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PubMed1987

Elimination half-life of methanol during hangover.

This paper reports the elimination half-life of methanol in human volunteers. Experiments were made during the morning after the subjects had consumed 1000-1500 ml red wine (9.5% w/v ethanol, 100 mg/l methanol) the previous evening. The washout of methanol from the body coincided with the onset of hangover. The concentrations of ethanol and methanol in blood were determined indirectly by analysis of end-expired alveolar air. In the morning when blood-ethanol dropped below the Km of liver alcohol dehydrogenase (ADH) of about 100 mg/l (2.2 mM), the disappearance half-life of ethanol was 21, 22, 18 and 15 min. in 4 test subjects respectively. The corresponding elimination half-lives of methanol were 213, 110, 133 and 142 min. in these same individuals. The experimental design outlined in this paper can be used to obtain useful data on elimination kinetics of methanol in human volunteers without undue ethical limitations. Circumstantial evidence is presented to link methanol or its toxic metabolic products, formaldehyde and formic acid, with the pathogenesis of hangover.

Alcoholic Intoxication↗
PubMed2004

Measurement and simulation of water and methanol transport in algal cells.

BACKGROUND: Experimental data and a complementary biophysical model are presented to describe the dynamic response of a unicellular microalga to osmotic processes encountered during cryopreservation. METHOD OF APPROACH: Chlorococcum texanum (C. texanum) were mounted on a cryoperfusion microscope stage and exposed sequentially to various solutions of sucrose and methanol. Transient volumetric excursions were determined by capturing images of cells in real time and utilizing image analysis software to calculate cell volumes. A biophysical model was applied to the data via inverse analysis in order to determine the plasma membrane permeability to water and to methanol. The data were also used to determine the elastic modulus of the cell wall and its effect on cell volume. A three-parameter (hydraulic conductivity (Lp), solute permeability; (omega), and reflection coefficient, (sigma)) membrane transport model was fit to data obtained during methanol perfusion to obtain constitutive property values. These results were compared with the property values obtained for a two coefficient (Lp and omega) model. RESULTS: The three-parameter model gave a value for sigma not consistent with practical physical interpretation. Thus, the two-coefficient model is the preferred approach for describing simultaneous water and methanol transport. The rate of both water and methanol transport were strongly dependent on temperature over the measured temperature range (25 degrees C to -5 degrees C) and cells were appreciably more permeable to methanol than to water at all measured temperatures. CONCLUSION: These results may explain in part why methanol is an effective cryoprotective agent for microalgae.

Biological Transport↗
PubMed1992

Cloning of a methanol-inducible moxF promoter and its analysis in moxB mutants of Methylobacterium extorquens AM1rif.

In Methylobacterium extorquens AM1, gene encoding methanol dehydrogenase polypeptides are transcriptionally regulated in response to C1 compounds, including methanol (M. E. Lidstrom and D. I. Stirling, Annu. Rev. Microbiol. 44:27-57, 1990). In order to study this regulation, a transcriptional fusion has been constructed between a beta-galactosidase reporter gene and a 1.55-kb XhoI-SalI fragment of M. extorquens AM1rif DNA encoding the N terminus of the methanol dehydrogenase large subunit (moxF) and 1,289 bp of upstream DNA. The fusion exhibited orientation-specific promoter activity in M. extorquens AM1rif but was expressed constitutively when the transcriptional fusion was located on the plasmid. However, correct regulation was restored when the construction was inserted in the M. extorquens AM1rif chromosome. This DNA fragment was shown to contain both the moxFJGI promoter and the sequences necessary in cis for its transcriptional regulation by methanol. Transcription from this promoter was studied in the M. extorquens AM1rif moxB mutant strains UV4rif and UV25rif, which have a pleiotropic phenotype with regard to the components of methanol oxidation. In these mutants, beta-galactosidase activity from the fusion was reduced to a level equal to that of the vector background when the fusion was present in both plasmid and chromosomal locations. Since both constitutive and methanol-inducible promoter activities were lost in the mutants, moxB appears to be required for transcription of the genes encoding the methanol dehydrogenase polypeptides.

