Question
Asked 7th Jul, 2012

What is the source of methanol in human blood?

During a 1H NMR metabonomic analysis, we found methanol (but not ethanol) in the serum of healthy athletes. What is more, methanol decreased after acute exercise but increased in the long run (with exercise training). How can one explain these findings?

Most recent answer

21st Jul, 2012
Carlos Viana
Viana Healing Center N.V.
bacterial dysfunction or overgrowth in the mid- or transitional gut is where aromatics come from that appear in breath and urine. It would be interesting to co-relate methanol amount per blood type [including secretor status] I hypothesize Type A non- secretors would present with the largest amount of methanol and O secretors with the least amount
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Popular Answers (1)

9th Jul, 2012
Maroof Ahmed
University of Jammu
Methanol occurs naturally in humans, animals and plants. It is a natural constituent in blood, urine, saliva and expired air. ... The two most important sources of background body burdens for methanol and formate are diet and metabolic processes. Methanol is available in the diet principally from fresh fruits and vegetables, fruit juices ... fermented beverages ... and diet foods (principally soft drinks). The artificial sweetner aspartame is widely used and, on hydrolysis, 10% (by weight) of the molecule is converted to free methanol, which is available for absorption. ... Exposures to methanol can occur in occupational settings through inhalation or dermal contact. ... Methanol is readily absorbed by inhalation, ingestion and dermal exposure, and it is rapidly distributed to tissues according to the distribution of body water. A small amount of methanol is excreted unchanged by the lungs and kidneys. ... Methanol is metabolized primarily in the liver by sequential oxidative steps to formaldehyde, formic acid and carbon dioxide. The initial step involves oxidation to formaldehyde by hepatic alcohol dehydrogenase ... In step 2, formaldehyde is oxidized by formaldehyde dehydrogenase to formic acid/or formate depending on the pH. In step 3, formic acid is detoxified to carbon dioxide by folate-dependent reactions. Elimination of methanol from the blood via the urine and exhaled air and by metabolism appears to be slow in all species, especially when compared to ethanol. ... It is the rate of metabolic detoxification, or removal of formate that is vastly different between rodents and primates and is the basis for the dramatic differences in methanol toxicity observed between rodents and primates. The acute and short term toxicity of methanol varies greatly between different species, toxicity being highest in species with a relatively poor ability to metabolize formate. In such cases of poor metabolism of formate, fatal methanol poisoning occurs as a result of metabolic acidosis and neuronal toxicity, whereas, in animals that readily metabolize formate, consequences of CNS depression (coma, respiratory failure, etc.) are usually the cause of death. Sensitive primate species (humans and monkeys) develop increased blood formate concentrations following methanol exposure, while resistant rodents, rabbits and dogs do not. Humans and non-human primates are uniquely sensitive to the toxic effects of methanol. Overall methanol has a low acute toxicity to non-primate animals. ... In the rabbit, methanol is a moderate irritant to the eye. It was not skin sensitizing ... There is no evidence from animal studies to suggest that methanol is a carcinogen ... The inhalation of methanol by pregnant rodents throughout the period of embryogenesis induces a wide range of concentration-dependent teratogenic and embryolethal effects. Treatment-related malformations, primarily extra or rudimentary cervical ribs and urinary or cardiovascular defects, were found in fetuses of rats ... Increased incidences of exencephaly and cleft palate were found in the offspring of ... mice ... There was increased embryo/fetal death ... and an increasing incidence of full litter resorptions. Reduced fetal weight was observed ... Fetal malformations ... included neural and ocular defects, cleft palate, hydronephrosis and limb anomalies. Humans (and non-human primates) are uniquely sensitive to methanol poisoning and the toxic effects in these species are characterized by formic acidemia, metabolic acidosis, ocular toxicity, nervous system depression, blindness, coma