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PubMed1986

Inhibition of the acute toxicity of methyl chloride in male B6C3F1 mice by glutathione depletion.

Previous data have demonstrated that methyl chloride (MeCl) is toxic to B6C3F1 mice under both acute and chronic exposure conditions, and that conjugation of MeCl with glutathione (GSH) is a key step in the metabolism of MeCl. This study examined the role of GSH in mediating the acute toxicity of MeCl to liver, kidney, and brain of male B6C3F1 mice. The lethal effects of a single 6-hr inhalation exposure of B6C3F1 males to 2500 ppm MeCl were completely prevented by pretreatment with the GSH synthesis inhibitor, L-buthionine-S,R-sulfoximine (4 mmol L-BSO/kg, ip 1.5 hr prior to MeCl exposure). GSH levels (measured as nonprotein sulfhydryl) in liver and kidney were depleted to 19 and 25% of control values, respectively, at the start of the exposure; the ratio of dead/exposed mice during the 18-hr postexposure declined from 14/15 mice to 0/10. Also, the LC50 for MeCl increased from 2200 to 3200 ppm in male mice pretreated with BSO. The hepatic toxicity of MeCl was detected by increased alanine aminotransferase (ALT) activities in serum 18 hr after a 6-hr exposure to 1500 ppm MeCl (2147 +/- 1327 IU/liter vs 46 +/- 6 in controls). Liver toxicity was inhibited when B6C3F1 males were depleted of GSH prior to MeCl exposure by BSO pretreatment (43 +/- 2), fasting (100 +/- 47), or injection of diethyl maleate (42 +/- 16). The effects of GSH depletion on MeCl toxicity to brain and kidney were determined in B6C3F1 males exposed to 1500 ppm MeCl 6 hr/day, 5 days/week for 2 weeks, with and without daily pretreatment with 2 mmol L-BSO/kg. This dose of BSO depleted hepatic and renal GSH by 28 and 60%, respectively, at the start of MeCl exposure. BSO-pretreated mice were protected from the central nervous system toxicity of MeCl, as assessed by microscopic examination of the granule cell layer of the cerebellum. BSO pretreatment also inhibited the renal toxicity of MeCl as measured by incorporation of [3H]thymidine ([3H]TdR) into renal DNA, an indicator of cell regeneration after cortical necrosis. [3H]TdR incorporation was 105 +/- 10,337 +/- 40, and 60 +/- 15 dpm/microgram DNA in nonexposed controls, MeCl, and MeCl + BSO treatment groups, respectively. These results indicate that GSH is an important component in the toxicity of MeCl to multiple organ systems in B6C3F1 mice. Reaction of MeCl with GSH appears to constitute a mechanism of toxication, contrary to the role usually proposed for GSH in detoxifying xenobiotics.

Animals↗
PubMed1985

Reproductive effects of inhaled methyl chloride in the male Fischer 344 rat. I. Mating performance and dominant lethal assay.

Methyl chloride (MeCl) is a direct-acting mutagen in bacteria, induces renal adenocarcinomas in male mice, and is a potent reproductive toxicant in the male Fischer 344 (F-344) rat. A dominant lethal assay was performed to examine the possibility that MeCl may be a germ cell mutagen in the F-344 male rat. Groups of 40 rats each were exposed to 0, 1000, or 3000 ppm MeCl 6 hr/day for 5 consecutive days, or received a single ip injection of 0.2 mg triethylenemelamine (TEM)/kg as a positive control. Each male was bred to a single female weekly for 8 weeks, and the standard criteria of dominant lethal tests were recorded. Exposure to 1000 ppm MeCl caused no consistent change in any parameter relative to control values. TEM caused increases in pre- and postimplantation loss indices in Weeks 1 to 5 postexposure, corresponding to sperm exposed in the epididymis and as early to late stage spermatids in the testis. Exposure to 3000 ppm MeCl caused a slight increase in postimplantation loss at Week 1 postexposure only, i.e., in sperm exposed in the epididymis or vas deferens, and increases in preimplantation loss throughout the 8 weeks postexposure. Fertility of the 3000 ppm MeCl-exposed males was significantly decreased by Week 2 after exposure, and never recovered to control values during the period of observation. It is suggested that the increased preimplantation losses are due, at least in part, to cytotoxic rather than genotoxic effects. High concentrations of inhaled MeCl, however, do induce dominant lethal mutations (reflected as an increased level of postimplantation fetal deaths) in sperm located within the vas deferens and epididymis at the time of exposure.

Animals↗
PubMed2005

A method for determination of methyl chloride concentration in air trapped in ice cores.

