Methanol

Tephly, Thomas R.; Makar, A B; McMartin, Kenneth E.; Hayreh, S S; Martin-Amat, G.

doi:10.1007/978-1-4684-8577-6_9

Cited by 10 publications

(5 citation statements)

References 48 publications

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“…In addition, methanol is metabolized in humans by the same enzymes that metabolize ethanol: alcohol dehydrogenase and aldehyde dehydrogenase, to form formaldehyde and formic acid. (27). Oxidation of methanol, like that of ethanol, proceeds at a rate that is independent of its concentration in plasma.…”

Section: Absorption and Eliminationmentioning

confidence: 98%

Clinical and Pharmaceutical Applications of Gas Chromatography

Álvarez

2004

Modern Practice of Gas Chromatography

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Section: Absorption and Eliminationmentioning

confidence: 98%

Clinical and Pharmaceutical Applications of Gas Chromatography

Álvarez

2004

Modern Practice of Gas Chromatography

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“…It is well documented that the ingestion of methanol causes visual toxicity, metabolic acidosis, central nervous system depression and abdominal pain. The individual susceptibility for methanol damage varies widely depending on the amount ingested which causes toxic symptoms (Mc -Martin et al, 1975;Tephly et al, 1979 andSwartz et al, 1981). In regards to the changes in the liver, Upreti and Shanker (1978), Lamb et al, (1979) and Anderson et al , (1979) investigated the histological and enzymatic pattern in cases of alcoholism.…”

Section: Introductionmentioning

confidence: 99%

Histological and Histochemical Changes in the Liver of Albino Rats Due to Methyl Alcohol Administration

Aziz¹

1997

An-Najah University Journal for Research - A

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Histological and histochemical changes in the livers of 40 adult male albino rats (Rattus norvegicus) were studied at different intervals following methyl alcohol administration. The animates were divided into three groups. Methanol was administrated by oral a intubation in two doses (1m1/Kg. body weight and 2m1/Kg. body weight, respectively) for twenty consecutive days. Then the animals were killed after different periods of time (5, 10 and 20 days). The changes appeared to be time and/or dose dependent. Early signs of hepatic changes were characterized by hydropic degeneration, nuclear pyknosis, erosion of the endothelial lining of the blood vessels, vascular congestion and internal haemorrhage. Degenerative hepatic cells were seen invaded by inflammatory infiltrative cells. Maximum signs of deterioration were detected when 2m1/Kg. body weight was given. The first dose of methanol (1m1/Kg. body weight) caused depletion of liver glycogen, lipids, total proteins, proteins containing NH group, nucleic acids contents, and succinate dehydrogenase (SDH). Also, it caused a significant elevation of alkaline and acid phosphatase activities. The second dose of methanol (2m1/Kg. body weight) showed stronger effects on the 10th and 20th days of administration.

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“…A species difference exists in the susceptibility to methanol toxicity (1)(2)(3), which appears to be related to the regulation of folate-dependent one-carbon metabolism (4)(5)(6)(7). The syndrome of methanol poisoning in humans and monkeys is characterized by a mild central nervous system depression which is followed by a latent period, metabolic acidosis, ocular toxicity, and death (1)(2)(3).…”

mentioning

confidence: 99%

“…The syndrome of methanol poisoning in humans and monkeys is characterized by a mild central nervous system depression which is followed by a latent period, metabolic acidosis, ocular toxicity, and death (1)(2)(3). In contrast, rats and other rodents display only a mild central nervous system depression after methanol administration (1)(2)(3). This difference in response to methanol is related to elevated levels of formic acid in species susceptible to methanol poisoning (8)(9)(10)(11)(12)(13).…”

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Role of hepatic tetrahydrofolate in the species difference in methanol toxicity.

Black¹,

Eells²,

Noker³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

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The susceptibility of various species to methanol toxicity is inversely related to the rate of tetrahydrofolate (H4olate)-dependent formate oxidation to carbon dioxide.Thus, the levels of various folate derivatives and folatedependent enzyme activities present in the livers of monkeys, which are sensitive to methanol, and rats, which are not, were compared in order to investigate the biochemical basis of this species difference. Hepatic H4folate levels in monkeys were 60% of those in rats, and formylated-H4folate derivatives were 2-fold higher in monkeys than in rats. No significant difference between monkeys and rats in the levels of total hepatic folate or 5-methyl-H4folate was observed. The activities of formylH4folate synthetase (EC 6.3.4.3) and formyl-H4folate dehydrogenase (EC 1.5.1.6) were 4-and 2-fold higher, respectively, in monkeys than in rats. There was no significant difference between monkeys and rats in methionine synthetase activity (EC 2.1.1.13). Dihydrofolate reductase activity (EC 1.5.1.3) in monkeys was 20% of that in rats. 5,10-Methylene-H4folate reductase (NADPH) activity (EC 1.1.1.171) in monkeys was 40% and 25% of that in rats when the rates of the forward and reverse reactions, respectively, were compared. Serine hydroxymethyltransferase activity (EC 2.1.2.1) was 2-fold higher in monkeys than in rats. The differences in the activities of methylene-H4folate reductase and serine hydroxymethyltransferase between monkeys and rats may have contributed to the difference in hepatic Il4folate levels. The 40% lower level of hepatic H4folate in monkeys, as compared to rats, relates well to the 50% lower maximal rate of formate oxidation in monkeys. Thus, the species difference in susceptibility to methanol may be explained by the difference in the level of hepatic H4folate.A species difference exists in the susceptibility to methanol toxicity (1-3), which appears to be related to the regulation of folate-dependent one-carbon metabolism (4-7). The syndrome of methanol poisoning in humans and monkeys is characterized by a mild central nervous system depression which is followed by a latent period, metabolic acidosis, ocular toxicity, and death (1-3). In contrast, rats and other rodents display only a mild central nervous system depression after methanol administration (1-3). This difference in response to methanol is related to elevated levels of formic acid in species susceptible to methanol poisoning (8-13). Thus, marked elevations of formate in body fluids and tissues occur in humans and monkeys receiving toxic doses of methanol (8, 9, 11-13); but in rats, no significant accumulation of formate is observed (8, 9). The species variation in formate accumulation is explained by the observation that, over a range of formate dose levels, the rate of formate oxidation to carbon dioxide in vivo in rats is at least twice that observed in monkeys (4). In both rats and monkeys, the major route of formate oxidation in vivo is through a folatedependent pathway (4, 5) (Fig. 1) (Fig. 1, reaction 1) (1...

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Methanol

Cited by 10 publications

References 48 publications

Clinical and Pharmaceutical Applications of Gas Chromatography

Clinical and Pharmaceutical Applications of Gas Chromatography

Histological and Histochemical Changes in the Liver of Albino Rats Due to Methyl Alcohol Administration

Role of hepatic tetrahydrofolate in the species difference in methanol toxicity.

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