and death. Nearly all of the available information on methanol toxicity in humans relates to the consequences of acute rather than chronic exposures. A vast majority of poisonings involving methanol have occurred from drinking adulterated beverages and from methanol-containing products. Although ingestion dominates as the most frequent route of poisoning, inhalation of high concentrations of methanol vapor and percutaneous absorption of methanolic liquids are as effective as the oral route in producing acute toxic effects. The most noted health consequences of longer term exposure to lower levels of methanol is a broad range of ocular effects. ... The toxicity is manifest if formate generation continues at a rate that exceeds its rate of metabolism. ... The minimum lethal dose of methanol in the absence of medical treatment is between 0.3 and 1 g/kg. The minimum dose causing permanent visual defects is unknown. ... Wide interindividual variability of the toxic dose is a prominent feature in acute methanol poisoning. Two important determinants of human susceptibility to methanol toxicity appear to be (1) concurrent ingestion of ethanol, which slows the entrance of methanol into the metabolic pathway, and (2) hepatic folate status, which governs the rate of formate detoxification. The symptoms and signs of methanol poisoning, which may not appear until after an asymptomatic period ... include visual disturbances, nausea, abdominal and muscle pain, dizziness, weakness and disturbances of consciousness ranging from coma to clonic seizures. Visual disturbances ... range from mild photophobia and misty or blurred vision to markedly reduced visual acuity and complete blindness. In extreme cases death results. The principal clinical feature is severe metabolic acidosis of the anion-gap type. The acidosis is largely attributed to the formic acid produced when methanol is metabolized. ... Visual disturbances of several types (blurring, constriction of the visible field, changes in color perception, and temporary or permanent blindness) have been reported in workers ... No other adverse effects of methanol have been reported in humans except minor skin and eye irritation. ... Methanol is of low toxicity to aquatic organisms, and effects due to environmental exposure to methanol are unlikely to be observed, except in the case of a spill.
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All Answers (15)

9th Jul, 2012
Fan Wu
Celgene
This is a very interesting finding. As I knew, methanol in the blood may be absorbed from natural food (fruits, vegetables, fermented food or drinks) or from diet drinks containing aspartame, be associated with alcohol usage, or be related to air contamination. In terms of body synthesis, it may be produced by gut microflora.
Here is a paragraph from a useful website (http://www.inchem.org/documents/ehc/ehc/ehc196.htm#SectionNumber:3).
"It is believed that dietary sources are only partial contributors to the total body pool of methanol (Stegink et al., 1981). It has been suggested that methanol is formed by the activities of the intestinal microflora or by other enzymatic processes (Axelrod & Daly, 1965). The methanol-forming enzyme was shown to be protein carboxylmethylase, an enzyme that methylates the carboxyl groups of proteins (Kim, 1973; Morin & Liss, 1973)."
Following this microflora hypothesis, I guess the observed varying levels of blood methanol in exercising people may be associated with the adjustment of microenvironment in the intestine in response to exercise intensity and duration.
The same website also provides a good summary of other analytic methods, toxicity, and other useful information for methanol along with references. Hope it helps.
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9th Jul, 2012
Julio Francisco Turrens
University of South Alabama
I agree. The likely sources are: the intestinal flora, food and air pollution. Methanol is a pretty powerful poison and causes blindness at low concentrations and death at higher concentrations (about 100 ml). Still, trace amounts are non toxic
2 Recommendations
9th Jul, 2012
Santhosh Satapati
MERCK, kenilworth, USA
I agree. Methanol occurs naturally in blood with mean concentration of 0.73mg/l. As the other replies mentioned fresh citrus fruits, vegetables and beverages contain methanol. And in artificially sweetened beverages such as soft drinks also contain methanol.
