible for controlling the degree of inflammatory response that can affect blood flow in the liver. In this study, NS-398, a specific COX-2 inhibitor, and indomethacin, a COX-1 and COX-2 inhibitor, were administered 24 h after chloroform dosing to determine their effect on liver injury in Sprague-Dawley rats. The extent of necrosis was evaluated by H&E staining, while injury to hepatocytes was evaluated by measuring plasma levels of alanine transaminase (ALT). Both COX inhibitors, indomethacin and NS-398, prevented an increase in (ALT) at 48 h after initial toxicant insult and attenuated further liver necrosis. No changes in cellular proliferative activity occurred in all the treatment groups, which indicates that protection from the Cyclooxygenase (COX) inhibitors did not have an effect on regeneration of cells at 32 and 48 h. These results indicate COX inhibitors provide a significant protective effect on liver cells against CHCl(3) injury and may provide further insight into therapeutic interventions against hepatotoxicants.

Alanine Transaminase↗