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Detailed structural study of the major triterpenoids from chloroform extract of Agarista mexicana revealed the presence of new pentacyclic triterpene lactone 3ss-hydroxy-ursan-28ss, 19ss-olide together with four known compounds, 12-ursene, campesterol, stigmasterol, sitosterol. These compounds were isolated by chromatography and their structures confirmed by NMR experiments and by MS.
Chloroform (CHCl3) is a near-ubiquitous environmental contaminant, a by-product of the disinfection of drinking water sources and a commercially important compound. Standards for safe exposure have been established based on information defining its toxicity, which is mediated by metabolites. The metabolism of CHCl3 is via cytochrome P-450 2E1 (CYP2E1)-mediated oxidation to phosgene, which is known to obey a saturable mechanism. CYP2E1 is a highly conserved form, expressed in all mammalian systems studied, and is responsible for the metabolism of a great many low-molecular-weight (halogenated) compounds. However, the Michaelis-Menten rate constants for CHCl3 oxidation have not been derived in vitro, and the specific activity of CYP2E1 toward CHCl3 has not been reported. In this investigation with microsomal protein (MSP), apparent Vmax values of 27.6 and 28.3 nmol/h/mg MSP and apparent K(m) values of 1 and 0.15 microM in rats and human organ donors, respectively, were demonstrated. The specific activity of CYP2E1 toward CHCl3 in rats and humans was 5.29 and 5.24 pmol/min/pmol CYP2E1, respectively. Toluene metabolism to benzyl alcohol (BA), another CYP2E1-dependent reaction, was also highly dependent on CYP2E1 content in humans, and was more efficient than was CHCl3 metabolism. The specific activity of human CYP2E1 toward toluene metabolism in human MSP was 23 pmol/min/pmol CYP2E1. These results demonstrate that differences in CYP2E1 content of MSP among individuals and between species are largely responsible for observed differences in toluene and CHCl3 metabolism in vitro.
The disposition of metabolites from 14C-labeled 1,2-dibromoethane (DBE) and chloroform (CF) in juvenile rainbow trout was studied by autoradiography and quantitation of tissue radioactivity. Whole-body autoradiography of heated tissue sections showed a considerable level of nonvolatile metabolites of DBE and CF in the liver and certain areas of the body kidney. A lower level of metabolites appeared in the gills, intestinal mucosa, and olfactory rosettes in trouts exposed to DBE- or CF-containing water. Unlike previous studies in rodents, no specific uptake or binding of DBE or CF occurred in the surface epithelia of the upper alimentary tract. Microautoradiography and exhaustive tissue extraction confirmed a high irreversible binding of DBE metabolites in the liver and in a proximal tubular segment of the body kidney in fish exposed to DBE-containing water. A high level of radioactivity in the bile indicated fecal excretion of metabolites from both compounds. The results suggest that there is marked metabolism of DBE and CF in the liver and kidney, whereas the metabolism in the surface epithelia is low. The liver and kidney are proposed to be target organs of toxicity in fish.
Dichloro- and trichloroacetic acids (DCA and TCA) and chloroform are formed during chlorination disinfection of drinking water. The effects of DCA and TCA treatment on CHCl3 toxicity were assessed in these studies. Male and female rats were gavaged with DCA or TCA (0.92 and 2.45 mmol/kg administered 3 times over 24 h). Three hours after the last dose CHCl3 was injected ip (0.75 mg/kg). Male rats experienced some weight loss (15%) and slight increases of ALT and BUN, but there were no effects of either DCA or TCA on any of these responses. In females, CHCl3 increased plasma ALT and this response was greater (up to threefold) in the DCA group, compared to saline controls. Similarly, BUN was increased by CHCl3 and this was more severe (up to threefold) in both the DCA and TCA pretreated groups. These results show that CHCl3 toxicity is increased by DCA and TCA, and this effect is gender-specific, occurring only in females. DCA increases both liver and kidney toxicity, whereas TCA affects only kidney toxicity.
Halothane with and without nitrous oxide and chloroform alone were tested for mutagenic effects at the 8-azaguanine locus on the chromosomes of Chinese hamster lung fibroblast cells in culture. No significant numbers of mutations were found after 24 h exposures to 1-3% of these anaesthetics, or to 75% nitrous oxide.