1 Recommendation
9th Jul, 2012
Sami Saadi
Universiti Putra Malaysia
Dorokhov et al. (2012) stated that methanol may function as a cross-kingdom signal. They verified whether animal methanol is a metabolic waste product or whether methanol has specific function similar to the signaling function of methanol in plant life, they studied animal responses to digested and inhaled methanol. They showed that plant leaf wounding resulted in the emission of gaseous methanol, which increased methanol content in plasma of mice. Moreover, they identified methanol-responsive genes (MRGs) as methanol gene targets and detected the up- or downregulation of MRGs in the brains of mice after breathing methanol and leaf vapors. They revealed a preference of the mice for the odor of methanol over other plant volatiles in a Y-maze setup and suggested that methanol may function as a cross-kingdom signal.
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9th Jul, 2012
Hannelore Daniel
Technische Universität München
We also found methanol in human breath when analysing volatiles by PPTR-MS. As we can be sure that our volunteers did not consume any fruits, alcoholic drinks etc (kept in our study unit for 2 days with an absolutely defined liquid diet) I favor production of methanol by gut microbiota. Acute intensive exercise may just lower blood levels via breath.
5 Recommendations
9th Jul, 2012
Maroof Ahmed
University of Jammu
Methanol occurs naturally in humans, animals and plants. It is a natural constituent in blood, urine, saliva and expired air. ... The two most important sources of background body burdens for methanol and formate are diet and metabolic processes. Methanol is available in the diet principally from fresh fruits and vegetables, fruit juices ... fermented beverages ... and diet foods (principally soft drinks). The artificial sweetner aspartame is widely used and, on hydrolysis, 10% (by weight) of the molecule is converted to free methanol, which is available for absorption. ... Exposures to methanol can occur in occupational settings through inhalation or dermal contact. ... Methanol is readily absorbed by inhalation, ingestion and dermal exposure, and it is rapidly distributed to tissues according to the distribution of body water. A small amount of methanol is excreted unchanged by the lungs and kidneys. ... Methanol is metabolized primarily in the liver by sequential oxidative steps to formaldehyde, formic acid and carbon dioxide. The initial step involves oxidation to formaldehyde by hepatic alcohol dehydrogenase ... In step 2, formaldehyde is oxidized by formaldehyde dehydrogenase to formic acid/or formate depending on the pH. In step 3, formic acid is detoxified to carbon dioxide by folate-dependent reactions. Elimination of methanol from the blood via the urine and exhaled air and by metabolism appears to be slow in all species, especially when compared to ethanol. ... It is the rate of metabolic detoxification, or removal of formate that is vastly different between rodents and primates and is the basis for the dramatic differences in methanol toxicity observed between rodents and primates. The acute and short term toxicity of methanol varies greatly between different species, toxicity being highest in species with a relatively poor ability to metabolize formate. In such cases of poor metabolism of formate, fatal methanol poisoning occurs as a result of metabolic acidosis and neuronal toxicity, whereas, in animals that readily metabolize formate, consequences of CNS depression (coma, respiratory failure, etc.) are usually the cause of death. Sensitive primate species (humans and monkeys) develop increased blood formate concentrations following methanol exposure, while resistant rodents, rabbits and dogs do not. Humans and non-human primates are uniquely sensitive to the toxic effects of methanol. Overall methanol has a low acute toxicity to non-primate animals. ... In the rabbit, methanol is a moderate irritant to the eye. It was not skin sensitizing ... There is no evidence from animal studies to suggest that methanol is a carcinogen ... The inhalation of methanol by pregnant rodents throughout the period of embryogenesis induces a wide range of concentration-dependent teratogenic and embryolethal effects. Treatment-related malformations, primarily extra or rudimentary cervical ribs and urinary or cardiovascular defects, were found in fetuses of rats ... Increased incidences of exencephaly and cleft palate were found in the offspring of ... mice ... There was increased embryo/fetal death ... and an increasing incidence of full litter resorptions. Reduced fetal weight was observed ... Fetal malformations ... included neural and ocular defects, cleft palate, hydronephrosis and limb anomalies. Humans (and non-human primates) are uniquely sensitive to methanol poisoning and the toxic effects in these species are characterized by formic acidemia, metabolic acidosis, ocular