Synopsis
0
USDMF
0
CEP/COS
0
JDMF
0
EU WC
0
KDMF
0
NDC API
0
VMF
0
FDF
0
FDF Dossiers
0
FDA Orange Book
0
Europe
0
Canada
0
Australia
0
South Africa
0
Listed Dossiers
DRUG PRODUCT COMPOSITIONS
0
US Patents
0
US Exclusivities
0
Health Canada Patents
0
Data Compilation #PharmaFlow
0
Stock Recap #PipelineProspector
0
Weekly News Recap #Phispers
US Medicaid
NA
Annual Reports
NA
Finished Drug Prices
NA
1. Alcohol, Methyl
2. Alcohol, Wood
3. Carbinol
4. Methoxide, Sodium
5. Methyl Alcohol
6. Sodium Methoxide
7. Wood Alcohol
1. Methyl Alcohol
2. 67-56-1
3. Wood Alcohol
4. Carbinol
5. Wood Spirit
6. Wood Naphtha
7. Methylol
8. Methyl Hydroxide
9. Pyroxylic Spirit
10. Colonial Spirit
11. Columbian Spirit
12. Monohydroxymethane
13. Methylalkohol
14. Columbian Spirits
15. Alcohol, Methyl
16. Alcool Methylique
17. Meoh
18. Methyl Hydrate
19. Ch3oh
20. Metanolo
21. Alcool Metilico
22. Bieleski's Solution
23. Colonial Spirits
24. Metylowy Alkohol
25. Pyroxylic Spirits
26. Hydroxymethane
27. Freers Elm Arrester
28. Surflo-b17
29. Rcra Waste Number U154
30. Wilbur-ellis Smut-guard
31. Metanol [spanish]
32. Metanolo [italian]
33. Coat-b1400
34. Eureka Products, Criosine
35. Metanol
36. Caswell No. 552
37. Methylalkohol [german]
38. Spirit Of Wood
39. Alcool Metilico [italian]
40. Metylowy Alkohol [polish]
41. Alcool Methylique [french]
42. X-cide 402 Industrial Bactericide
43. Hsdb 93
44. Ideal Concentrated Wood Preservative
45. Methyl Alcohol [nf]
46. Eureka Products Criosine Disinfectant
47. Nsc 85232
48. Un1230
49. Ccris 2301
50. Alcohol,methyl
51. Pyro Alcohol
52. Ai3-00409
53. Metoh
54. Rcra Waste No. U154
55. Epa Pesticide Chemical Code 053801
56. Methanol-water Mixture
57. Chebi:17790
58. Nsc-85232
59. Y4s76jwi15
60. Methanol, Anhydrous
61. Mfcd00004595
62. Methyl Alcohol (nf)
63. Ncgc00091172-01
64. Aqualine™ Solvent
65. Methanol-[17o]
66. Dsstox_cid_1731
67. Aqualine™ Titrant 5
68. Dsstox_rid_76297
69. Dsstox_gsid_21731
70. 170082-17-4
71. Ch4o
72. Methanol, For Hplc, >=99.9%
73. Methanol, Acs Reagent, >=99.8%
74. Methanol, Or Methyl Alcohol [un1230] [flammable Liquid, Poison]
75. Cas-67-56-1
76. Moh
77. Einecs 200-659-6
78. Unii-y4s76jwi15
79. Methylalcohol
80. Methly Alcohol
81. Primary Alcohol
82. Methanol-
83. Wood
84. Primary Alcohols
85. Methanol Cluster
86. Methanol Nf
87. Nat. Methanol
88. A Primary Alcohol
89. Methanol Lc-ms
90. Methanol, For Hplc
91. Methanol (recovered)
92. Methanol, Acs Grade
93. Solutions, Bieleski's
94. Methanol, Hplc Grade
95. Methanol, Lcms Grade
96. Columbian Spirits
97. Methanol [mi]
98. Hydroxymethylidyne Radical
99. 3'-hydroxystanozolol-d3
100. Methanol (peptide Grade)
101. Methanol, Histology Grade
102. Bmse000294
103. Epitope Id:116865
104. Methanol [usp-rs]
105. Methanol [who-dd]
106. Ec 200-659-6
107. Aqualine™ Solvent Cm
108. Methanol Reagent Grade Acs
109. Methanol, Or Methyl Alcohol
110. Methyl Alcohol [ii]
111. Methanol, Lr, >=99%
112. Methanol, Saj Special Grade
113. Methanol, Analytical Standard
114. Methyl Alcohol [fcc]
115. Wln: Q1
116. Methanol Hplc Gradient Grade
117. Methanol, Environmental Grade
118. Aqualine™ Electrolyte A
119. Chembl14688
120. Methyl Alcohol [hsdb]
121. Methyl Alcohol [inci]
122. Alcohol,methyl [vandf]