Factors enhancing renal carcinogenesis induced by formic acid 2-[4-(5-nitro-2-furyl)-2-thiazolyl] hydrazide (FNT) were studied. Five groups of rats were used. Groups 1 and 2 were subjected to right nephrectomy and 2 days late they were injected with 20 mg/kg body weight of dimethylnitrosamine (DMN). From one week after nephrectomy, group 1 was fed on 0.2% FNT diet continuously to the end of the experiment, and group 2 was given normal diet. In week 2, they were given 400 mg/kg body weight of chloroform (CHCl3) orally. Groups 3 and 4 were given ChCl3 first and 2 days later injected with DMN. Group 3 was then fed FNT diet and group 4 was fed basal diet continuously. In week 2, groups 3 and 4 were subjected to unilateral nephrectomy. Group 5 was given FNT diet without other treatment. The incidences of tubular hyperplasia in groups 1, 3 and 5 were 53.3%, 52.9%, and 0%, respectively, at week 16 and 100%, 94.9% and 94.1%, respectively, at week 32. Moreover, the incidences of renal cell tumors in these groups were 85.0%, 88.9% and 17.6%, respectively, at week 32. Thus, the inductions of tubular hyperplasia and renal cell tumor were markedly enhanced by combined treatment with CHCl3, DMN, unilateral nephrectomy and FNT in the initiating and promoting stages.
A case of suicide is described that combined elements of psychotic self-mutilation, both chronic and terminal, and poisoning with ingested chloroform. This illustrates the need to consider unusual methods when investigating the deaths of people with patterns of bizarre behavior and access to unusual, fatal materials.
The effect of proteins soluble in acidic chloroform-methanol (ACMS proteins) on the transcriptase activity of virus ribonucleoproteins (RNPs) in vitro has been studied. Experiments with ACMS membrane (M) proteins from type A and B orthomyxoviruses, as well as from vesicular stomatitis virus, showed that inhibition of the viral RNP transcriptase activity occurred when they interacted with M proteins isolated from viruses of a different serotype, or even of a different family. The presence of ACMS proteins capable of inhibiting the transcriptase activity of orthomyxovirus RNP in vitro was also detected in human blood plasma and among proteins produced by human leukocytes. Determination of the minimum concentration of M protein inhibiting the RNP transcriptase activity, and analysis of the fowl plague virus M protein-RNP complex formed in the in vitro system, showed that the M protein was capable of inhibiting RNP transcriptase activity at a M:RNP ratio of 0.1 to 0.2:1.
The title compound, N,N'-difluoro-N,N'-ethylenedi-p-toluenesulfonamide, C(16)H(18)F(2)N(2)O(4)S(2).CHCl(3), is a novel stable compound of the N-F class of reagents containing two R(2)N-F functionalities. The compound, as the chloroform solvate, is the first such bis(N-F) compound to be structurally characterized. It adopts a solid-state structure in which the two aromatic rings are antiperiplanar and a combination of weak C-H...F and C-H...O hydrogen bonds [distances and angles range from 3.265 (4) to 3.439 (4) A and 150 to 170 degrees, respectively] and pi-stacking between the rings of different molecules (separations of 3.717 and 3.926 A) results in a solid-state structure containing well defined channels in which CHCl(3) solvent molecules are located. The N-F distances are 1.428 (3) and 1.433 (3) A.
The X-ray crystallographic analysis of the title complex, chloro[3,10,13,20-tetraethyl-4,9,14,19-tetramethylpentacyclo[16.2.1.1(2,5).1(8,11).1(12,15)]tetracosa-2,4,6,8(23),9,12,14,16,18(21),19-decaene]iron(III) chloroform solvate, [Fe(C(33)H(37)N(4))Cl].CHCl(3), reveals a twisted macrocyclic framework with a slightly distorted rectangular pyramidal core, where the deviation of the central Fe(III) atom from the least-squares plane of the C(20)N(4) core is 0.594 (1) A. Some important bond distances are as follows: Fe-N 2.019 (3), 2.026 (3), 2.028 (3) and 2.034 (3) A; Fe-Cl 2.232 (1) A.