toxicity, nervous system depression, blindness, coma and death. Nearly all of the available information on methanol toxicity in humans relates to the consequences of acute rather than chronic exposures. A vast majority of poisonings involving methanol have occurred from drinking adulterated beverages and from methanol-containing products. Although ingestion dominates as the most frequent route of poisoning, inhalation of high concentrations of methanol vapor and percutaneous absorption of methanolic liquids are as effective as the oral route in producing acute toxic effects. The most noted health consequences of longer term exposure to lower levels of methanol is a broad range of ocular effects. ... The toxicity is manifest if formate generation continues at a rate that exceeds its rate of metabolism. ... The minimum lethal dose of methanol in the absence of medical treatment is between 0.3 and 1 g/kg. The minimum dose causing permanent visual defects is unknown. ... Wide interindividual variability of the toxic dose is a prominent feature in acute methanol poisoning. Two important determinants of human susceptibility to methanol toxicity appear to be (1) concurrent ingestion of ethanol, which slows the entrance of methanol into the metabolic pathway, and (2) hepatic folate status, which governs the rate of formate detoxification. The symptoms and signs of methanol poisoning, which may not appear until after an asymptomatic period ... include visual disturbances, nausea, abdominal and muscle pain, dizziness, weakness and disturbances of consciousness ranging from coma to clonic seizures. Visual disturbances ... range from mild photophobia and misty or blurred vision to markedly reduced visual acuity and complete blindness. In extreme cases death results. The principal clinical feature is severe metabolic acidosis of the anion-gap type. The acidosis is largely attributed to the formic acid produced when methanol is metabolized. ... Visual disturbances of several types (blurring, constriction of the visible field, changes in color perception, and temporary or permanent blindness) have been reported in workers ... No other adverse effects of methanol have been reported in humans except minor skin and eye irritation. ... Methanol is of low toxicity to aquatic organisms, and effects due to environmental exposure to methanol are unlikely to be observed, except in the case of a spill.
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10th Jul, 2012
Abdul Razak Mohamed Sikkander
Velammal Engineering College
DEAR VASSILIS MOUGIOUS,
Greetings! you may refer the following paper.
Experiences with Volatile Alcoholism Indicators (Methanol, Acetone, Isopropanol) in DWI Car Drivers
R. Iffland, G. Berghaus
Institute of Forensic Medicine, University of Cologne, Melatengürtel 60-62, 50823 Cologne, Germany
ABSTRACT
State markers of alcoholism can be divided into (1) the indicators connected directly to ethanol metabolism and the substances involved in or by ethanol metabolism, and (2) the indicators that are not associated with actual blood alcohol concentrations, such as GGT, CDT, or MCV. Methanol, acetone, and isopropanol belong to the first group. These substances were detected and proposed as alcoholism indicators in connection with congener alcohol analyses of blood samples from DWIs. Methanol, in particular, has been adopted as a powerful indicator of alcohol misuse. Levels greater than 10.0 mg/kg blood indicate, in most cases, addictive drinking of long duration.
Acetone and isopropanol are bound by a redox-reaction. During the storage of blood samples, acetone can be altered to isopropanol. Therefore, it is reasonable to adopt the combination of acetone + isopropanol as a new alcoholism indicator, with 9.0 mg/kg as the cut-off. Experiences with these volatile alcoholism indicators are reported in re-analysis of blood samples obtained from intoxicated drivers.
INTRODUCTION
Blood samples are obligatory in Germany at drunken driving to estimate blood alcohol concentrations (BAC). Jurisdiction affords high accuracy in determination to prevent misjudgment. Congener analyses of blood samples are carried out in cases of claiming after drinks to prove these answers. The concentrations of these alcohols like methanol, n-propanol or isobutanol in blood compared with ethanol are very low. They don't exceed hardly 1 mg/kg except of methanol, which may reach levels of 20 mg/kg. Acetone and isopropanol are physiological substances with similar blood levels. They are measured by the same gaschromatographic method like the congener alcohols. These analyses are usual since the beginning of the eighties in many German institutes of forensic medicine but not in other parts of the world. Most of the papers about this new field of research are written in German. This and different systems in justice are the main reasons of the poor knowledge in English spoken countries about German alcohol investigations.