123. Methanol, Anhydrous, 99.8%
124. Methanol, P.a., 99.8%
125. Methanol, P.a., 99.9%
126. Aqualine™ Electrolyte Ag
127. Aqualine™ Electrolyte Cg
128. Methanol [ep Monograph]
129. Methyl Alcohol [mart.]
130. Dtxsid2021731
131. Methanol, Ar, >=99.5%
132. Methyl Alcohol [usp-rs]
133. Chebi:15734
134. Methanol, Nmr Reference Standard
135. Methanol, Ultrapure, Hplc Grade
136. Methyl Alcohol (methanol)
137. Methanol, 99.8%, Acs Reagent
138. Methanol, Anhydrous, >=99.5%
139. Methanol, Low Water For Titration
140. Methanol Gc, For Residue Analysis
141. Eriochrome™ Black T Solution
142. Methanol, Absolute - Acetone Free
143. Methanol, Low Benzene, Hplc Grade
144. Methanol, Hplc Gradient, 99.9%
145. Methanol, Or Methyl Alcohol [un1230] [flammable Liquid, Poison]
146. Nsc85232
147. Methanol, For Hplc, >=99.8%
148. Methanol, Pra Grade, >=99.9%
149. Tox21_111094
150. Tox21_202523
151. Methanol, Hplc Plus, >=99.9%
152. Akos000269045
153. Methanol, Purification Grade, 99.8%
154. Un 1230
155. Methanol, Uhplc, For Mass Spectrometry
156. Acetone Impurity A [ep Impurity]
157. Methanol Solution, Technical Grade, 95%
158. Methanol, >=99.8%, For Chromatography
159. Methanol, Saj First Grade, >=99.5%
160. Ncgc00260072-01
161. Methanol, Jis Special Grade, >=99.8%
162. Methanol, Laboratory Reagent, >=99.6%
163. Methanol, Uv Hplc Spectroscopic, 99.9%
164. Methanol, Anhydrous, Zero2(tm), 99.8%
165. Methanol, Spectrophotometric Grade, >=99%
166. Ft-0623465
167. Ft-0628297
168. Ft-0628299
169. Ft-0700908
170. Ft-0700959
171. M0097
172. M0628
173. Methanol, Ultrapure, Spectrophotometric Grade
174. C00132
175. D02309
176. Methanol, For Hplc, Gradient Grade, 99.93%
177. Methanol, Suitable For Determination Of Dioxins
178. Q14982
179. Methanol 100 Microg/ml In N,n-dimethylacetamide
180. Methanol, For Hplc, Gradient Grade, >=99.9%
181. Methanol, Glass Distilled Hrgc/hplc Trace Grade
182. Methanol, Low Benzene, Acs Reagent, = 99.8%
183. Methanol, Low Benzene, Acs Reagent, >=99.8%
184. Methanol, Acs Spectrophotometric Grade, >=99.9%
185. Methanol Hplc, Uv-ir Min. 99.9% Isocratic Grade
186. Methanol, Bioreagent, Suitable For Protein Sequencing
187. Methanol, For Hplc, Gradient Grade, >=99.8% (gc)
188. Methanol, Hplc Plus, >=99.9%, Poly-coated Bottles
189. Q27115113
190. Methanol Solution, (methanol:acetonitrile 1:1 (v/v))
191. Methanol Solution, Contains 0.50 % (v/v) Triethylamine
192. Methanol, Vetec(tm) Reagent Grade, Anhydrous, >=99.8%
193. Methanol Solution, (methanol:dichloromethane 1:1 (v/v))
194. Methanol, For Residue Analysis, Suitable For 5000 Per Jis
195. Moisture In Methanol, 325 Mg/kg, Nist(r) Srm(r) 8510
196. Moisture In Methanol, 93 Mg/kg, Nist(r) Srm(r) 8509
197. Methanol Solution, (methanol:dimethyl Sulfoxide 1:1 (v/v))
198. Methanol Solution, Contains 0.1 % (v/v) Trifluoroacetic Acid
199. Methanol Solution, For Protein Sequence Analysis, ~50% In H2o
200. Methanol With 0.1% Trifluoroacetic Acid, Tested For Uhplc-ms
201. Methanol, >=99.8%, Suitable For Absorption Spectrum Analysis
202. Methanol, Semiconductor Grade Puranal(tm) (honeywell 17824)
203. Methanol, P.a., Acs Reagent, Reag. Iso, Reag. Ph. Eur., 99.9%
204. Methanol, Puriss. P.a., Absolute, Acs Reagent, >=99.8% (gc)