Alcohol Oxidoreductases↗
PubMed1985

Isolation of alcohol oxidase and two other methanol regulatable genes from the yeast Pichia pastoris.

The oxidation of methanol follows a well-defined pathway and is similar for several methylotrophic yeasts. The use of methanol as the sole carbon source for the growth of Pichia pastoris stimulates the expression of a family of genes. Three methanol-responsive genes have been isolated; cDNA copies have been made from mRNAs of these genes, and the protein products from in vitro translations have been examined. The identification of alcohol oxidase as one of the cloned, methanol-regulated genes has been made by enzymatic, immunological, and sequence analyses. Methanol-regulated expression of each of these three isolated genes can be demonstrated to occur at the level of transcription. Finally, DNA subfragments of two of the methanol-responsive genomic clones from P. pastoris have been isolated and tentatively identified as containing the control regions involved in methanol regulation.

Alcohol Oxidoreductases↗
PubMed2005

Vapor-phase photo-oxidation of methanol over nano-size titanium dioxide clusters dispersed in MCM-41 host material part 2: catalytic properties and surface transient species.

We report in this paper on the ultraviolet-assisted vapor-phase oxidation of methanol at room temperature, with the help of nano-size clusters of titanium dioxide dispersed in an MCM-41 silicate matrix. The surface species formed during the adsorption/oxidation of methanol and the transformation that they undergo as a result of ultraviolet irradiation were monitored using in-situ Fourier transform infrared and thermal desorption spectroscopy techniques. Parallel experiments conducted on TiO2/MCM, bulk titania, and pristine MCM-41 samples helped in identifying the individual role of titanium dioxide and host matrix in these processes. The photo-catalytic oxidation of methanol, at concentrations of 0.1 to 1.1 mol% in air, gave rise to formation of CO2 and H2O as products, for both the TiO2/MCM and bulk TiO2 samples. No such reaction occurred on titania-free MCM. Furthermore, the rate of reaction depended upon the TiO2 content of a sample and also on the concentration of methanol in reaction mixture. Thus, the rate of conversion increased progressively with the increase in TiO2 loading from 5 to 21 wt% in TiO2/MCM samples, particularly for the experiments with high concentration of methanol. For low methanol concentration (0.1 mol%) in air, the effect of titania content in MCM was very small. The specific activity (per g of titania) of a sample, on the other hand, showed an inverse relationship with the loading of titanium dioxide in a sample. Infrared and temperature-programmed desorption results revealed that the mode of CH3OH adsorption and the reactivity of the transient species formed during the oxidation process were independent of the size of dispersed titania particles. Thus, the particles of approximately 2-6 nm size, present in TiO2/MCM, exhibited a chemisorption behavior similar to that of the bulk titania. The results of the present study provide strong evidence that the hydroxyl groups, both on the host matrix and at the titania sites, participate independently in the formation of methoxyl groups and at the same time promote the heterogeneous photo-catalytic oxidation of methanol molecules via formation of transient formate groups. Our results also show that the effect of titania crystallite size in the photo-catalytic properties relate mainly to the larger surface area and hence to the enhanced number of chemisorption sites, rather than to the changes in electronic properties.

Catalysis↗
PubMed2005

Formate kinetics in methanol poisoning.