METHANOL
Nearly all alcoholic beverages contain methanol (Table 1). In contrast to n-propanol or isobutanol methanol of these beverages is completely resorbed on account of the total inhibition of methanol metabolism by ethanol. Methanol blood levels exceed however the expected concentrations. Also if dinking is stopped and no more ethanol resorbed, the blood levels of methanol increase until ethanol concentrations are fallen down to nearly 0.2 g/kg (Iffland et al. 1994). This is only to explain by endogenous sources of methanol. Majchrowicz and Mendelson (1971) were the first, who described this phenomenon.
Table 1
Methanol and Ethanol Contents of Alcoholic Beverages
Beverage Methanol (mg/l) Ethanol (g/l)
Beer 1 - 10 30 - 50
White Wine 20 - 40 60 - 100
Red Wine 60 - 100 70 - 110
Brandy 200 - 300 300
Vodka 1 - 100 300 - 400
Whisky 80 - 200 300 - 320
Fruiterer 1000 - 4000 300 - 350
Methanol levels of 0.5 - 1.0 mg/kg exist in humans already in sober condition. During drinking most methanol is formed endogenous. Levels of 0.2 - 0.3 mg/kg are formed hourly as long as blood ethanol concentrations exceed 0.2 g/kg. The source of this methanol is not found till now. There exist some hypotheses like reduction of formic aldehyde built by methyl donators, bacterial formation of methanol in intestine or splitting of methyl esters like pectines in food. But these are no explanations for a constant endogenous formation of methanol. Tiess and Stöhlmacher (1990) assume a minor metabolic way of ethanol forming small amounts of methanol. This hypothesis is supported by drinking trials with isopropanol which also inhibits methanol metabolism at the ADH. But no increasing methanol levels like at ethanol were observed in these attempts (Iffland et al. 1989).
First hints to methanol as an indicator of alcohol abuse were given by Iffland et al. (1984). They found more frequent methanol levels higher than 10 mg/kg in the blood of alcoholics, who were hospitalized drunken, or people known as alcoholics, who died alcoholized. The main source of blood methanol was in these cases endogenous methanol for it is impossible to reach such high methanol levels by the most alcoholic beverages except by fruiterers. High methanol levels require a permanent alcoholization of more than one day and continuing drinking on the next day not interrupted by sobriety. This behaviour characterizes an addicted drinking and makes methanol to a potent indicator of alcohol misuse.
ACETONE
Crato et al. (1978) described first enlarged acetone blood levels > 7.0 mg/kg in cases of blood ethanol concentrations higher than 2.0 g/kg. Acetone is formed by decarboxylation of aceto-acetic-acid which has acetyl-coenzyme A as precursor. Increased formation of NADH - directly connected to ethanol metabolism - delays degradation of acetyl coenzyme A and enlarges on this way acetone blood levels. Condensation of pyruvate and acetaldehyde is seen as an explanation of acetone formation too. Metabolism of ethanol is increased at blood levels > 2.0 g/kg and connected thereby with higher amounts of NADH and acetaldehyde the reasons to form higher amounts of acetone. Acetone blood levels > 7.0 mg/l are seen as indicators for alcohol misuse (Iffland et al. 1994). Alcoholic ketoacidosis is the final form of ethanol induced enlarged endogenous formation of ketones in humans (Caspar et al. 1993).