205. Methanol, Semiconductor Grade Vlsi Puranal(tm) (honeywell 17744)
206. Methanol, Suitable For Protein Sequencing, Bioreagent, >=99.93%
207. Methyl Alcohol, United States Pharmacopeia (usp) Reference Standard
208. Methanol, Pharmaceutical Secondary Standard; Certified Reference Material
209. Methanol, Puriss., Meets Analytical Specification Of Ph Eur, >=99.7% (gc)
210. Methanol, Suitable For 1000 Per Jis, >=99.8%, For Residue Analysis
211. Methanol, Suitable For 300 Per Jis, >=99.8%, For Residue Analysis
212. (5beta,17beta)-17-hydroxy-17-(methyl-d3)-2'h-androst-2-eno[3,2-c]pyrazol-5'(1'h)-one
213. Methanol Solution, Contains 0.1 % (v/v) Trifluoroacetic Acid, 5 % (v/v) Water, For Hplc
214. Methanol Solution, Contains 0.10 % (v/v) Trifluoroacetic Acid, 10 % (v/v) Water
215. Methanol Solution, For Hplc, Contains 10 % (v/v) Water, 0.1 % (v/v) Trifluoroacetic Acid
216. Methanol, For Hplc, Gradient Grade, Suitable As Acs-grade Lc Reagent, >=99.9%
217. Methanol, Puriss. P.a., Acs Reagent, Reag. Iso, Reag. Ph. Eur., >=99.8% (gc)
218. Residual Solvent Class 2 - Methanol, United States Pharmacopeia (usp) Reference Standard
219. Jandajel(tm)-oh, 100-200 Mesh, Extent Of Labeling: 1.0 Mmol/g Oh Loading, 2 % Cross-linked
220. Jandajel(tm)-oh, 200-400 Mesh, Extent Of Labeling: 1.0 Mmol/g Oh Loading, 2 % Cross-linked
221. Jandajel(tm)-oh, 50-100 Mesh, Extent Of Labeling: 1.0 Mmol/g Oh Loading, 2 % Cross-linked
222. Methanol Solution, Contains 0.10 % (v/v) Formic Acid, Uhplc, For Mass Spectrometry, >=99.5%
223. Methanol Solution, Nmr Reference Standard, 4% In Methanol-d4 (99.8 Atom % D), Nmr Tube Size 3 Mm X 8 In.
224. Methanol Solution, Nmr Reference Standard, 4% In Methanol-d4 (99.8 Atom % D), Nmr Tube Size 5 Mm X 8 In.
| Molecular Weight | 32.042 g/mol |
|---|---|
| Molecular Formula | CH4O |
| XLogP3 | -0.5 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 1 |
| Rotatable Bond Count | 0 |
| Exact Mass | 32.026214747 g/mol |
| Monoisotopic Mass | 32.026214747 g/mol |
| Topological Polar Surface Area | 20.2 Ų |
| Heavy Atom Count | 2 |
| Formal Charge | 0 |
| Complexity | 2 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
The minimum lethal dose of methanol in the absence of medical treatment is between 0.3 and 1 g/kg.
Environmental Health Criteria 196: Methanol pp. 8 (1997) by the International Programme on Chemical Safety (IPCS) under the joint sponsorship of the United Nations Environment Programme, the International Labour Organisation and the World Health Organization.
... A 67-year-old woman ... committed suicide by ingestion of 500 mL of absolute methanol. ...
PMID:22398189 Cascallana JL et al; Forensic Sci Int 220 (1-3): e9-12 (2012)
Solvents
Liquids that dissolve other substances (solutes), generally solids, without any change in chemical composition, as, water containing sugar. (Grant and Hackh's Chemical Dictionary, 5th ed) (See all compounds classified as Solvents.)
Methanol is absorbed following inhalation or ingestion, and inhalation is the major route of absorption in the occupational environment. There is no agreement on the potential risk of dermal exposure to methanol. Methanol is uniformly distributed according to the relative water content of the tissue.
Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 374
Methyl alcohol is readily absorbed from GI and respiratory tracts.
Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. III-275
The rate of absorption /of methanol from the gastrointestinal tract is approximately/... 8.4 mg/sq cm/hr. Time to peak serum concentration... after ingestion /is/... 30-60 minutes for methanol... .
Goldfrank, L.R. (ed). Goldfrank's Toxicologic Emergencies. 7th Edition McGraw-Hill New York, New York 2002., p. 982
... Under ... experimental conditions in man following ingestion and inhalation, dosages of 71-84 mg/kg orally resulted in blood levels of 4.7-7.6 mg/100 mL ... 2-3 hr afterward. urine/blood concentration ratio was ... constant at about 1.3. ... Inhalation of ... 500-1000 ppm ... for ... 3-4 hr gave urine concentration of about 1-3 mg/100 mL. ...
Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982., p. 4537
For more Absorption, Distribution and Excretion (Complete) data for Methanol (27 total), please visit the HSDB record page.
We recently showed that methanol emitted by wounded plants might function as a signaling molecule for plant-to-plant and plant-to-animal communications. In mammals, methanol is considered a poison because the enzyme alcohol dehydrogenase (ADH) converts methanol into ... formaldehyde /and other products/. However, the detection of methanol in the blood and exhaled air of healthy volunteers suggests that methanol may be a chemical with specific functions rather than a metabolic waste product. Using a genome-wide analysis of the mouse brain, we demonstrated that an increase in blood methanol concentration led to a change in the accumulation of mRNAs from genes primarily involved in detoxification processes and regulation of the alcohol/aldehyde dehydrogenases gene cluster. To test the role of ADH in the maintenance of low methanol concentration in the plasma, we used the specific ADH inhibitor 4-methylpyrazole (4-MP) and showed that intraperitoneal administration of 4-MP resulted in a significant increase in the plasma methanol, ethanol and formaldehyde concentrations. Removal of the intestine significantly decreased the rate of methanol addition to the plasma and suggested that the gut flora may be involved in the endogenous production of methanol. ADH in the liver was identified as the main enzyme for metabolizing methanol because an increase in the methanol and ethanol contents in the liver homogenate was observed after 4-MP administration into the portal vein. Liver mRNA quantification showed changes in the accumulation of mRNAs from genes involved in cell signaling and detoxification processes. We hypothesized that endogenous methanol acts as a regulator of homeostasis by controlling the mRNA synthesis.
PMID:24587296 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3937363 Komarova TV et al; PLoS One 9 (2): e90239 (2014)
Many studies have reported that methanol toxicity to primates is mainly associated with its metabolites, formaldehyde (FA) and formic acid. While methanol metabolism and toxicology have been best studied in peripheral organs, little study has focused on the brain and no study has reported experimental evidence that demonstrates transformation of methanol into FA in the primate brain. In this study, three rhesus macaques were given a single intracerebroventricular injection of methanol to investigate whether a metabolic process of methanol to FA occurs in nonhuman primate brain. Levels of FA in cerebrospinal fluid (CSF) were then assessed at different time points. A significant increase of FA levels was found at the 18th hour following a methanol injection. Moreover, the FA level returned to a normal physiological level at the 30th hour after the injection. These findings provide direct evidence that methanol is oxidized to FA in nonhuman primate brain and that a portion of the FA generated is released out of the brain cells. This study suggests that FA is produced from methanol metabolic processes in the nonhuman primate brain and that FA may play a significant role in methanol neurotoxicology.
PMID:27066393 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4811046 Zhai R et al; Anal Cell Pathol (Amst) 2016: 4598454 (2016)
Methanol is among the most common short-chain alcohols in fermenting fruits, the natural food and oviposition sites of the fruit fly Drosophila melanogaster. Our previous results showed that cytochrome P450 monooxygenases (CYPs) were associated with methanol detoxification in the larvae. Catalases, alcohol dehydrogenases (ADHs), esterases (ESTs) and glutathione S-transferases (GSTs) were specifically inhibited by 3-amino-1,2,4-triazole (3-AT), 4-methylpyrazole (4-MP), triphenyl phosphate (TPP) and diethylmeleate (DEM), respectively. CYPs were inhibited by piperonyl butoxide (PBO) and 1-aminobenzotriazole (1-ABT). In the present paper, the involvements of these enzymes in methanol metabolism were investigated in female and male adults by determining the combination indices of methanol and their corresponding inhibitors. When PBO, 1-ABT, 3-AT, 4-MP and TPP were individually mixed with methanol, they exhibited significant synergism to the mortality of the adults after 72 hr of dietary exposure. In contrast, the DEM and methanol mixture showed additive effects. Moreover, methanol exposure dramatically increased CYP activity and up-regulated mRNA expression levels of several Cyp genes. Bioassays using different strains revealed that the variation in ADH activity and RNAi-mediated knockdown of alpha-Est7 significantly changed LC50 values for methanol. These results suggest that CYPs, catalases, ADHs and ESTs are partially responsible for methanol elimination in adults. It seems that there are some differences in methanol metabolism between larvae and adults, but not between female and male adults.