OBJECTIVE: The objective is to describe the kinetics of formate, the main toxic metabolite of methanol, in a series of consecutive patients treated in the same intensive care unit for severe methanol poisoning. METHODS: The charts of the patients admitted between 1987 and 2001 were reviewed. Inclusion criteria were: a history of deliberate methanol ingestion, with a blood methanol concentration greater than 20 mg/dL (6.2 mmol/L) or a high anion gap metabolic acidosis. Indications for hemodialysis were: blood methanol concentration >50 mg/dL (15.8 mmol/L), metabolic acidosis (bicarbonate <15 mmol/L, arterial pH <7.30), visual toxicity. Antidotal therapy included ethanol administration in 22 cases, and fomepizole in three cases. Serial blood measurements were obtained for pH, bicarbonate, methanol and formate. Endogenous and hemodialysis elimination half-lives were calculated as t1/2 =0.693/Ke. Fick principle was applied for hemodialysis clearance calculation. RESULTS: The records of 25 methanol poisoned patients were analysed. Among them, 18 patients had sufficient data to allow accurate determinations of formate kinetics. Formate half-life elimination during hemodialysis was 1.80+/-0.78 h, which was statistically different from the values observed before or in the absence of dialysis (6.04+/-3.26 h, P =0.004). The mean hemodialysis formate clearance rate calculated in eight cases was 176+/-43 mL/min. A rebound in plasma formate concentration was observed in three patients after the discontinuation of hemodialysis. CONCLUSIONS: In accordance with previous isolated case reports and in contrast with a recent case series, our data document that hemodiaysis is effective in reducing formate elimination half-life. The impact on clinical outcome is still debatable.

Adult↗
PubMed2000

Protective effect of N-acetylcysteine on rat liver cell membrane during methanol intoxication.

Methanol is oxidized in-vivo to formaldehyde and then to formate, and these processes are accompanied by the generation of free radicals. We have studied the effect of N-acetylcysteine on liver cell membrane from rats intoxicated with methanol (3.0 g kg(-1)). Evaluation of the effect was achieved by several methods. Lipid peroxidation and surface charge density were measured. An ultrastructural study of the liver cells was undertaken. The concentration of marker enzymes of liver damage (alanine aminotransferase and aspartate aminotransferase) in blood serum was measured. Methanol administration caused an increase in lipid peroxidation products (approximately 30%) as well as in surface charge density (approximately 60%). This might have resulted in the membrane liver cell damage visible under electron microscopy and a leak of alanine aminotransferase and aspartate aminotransferase into the blood (increase of approximately 70 and 50%, respectively). Ingestion of N-acetylcysteine with methanol partially prevented these methanol-induced changes. Compared with the control group, lipid peroxidation was increased by approximately 3% and surface charge density by approximately 30%. Alanine aminotransferase and aspartate aminotransferase activity increased by 9 and 8%, respectively, compared with the control group. The results suggested that N-acetylcysteine was an effective antioxidant in methanol intoxication. It may have efficacy in protecting free radical damage to liver cells following methanol intoxication.

Acetylcysteine↗
PubMed1990

Peroxisomes induced in Candida boidinii by methanol, oleic acid and D-alanine vary in metabolic function but share common integral membrane proteins.

Peroxisomes massively proliferate in the methylotrophic yeast Candida boidinii when cultured on methanol as the only carbon and energy source. These organelles contain enzymes that catalyze the initial reactions of methanol utilization. The membranes contain abundant proteins of unknown function; their apparent molecular masses are 20, 31, 32 and 47 x 10(3) Mr and are termed PMP20, PMPs31-32 and PMP47. Recently, we reported that peroxisomes in this yeast are also induced by oleic acid and D-alanine as carbon sources, and that these peroxisomes contain increased concentrations of the enzymes of fatty acid beta-oxidation or D-amino acid oxidase, respectively. This report extends these findings and further compares the enzyme composition from peroxisomes induced by methanol, oleic acid and D-alanine. the patterns of matrix proteins represented on SDS-polyacrylamide gels from peroxisomes induced by oleic acid or D-alanine were found to be very different from those of peroxisomes induced by methanol. In order to differentiate between membrane proteins that have specific functions in pathways of substrate utilization from those with more generalized functions, peroxisomal membranes from cultures grown on methanol, oleic acid or D-alanine were purified. Analysis of these fractions demonstrated that while PMP20 is found only in peroxisomes induced by methanol, the PMPs31-32 and PMP47 were the abundant peroxisomal membrane proteins (PMP) regardless of inducing substrate. The data strongly suggest that the function of PMP20 is related to methanol metabolism. In contrast, the functions of PMPs31-32 and PMP47 are 'substrate-nonspecific'. We speculate that they may relate to the structure, assembly or general function of the organelle.