ISOPROPANOL
Isopropanol is metabolized by hepatic ADH to acetone like ethanol to acetaldehyde. The balance of these reactions is shifted in the liver on the side of the alcohols. In contrast to acetaldehyde there exists no further metabolism of acetone. This explains the observations of Tiess (1985) that in liver slices isopropanol was formed from acetone. Decarboxylation of b-hydroxybutyracid is supposed as another way similar to acetone forming isopropanol. This narrow connection to ketones makes also isopropanol to an important indicator of alcohol abuse. Normal physiological blood levels of isopropanol don't exceed 0.1 - 0.2 mg/kg. Isopropanol was proposed as an indicator of alcohol misuse first by Iffland et al. (1989, 1994). The cut-off was set to 2.0 mg/kg.
The narrow connection of acetone and isopropanol suggests to summarize both indicators and to define it as a new marker, AcIp = acetone+isopropanol. During storage of blood samples parts of acetone undergo a reduction to isopropanol. The new marker AcIp is for reanalyses of blood samples appropriate. The cut-off was set to 9.0 mg/kg (Krambrich 1993, Iffland et al. 1994).
METHANOL AND AcIp IN AN EPIDEMIOLOGICAL STUDY OF ALCOHOLIZED CAR DRIVERS
Four different indicators of alcohol abuse - GGT, CDT, methanol and acetone+isopropanol - were determined in blood samples of 534 male alcoholized car drivers representative for German conditions (Iffland and Grassnack, 1995). The men were at least 18 years old and had minimum blood ethanol levels of 0.80 g/kg. Included blood alcohol concentration five indicators were measured in every case characteristic for different drinking behaviour (Table 2)(Iffland et al. 1994).
Table 2
Discrimination of Drinking Behaviour by High Levels of Indicators of Alcohol Abuse
BAC Acute drinking of large amounts of alcohol
Methanol Consuming alcohol without time of sobriety
AcIp Alcohol induced disturbances of metabolism
CDT Drinking alcohol (> 100 g/d) for some weeks
GGT Drinking large amounts of alcohol for years
The distributions of methanol and AcIp are similar in this study and don't exceed most of all 5.00 mg/kg. Cases with higher levels were found at methanol 121 (22.7 percent) and at AcIp 64 (12.0 percent). Blood concentrations of methanol are normal up to 5.00 mg/kg and may be reached after consuming 60 - 100 g ethanol with alcoholic beverages in some hours for example during an evening with good friends. Levels between 7.00 and 9.99 mg/kg are suspicious for alcohol abuse. They were found in 37 (6.9 percent) car drivers and in 30 (5.6 percent) alcohol abuse is sure. AcIp exceeded in 17 cases (3.2 percent) the level of 9.00 mg/kg and laid at 27 (5.1 percent) between 6.00 and 8.99 mg/kg comparable with the group of suspicious alcohol abuse.
There exist no functional but sometimes high stochastic correlations between methanol (MeOH), AcIp and other parameters in this study. Ranking correlations were calculated for two groups. Group A contains all cases (534) and group B car drivers (104) with BAC from 2.00 g/kg (Table 3). The highest correlations are between MeOH and AcIp. The coefficients of methanol to GGT and BAC are remarkably high in group B. Poor correlation exists to CDT. This indicator seems to be most independent from other indicators.
Table 3
Ranking Correlation Coefficients of the Indicators
Group BAC GGT CDT AcIp MeOH
Methanol A 0.1308 0.1706 0.1568 0.5119 1.0000
B 0.4018 0.4143 0.1646 0.6394 1.0000
AcIp A 0.1998 0.3945 0.2365 1.0000 0.5119
B 0.2925 0.4900 0.2774 1.0000 0.6394
It is important to know, who of the drivers has heavy problems with alcohol. Important hints give the levels of these indicators. It was differed between three stages (Table 4). The cut-offs of heavy alcohol misuse were set for GGT at 70 U/1 (25°C) and for CDT at 60.0 U/1 (RIA-method, Kabi Pharmacia Diagnostics).