A method for measuring the concentration of methyl chloride (CH3Cl) in air trapped in an ice core was developed. The method combines the air extraction by milling the ice core samples under vacuum and the analysis of the extracted air with a cryogenic preconcentration/gas chromatograph/mass spectrometry system. The method was applied to air from Antarctic ice core samples estimated to have been formed in the pre-industrial and/or early industrial periods. The overall precision of the method deduced from duplicate ice core analyses was estimated to be better than +/-20 pptv. The measured CH3Cl concentration of 528+/-26 pptv was similar to the present-day concentration in the remote atmosphere as well as the CH3Cl concentration over the past 300 years obtained from Antarctic firn air and ice core analyses.

Air↗
PubMed1985

Neurotoxicity of methyl chloride in continuously versus intermittently exposed female C57BL/6 mice.

This study evaluated the relationship between methyl chloride (MeCl) exposure duration and neurotoxicity. Female C57BL/6 mice were exposed to MeCl for 11 days, either continuously (22 hr/day) to 15, 50, 100, 150, or 200 ppm, or intermittently (5.5 hr/day) to 150, 400, 800, 1600, or 2400 ppm. This strain and sex of mouse was chosen because it is sensitive to MeCl neurotoxicity and was a good candidate to allow the evaluation of morphological effects and the quantitation of functional effects. A simple quantitative relationship between neurotoxicity and continuous vs intermittent exposure was not observed. Although the no-observable-effect levels for continuous and intermittent MeCl exposures were very nearly proportionate to exposure concentration multiplied by duration, the dose-response curve was much steeper for continuously exposed mice. Cerebellar granular cell layer degeneration was observed in mice exposed continuously to 100 ppm MeCl and in mice exposed intermittently to 400 ppm. This histopathologic effect was observed at lower concentrations than a decrement in rotating rod running performance. No effects were observed in mice exposed to 50 ppm continuously or to 150 ppm intermittently. Continuous exposure to MeCl produced the cerebellar lesion with less effect on other tissues than did intermittent exposure. In mice exposed to 2400 ppm intermittently, there were renal and hematopoietic effects in addition to relatively slight cerebellar granular cell layer degeneration. These 2400-ppm exposed mice developed hemoglobinuria, apparently as a result of intravascular hemolysis. Although the effect of exposure duration on MeCl toxicity was complex, this study indicated that careful judgment is necessary when extrapolating intermittent exposure data to a continuous exposure situation.

Animals↗
PubMed2005

A pilot study of methyl chloride emissions from tropical woodrot fungi.

Flux chamber measurements made in a rainforest provide evidence that methyl chloride is emitted from rotting wood. However, its net flux was found to be into the soil, probably due to competing production and consumption processes within the soil. Evidence was found for a regional source, possibly vegetation, since its concentration above the canopy was substantially greater than reported average equatorial values.

Atmosphere↗
PubMed1990

Evaluation of the GMD systems, Inc., thermally-desorbable diffusional dosimeter for monitoring methyl chloride.

The GMD Systems, Inc., thermally-desorbable diffusional dosimeter using Anasorb GM solid sorbent was evaluated for monitoring methyl chloride (CH3Cl) in the workplace. The effects of CH3Cl concentration; dosimeter exposure time; relative humidity, temperature, and face velocity during exposure; excursion exposure behavior; and storage temperature and duration after collection were investigated. Only extremely low face velocities (0.020 m/sec) and storage periods of over 8 days at room temperature or of around 30 days at reduced (refrigerator or freezer) temperatures caused sample degradation. Side-by-side measurements of CH3Cl using the diffusional monitor and a validated charcoal tube method under field conditions yielded statistically indistinguishable results. This diffusional monitor used in combination with Anasorb GM solid sorbent is a satisfactory means of determining CH3Cl exposures in the workplace.

Air Pollutants, Occupational↗
PubMed2005

Dissociative adsorption of methyl chloride on Si(001) studied by scanning tunneling microscopy.

Chemical reactions of methyl chloride (CH3Cl) on a clean Si(001) surface at approximately 300 K are studied by means of scanning tunneling microscopy (STM) under ultra-high-vacuum conditions. The features appearing in the STM images are identified with the possible products of dissociated CH3 and Cl, and their distribution is also evaluated as well as the development of their distribution with increasing CH(3)Cl doses. The amount of Cl atoms found on the surface is approximately twice as large as that of the CH3 molecules. This leads to the conclusion that dissociative adsorption of CH3Cl on Si occurs in different processes: CH3Cl(precursor) --> CH3(ad) + Cl(ad) and CH3Cl(precursor) --> CH3(gas) + Cl(ad).

Journal Article↗
PubMed1973

Cholinesterases from Plant Tissues: II. Inhibition of Bean Cholinesterase by 2-Isopropyl-4-dimethylamino-5-methylphenyl-1-piperidine Carboxylate Methyl Chloride (AMO-1618).