Alanine↗
PubMed1990

The toxicity of inhaled methanol vapors.

Methanol could become a major automotive fuel in the U.S., and its use may result in increased exposure of the public to methanol vapor. Nearly all of the available information on methanol toxicity in humans relates to the consequences of acute, rather than chronic, exposures. Acute methanol toxicity evolves in a well-understood pattern and consists of an uncompensated metabolic acidosis with superimposed toxicity to the visual system. The toxic properties of methanol are rooted in the factors that govern both the conversion of methanol to formic acid and the subsequent metabolism of formate to carbon dioxide in the folate pathway. In short, the toxic syndrome sets in if formate generation continues at a rate that exceeds its rate of metabolism. Current evidence indicates that formate accumulation will not challenge the metabolic capacity of the folate pathway at the anticipated levels of exposure to automotive methanol vapor.

Administration, Inhalation↗
PubMed1975

A methanol resorcin-fuchsin stain for elastic tissues and nuclei.

The staining properties of conventional ethanol resorcin-fuchsin and of methanol resorcin-fuchsin were compared. Formula; Dissolve 0.2 g of commercial resorcin-fuschin in 70 ml of methanol or ethanol, add 30 ml of water and 1 m1 of concentrated HC1; stain sections for 4 hours. Both solutions colored elastic and pseudoelastic fibers, cartilage and some mucins. Methanol resorcin-fuchsin also colored nuclei in methacarn- (methanol-chloroform-glacial acetic acid 6:3:1) and formalin-fixed tissues; this nuclear stain withstood counterstaining with picro-dye mictures. Zenker-fixed sections showed diffuse coloration with little or no contrast between nuclei and cytoplasm. Extraction with hot trichloracetic acid abolished binding of methylene blue, but binding of methanol resorcin-fuchsin by nuclei remained unaltered or was enhanced. Experiments with solvents containing various concentrations of methanol, ethanol or isopropanol indicated that the staining patterns of resorcin-fuchsin are determined by the nature and concentration of the alcohol. Methanol resorcin-fuchsin proved useful for simultaneous visualization of elastic tissues and nuclei.

Elastic Tissue↗
PubMed1999

Morphological changes in the liver of rats intoxicated with methanol.

On the basis of morphological examinations in light and electron microscope, the evaluation of methanol influence on the liver of rats was conducted. The examination was carried out in the group of 36 rats that were given a single dose of methanol (1.5 g/kg b.w.) into the stomach through a gastric tube. The liver was taken from rats under the ether anaesthesia after 6, 12, and 24 hours as well as after 2, 5, and 7 days of methanol administration. Results showed that methanol intoxication caused visible changes in the examined organ. Only 6 h after intoxication, lobular peripheral hepatocytes presented characteristic features of vacuolar degradation persisting up to 48 h. Since the second day of intoxication, many cells with double nuclei were found more frequently than in controls. Single hepatocytes or small hepatocytic clusters with the features of deliquescent necrosis could be seen after 5 and 7 days of examination. All animals intoxicated with methanol showed distinct weakness of glycogen reaction. The loss of glycogen resources was highest at 24 h after methanol administration. The results indicate, that methanol causes morphological changes in the rat liver and that intensification of these changes depends on the time after intoxication.

Animals↗
PubMed2000

Effect of methanol on the activity and conformation of acid phosphatase from the prawn Penaeus penicillatus.