Table 4
Levels of the Indicators as Criteria of the Extent of Alcohol Abuse
Alcohol abuse BAC
g/kg Methanol
mg/kg AcIp
mg/kg CDT
U/l GGT
U/l
No proof < 1.60 < 7.00 < 6.00 < 30.0 < 40
Possible 1.60 - 2.49 7.00 - 9.99 6.00 - 8.99 30.0 - 59.9 40 - 69
Heavy > 2.49 > 9.99 > 8.99 > 60.0 > 70
The cut-offs marking heavy problems were exceeded by at least one of the five parameters in 116 cases (21,7 percent). Two or more parameters exceeded these limits in 37 cases. But the criterion for alcohol abuse is satisfied, if only one of the five parameters is higher than the cut-off. 8.1 percent of the car drivers aged 18 - 30 years belong to this group but one third of the older ones. The highest part with heavy alcoholic problems is to find in the group of 41 - 50 years with 38,6 percent. The high cut-offs were exceeded at GGT in 70 cases, methanol in 30, CDT in 29, BAC in 28 and AcIp in 17. The part of car drivers with indicators proving alcohol abuse is significantly increased at blood ethanol levels higher than 2.00 g/kg. Below this concentration there are no significant differences between groups of BAC like 0.80 - 1.29 g/kg, 1.30 - 1.59 g/kg or 1.60 - 1.99 g/kg. Car drivers with indicators above these high cut-offs are to find also at low BAC's. Therefore BAC alone is no sufficient criterion to detect alcohol misuse.
REFERENCES
Caspar, C B et al.: Schweiz. Med. Wschr. 123, 1929-1934 (1993)
Crato, H et al.: Beitr. Gerichtl. Med. 36, 275-279 (1978)
Iffland, R et al.: Beitr. Gerichtl. Med. 42, 231-236 (1984)
Iffland, R et al.: Blutalkohol 26, 87-97 (1989)
Iffland, R et al.: Blutalkohol 31, 273-314 (1994)
Iffland, R, Grassnack, F: Blutalkohol 32, 26-41 (1995)
Krambrich, T: Dissertation Köln (1993)
Majchrowicz, E, Mendelson, J H: J. Pharm. Exp. Therap. 179, 293-300 (1971)
Tiess, D: Z. ges. Hygiene 31, 530-531 (1985)
Tiess, D, Stöhlmacher, P: priv. communic. (1990)
1 Recommendation
10th Jul, 2012
Peter Jansen
Academisch Medisch Centrum Universiteit van Amsterdam
Very interesting discussion. I learned a lot!
Peter Jansen
3 Recommendations
10th Jul, 2012
Lakshmi Narasimha
Narayana Hrudayalaya Hospitals
its really worthy:) Thank you guys
2 Recommendations
10th Jul, 2012
Richard D Feinman
State University of New York Downstate Medical Center
Second others appreciation for this discussion. I wonder if there is a List of the amount of methanol in different foods. it is usually said that there is more methanol in a tomato than in the amount from aspartame in diet soda but I wonder if this is reliable.
11th Jul, 2012
Vijay Baladhye
Savirtibai Phule Pune University (Formerly University of Pune), Pune, India.
It may be because of intestinal flora. It is very interesting. Which type of microorganism is this and what type of metabolic is responsible for it? What are its advantages and disadvantages in humen body?
12th Jul, 2012
Bela Buslig
Florida Dept. of Citrus
Any food items containing pectic substances will contribute to the amounts of methanol formed in the human body. Similarly, hundreds of methoxylated compounds also can yield methanol.
16th Jul, 2012
Justin J. J. van der Hooft
Wageningen University & Research
Indeed, interesting discussion. One more thing we should keep in mind is the sample preparation. How were the NMR samples prepared for this human serum study?
17th Jul, 2012
Vassilis Mougios
Aristotle University of Thessaloniki
Sample pre-treatment was kept as simple as possible. The samples were thawed just before analysis and were centrifuged at 1500 g for 5 min. An amount of 300 μL of the supernatant was diluted with 150 μL of saline and 150 μL of D2O. The mixture was mixed gently and placed in a 5-mm wide NMR tube.
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