Isolates of Mycoplasma pneumoniae and M. salivarium could be subclassified at the strain level by inhibitors (ch-Mcin) derived from mycoplasmal cells treated with chloroform. Sixty-one isolates of M. pneumoniae obtained from oral cavities of patients were divided into three types by their ch-Mcin: a definite type which completely inhibits the growth of M. fermentans PG18, an indefinite type and a noinhibition type. Sixty-seven isolates of M. salivarium were also divided into similar types by their ch-Mcin which does or does not inhibit the growth of M. salivarium Hup127. In the case of isolates of M. pneumoniae and M. salivarium belonging to the indefinite type which gave ambiguous patterns in the ch-Mcin typing, it was demonstrated that they could be clearly typed by further testing after repeated cloning.
Thackeray's accurate knowledge of the pharmacology of chloroform and ether is considered and his source discussed.
James Young Simpson first administered chloroform to one of his obstetric patients on 5 November 1847. The speed with which the discovery caught the popular imagination is illustrated by a comic scene in a pantomime which formed part of an entertainment in Edinburgh presented on 27 December in the same year.
The attitude of Joseph Lister (1827-1912) to chloroform is considered with particular reference to contemporary methods of administration and the effect of the agent on cardiac and respiratory function.
A long-forgotten chloroform inhaler, probably the first accurately calibrated, temperature compensatable, plenum vaporizer, is described. Its place in the dosimetric movement at the beginning of the 20th century is considered, together with a brief account of the life of its designer.
Examination of contemporaneous publications suggests that the use of chloroform by Queen Victoria in 1853 did not result in the major breakthrough in the acceptability of obstetric anaesthesia with which the event has been credited by some later writers.
The effects of the non-ionic surfactant Triton X-100 on the biphasic induced CD spectra of bilirubin complexes of human and bovine serum albumins (HSA and BSA) are divergent. While Triton X-100 inverts the induced CD spectrum of HSA.bilirubin, this surfactant enhances the ellipticity values of induced CD of BSA.bilirubin without inversion. The effect of Triton X-100 on the characteristic ultraviolet-CD spectra of the albumins are similar; both the albumins are denatured from their native globular structures. The anionic surfactant SDS, unlike non-ionic Triton X-100, dislodges the ligand from its protein complexes, indicating that both electrostatic and hydrophobic forces are involved in binding of bilirubin to the albumins. The aprotic solvent chloroform inverts the biphasic induced CD spectra of HSA.bilirubin and BSA.bilirubin, whereas CHCl3 has relatively little effect on the ultraviolet CD spectra of the albumins. The combined effect of Triton X-100 and CHCl3 shows that the effect of CHCl3 predominates over that of Triton X-100. The perturbing effects of Triton X-100 and CHCl3 on the CD or induced CD spectra of the proteins or their bilirubin complexes are reversible, and independent of the order in which components were added. The observations suggest that the denaturation of the albumins by Triton X-100 or solvation of CHCl3 within albumins markedly alter the internal topography or dynamics of the receptor sites, triggering alterations of the chirality of the bound pigment in sign and/or magnitude.
The effects of naloxone and propranolol on cardiac arrhythmias and durations from respiratory arrest to ventricular asystole and cardiac standstill were studied in unanaesthetized young rats induced to suffer respiratory arrest and exhibit ventricular fibrillation (VF) by a modified chloroform hypoxia technique. Both naloxone and propranolol reduced the incidence of VF dose dependently, indicating that they have antiarrhythmic effects. Addition of naloxone to propranolol shifted the dose-response curve of propranolol to the left significantly, indicating an additive effect of the two drugs in their antiarrhythmic activity. Both naloxone and propranolol prolonged the duration from respiratory arrest to ventricular asystole. However, joint administration of both did not further prolong this duration indicating an absence of additive effects. Naloxone prolonged the duration from respiratory arrest to cardiac standstill, indicating that naloxone prolonged the survival time. In contrast, propranolol did not produce the same effect. That naloxone both produced antiarrhythmic effect and prolonged the survival time whereas propranolol only corrected cardiac arrhythmias suggests that the antiarrhythmic effect of naloxone may not result in prolongation of survival time and that different mechanisms may be involved in the antiarrhythmic effect.