Prawn (Penaeus penicillatus) acid phosphatase (EC 3.1.3.2) catalyzes the nonspecific hydrolysis of phosphate monoesters. The effects of some pollutants in sea water on the enzyme activity results in the loss of the biological function of the enzyme, which leads to disruption of phosphate metabolism in cells. This paper analyzes the effects of methanol on the activity and conformation of prawn acid phosphatase. The results show that low concentrations of methanol can lead to reversible inactivation. Inhibition of the enzyme by methanol is classified as non-competitive inhibition, and the inhibition constant (Ki) is 8.5%. Conformational changes of the enzyme molecule in methanol solutions of different concentrations were measured using fluorescence emission, differential UV-absorption, and circular dichroism spectra. Increased methanol concentrations caused the fluorescence emission intensity of the enzyme to increase. The ultraviolet difference spectra of the enzyme denatured with methanol had two negative peaks, at 222 and 270 nm, and a positive peak at 236 nm. The changes in the fluorescence and ultraviolet difference spectra reflected the changes of the microenvironments of tryptophan and tyrosine residues of the enzyme. The CD spectrum changes of the enzyme show that the secondary structure of the enzyme also changed some. These results suggest that methanol is a non-competitive inhibitor and the conformational integrity of the enzyme is essential for its activity.

Acid Phosphatase↗
PubMed2002

Modelling the competition between sulphate reducers and methanogens in a thermophilic methanol-fed bioreactor.

Sulphate can be removed from wastewater by means of biological anaerobic reduction to sulphide. The reduction requires the presence of a substrate that can serve as an electron donor. Methanol a suitable electron donor for sulphate reduction under thermophilic conditions. In an anaerobic system containing methanol and sulphate, acetogenic bacteria (AB) and methanogenic archaea (MA) compete with sulphate reducing bacteria (SRB) for methanol or its degradation intermediates. Previously obtained results indicate that at 65 degrees C SRB and MA mainly compete for the intermediate hydrogen instead of methanol. For efficient use of methanol as electron donor for sulphate reduction it is important that for the treatment of sulphate wastewater in an anaerobic reactor SRB out-compete MA. The mechanisms that determine the outcome of the competition are, however, not well understood. This paper describes a model based on growth kinetics of methanol-oxidising AB, and hydrogen-consuming SRB and MA, that can describe the competition between SRB and MA in a methanol-fed bioreactor. We present the model and its calibration using experimental data, and we discuss its shortcomings and suggest possible improvements.

Bioreactors↗
PubMed2004

[Methanol poisoning in Norway 2002].

BACKGROUND: In Norway methanol poisoning is rare. During the last four months of 2002, smuggled spirits containing about 20% methanol was distributed and ingested. MATERIAL AND METHODS: Epidemiological and clinical data concerning 33 patients admitted to hospital with methanol poisoning are presented. RESULTS: After a latency period of 12 to 72 hours, clinical features developed; visual disturbances and dyspnoea were particularly common. Diagnosis was based upon the anamnesis and clinical and laboratory findings. Calculation of anion gaps and osmolal gaps, were important diagnostic tools. Fomepizole was used as an antidote in 23 cases; 24 were dialysed. 28 patients were discharged, four of whom with permanent visual disturbances and signs of cerebral damage. Hospital mortality was 15% (five patients); eight patients died outside hospital with a post-mortem diagnosis of methanol poisoning. INTERPRETATION: Rapid diagnosis and treatment is mandatory in cases of methanol poisoning. The mixture of 20% methanol in ethanol resulted in a temporary block of methanol metabolism. The latency period therefore increased, leading to diagnostic problems.

Adult↗
PubMed2005

[Clinical cure for acute methanol poisoning].

OBJECTIVE: To analyze the treatment of 42 patients with acute methanol poisoning because of drinking alcohol containing methanol. METHODS: Clinical data of 42 cases of methanol poisoning were collected and analyzed. Methanol concentration in drinking alcohol and blood was determined by gas chromatography (GC). National standard for occupational medicine (GBZ53-2002) was used to diagnose the cases. RESULTS: The methanol concentration in the alcohol was 16% approximately 46%. 42 Patients (40 males, 2 females), at age of 46.1 (22 approximately 80), took 588.1 ml (50 approximately 2,000 ml) of the alcohol. The average methanol concentration in blood was 1.61 mmol/L (0.03 approximately 23.60 mmol/L). According to clinical diagnosis, there were 17 observed cases, 9 mild acute toxication, and 16 severe acute toxication. Among them, 35 (83.3%) patients were recovered, 2 (4.8%) blind, 4 (9.5%) with neuropsychic sequela and 1 (2.4%) dead after adopting 8 cure measures. CONCLUSION: To start using emergency plan for public health events suddenly happened, designate a special treatment hospital, clear blood methanol as soon as possible, correct acidosis, adequately administer folacin and hormone, protect optic nerve and retina, and take comprehensive symptomatic treatment as well as strict monitoring are the keys of clinical cure.