2-Isopropyl-4-dimethylamino-5-methylphenyl-1-piperidine carboxylate methyl chloride (AMO-1618) inhibits the activity of a cholinesterase isolated from mung bean (Phaseolus aureus) roots at concentrations comparable to those which retard growth and inhibit development of secondary roots of bean seedlings. Fifty per cent inhibition of the cholinesterase activity occurred at 0.21 mm. Inhibition of the cholinesterase is non-competitive and irreversible. The growth retardant seems to be a specific cholinesterase inhibitor since it has no effect on non-choline esterases.

Journal Article↗
PubMed1992

Anomalous binding of [3H]N-methyl-quinuclidinyl benzilate methyl chloride to human lymphocyte muscarinic receptors.

Using the muscarinic cholinergic ligand [3H]N-methyl quinuclidinyl benzilate methyl chloride ([3H]NM-QNB), we demonstrated that intact, viable human lymphocytes possess specific muscarinic binding sites. Equilibrium binding studies show that muscarinic acetylcholine receptor are divided into two subtype; high affinity (Ms) and low affinity types (Mw) for the ligand.

Adult↗
PubMed1981

Methyl chloride and diazepam effects on performance.

Human behavioral effects resulting from the ingestion of an average dose of diazepam and from 3 h of inhaling either 100 ppm or 200 ppm of methyl chloride (MeCl) were studied in the laboratory. Each of 56 volunteers was randomly assigned to one of six groups comprising the combinations of diazepam and placebo and one of the two levels of MeCl plus control. Each individual was tested in an environmental room on three tasks involving components of eye-hand coordination, mental alertness, and time discrimination. Both pretreatment and treatment data were obtained. Diazepam produced a significant 10% impairment in task performance, whereas the effect of 200 ppm of MeCl was marginally significant (average performance impairment of 4.5%). When the two agents were combined, total impairment was equal to the sum of the individually induced losses. Large interindividual differences in breath and blood levels were found for MeCl.

Adolescent↗
PubMed1984

Studies of lesions induced in the testis and epididymis of F-344 rats by inhaled methyl chloride.

Experiments were carried out in rats to characterize the development of the testicular and epididymal lesions and any associated effects on reproductive hormones. Adult F-344 rats were exposed to 3500 ppm methyl chloride (MeCl) 6 hr/day for 5 days, not exposed for 3 days, and exposed again for 4 days. The first consistent testicular lesion was a delay in spermiation which appeared on Day 9. Subsequently, germinal epithelial vacuolation and cellular exfoliation became widespread as exposure continued. All animals killed after 19 days also displayed bilateral epididymal granulomas in regions 5 or 6 of the cauda epididymis. The nature and distribution of inflammatory cells indicated that the primary neutrophilic response may be against the tubular epithelium and not extravasated sperm. After 5 days of exposure, circulating testosterone was below 6 ng/ml (control: 120 +/- 31 ng/ml). Both MeCl exposed and control animals responded similarly to challenge with hCG and LHRH ethylamide, suggesting that Leydig cell and gonadotrope function was unaffected. It is proposed that MeCl acts centrally to lower circulating testosterone. Nonprotein sulfhydryls were depleted in liver, testis, and epididymis after MeCl exposure, but not in whole blood. This finding indicates that sulfhydryl depletion is not due to direct alkylation, but is enzymatically mediated. Sulfhydryl depletion did not correlate with lesion development. It was concluded that the initial testicular effects of MeCl are directed at either the late stage spermatids or the Sertoli cells with a resultant delay in spermiation.

Animals↗
PubMed2005

Evidence for different types of water participation in the solvolysis of 1-adamantyl, tert-butyl, and methyl chlorides from density functional theory computations.

[structure: see text] The activation energy in the gas phase (deltaE(double dagger)) and the free energy of activation (deltaG(double dagger)) in water solution for the hydrolysis of the monohydrates of methyl chloride (MeCl), tert-butyl chloride (t-BuCl), and 1-adamantyl chloride (AdCl) have been computed with the B3LYP/631-G(d) method and the polarizable continuum (PCM) solvation model. There is a fair agreement between the deltaG(double dagger) values computed by us and the experimental data. The mechanistic implications of our computations are in severe contradiction with conventional representations. Thus, the computed nucleophilic solvent assistance (NSA) for the backside attack of a water molecule in the hydrolysis of MeCl is slightly lower than the corresponding NSA for t-BuCl. Hence, the hydrolysis of both MeCl and t-BuCl takes place mainly according to the classical S(N)2 mechanism. The most relevant difference is that deltaG(double dagger) for the frontside attack of water to t-BuCl is disfavored only by ca. 2 kcal/mol with regard to the backside attack but by ca. 23 kcal/mol in the case of MeCl. The higher solvolysis rate in water of t-BuCl in relation to AdCl is not due to steric factors affecting the specific solvation of the corresponding transition states, but to differential bulk solvent effects, which are accounted for by the PCM model.

Adamantane↗