Acute Disease↗
PubMed2006

[Serious intoxication after inhaling methanol].

A 38-year-old man presented with severe methanol intoxication after inhaling methanol over a period of 36 hours in a poorly-ventilated laboratory. He complained of visual disturbances, mild photophobia, hyperventilation and nausea. Laboratory results showed severe metabolic acidosis with a toxic serum-methanol level. He was treated by acute haemodialysis and ethanol infusions. After 9 hours of haemodialysis the serum-methanol value fell below toxic levels. Therapy resulted in the complete disappearance of symptoms and he was able to leave the intensive-care unit 24 hours after presentation. Often, late presentation is a cause of serious morbidity and even mortality in severe methanol intoxication, so early recognition is essential. This is the first published case of methanol intoxication due to inhalation, which is as serious and requires the same treatment as ingestion of methanol.

Adult↗
PubMed1991

Methanol-induced visual toxicity in the rat.

Human methanol poisoning is characterized by formic acidemia, metabolic acidosis and blindness or serious visual impairment. Nonprimate species are ordinarily resistant to the accumulation of formate and the associated metabolic and visual toxicity. A nonprimate model of methanol-induced visual toxicity was developed using rats treated with subanesthetic concentrations of nitrous oxide to inhibit the oxidation of methanol's toxic metabolite, formic acid. Methanol-intoxicated rats developed formic acidemia, metabolic acidosis and visual toxicity within 36 hr of methanol administration analogous to the human methanol poisoning syndrome. Visual dysfunction was measured as reductions in the flash-evoked cortical potential and electroretinogram, which occurred coincident with blood formate accumulation. Alterations in the electroretinogram occurred at formate concentrations lower than those associated with other visual changes and provide functional evidence of direct retinal toxicity in methanol poisoning.

Acidosis↗
PubMed1983

Methanol toxicity in the monkey: effects of nitrous oxide and methionine.

Methanol poisoning in monkeys and humans is characterized by the development of formic acidemia, metabolic acidosis and ocular toxicity. Formate, the metabolite associated with the toxicity of methanol, is oxidized to carbon dioxide by a tetrahydrofolate-dependent pathway. Nitrous oxide treatment was used to inhibit the tetrahydrofolate-generating enzyme, 5-methyltetrahydrofolate homocysteine methyltransferase (methionine synthetase, E.C. 2.1.1.13.), to delineate the role of this enzyme in regulating formate oxidation in the monkey. The importance of methionine in the regulation of formate oxidation in the monkey also was evaluated. Nitrous oxide inhibited the oxidation of formate generated from the metabolism of methanol (1 g/kg i.p.) in the monkey, resulting in the development of severe metabolic acidosis and high blood formate levels in these animals compared with air-breathing monkeys administered the same dose of methanol. Treatment of nitrous oxide-exposed monkeys with repetitive doses of methionine (100 mg/kg 10, 12 and 14 hr after methanol) reversed the effects of nitrous oxide on formate oxidation, resulting in a marked decrease in blood formate levels and an increase in the rate of [14C]O2 formation from methanol. Methionine treatment also reversed the development of metabolic acidosis and bicarbonate depletion observed in nitrous oxide-exposed monkeys. These results indicate that hepatic methionine synthetase is important in the regulation of tetrahydrofolate-dependent metabolism in the monkey and that the generation of tetrahydrofolate by this enzyme is a major factor in determining the sensitivity of a species to methanol poisoning.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