PMID:23751173 Wang SP et al; Comp Biochem Physiol B Biochem Mol Biol 166 (1): 7-14 (2013)
Metabolism of methanol occurs in a three-step process initially involving oxidation to formaldehyde by hepatic alcohol dehydrogenase, which is a saturable rate-limiting process. In the second step, formaldehyde is oxidized by aldehyde dehydrogenase to formic acid or formate depending on the pH. In the third step, formic acid is detoxified by a folate-dependent pathway to carbon dioxide. Elimination of methanol from the blood appears to be slow in all species, especially when compared to ethanol. In humans, urinary methanol concentrations have been found to be proportional to the concentration of methanol in blood.
WHO/Health and Safety Guide No. 105 for Methanol (67-56-1) (1997). Available from, as of September 29, 2011: https://www.inchem.org/pages/hsg.html
For more Metabolism/Metabolites (Complete) data for Methanol (18 total), please visit the HSDB record page.
... The mean plasma half-life of methanol during fomepizole treatment was 52 hr (range 22-87); the higher the serum methanol, the longer the half-life. ...
PMID:16035197 Hovda KE et al; Clin Toxicol (Phila). 43 (4): 221-7 (2005)
Biological half-life of methanol elimination in expired air is 1.5 hr after either oral or dermal application.
Dutkiewicz B; Int Congr Ser- Excerpta Med 440 (Ind Environ Xenobiotics): 106-9 (1978)
... Experiments were made during the morning after /human volunteers/ had consumed 1000-1500 mL red wine (9.5% weight/volume 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 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. ...
PMID:3588516 Jones AW; Pharmacol Toxicol 60 (3): 217-20 (1987)
Urinary methanol levels decreased exponentially with a half-life of about 2.5 to 3 hr in four volunteers exposed by inhalation to 102, 205, or 300 mg/cu m for 8 hr.
Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V6 381
For more Biological Half-Life (Complete) data for Methanol (7 total), please visit the HSDB record page.
... The metabolic mechanisms of methanol toxicity /are/ reviewed. ... It is noted that the most severe toxicity occurs many hours following peak blood and tissue methanol concentrations so that these do not necessarily provide an accurate indication of toxicity. Individual differences are seen both in this latent period and in individual susceptibility to methanol. This susceptibility may depend on the activity of folic acid requiring metabolic reactions involved in formate metabolism, formate being an intermediate produced during methanol oxidation and responsible for many toxic effects of methanol. Studies of the characteristics of methanol poisoning in non-primates and monkeys are examined. Despite the ingestion of lethal doses of methanol, non-primates generally do not develop significant metabolic acidosis nor impairment of vision, and no consistent histopathology has been demonstrated in these species. In monkeys, results suggest that the latent period represents a period of compensated metabolic acidosis; when compensatory mechanisms are exhausted, blood pH begins to drop. Formate accumulates and produces acidosis in the methanol poisoned monkey, but not in the rat, apparently due to a slower rate of formate metabolism to carbon dioxide in the monkey. ... Studies demonstrating the role of alcohol dehydrogenase in methanol metabolism in the monkey are reported; however, the catalase/peroxidative system which participates in methanol metabolism in rats apparently does not function in the monkey. Formaldehyde and formate metabolism are also examined. The regulation of the rate of formate metabolism is governed by regulation of the hepatic tetrahydrofolate concentrations. ... Further research is needed to determine what step or process it is which places the primate at a distinct liability in the metabolic disposition of one carbon moieties.
Tephly TR, Martin KE; Food Sci Technol 12: 111-40 (1984)
Methanol toxicity is observed in monkeys and humans but is not seen in rats or mice. The expression of methanol poisoning is related to the ability of an animal to metabolize formate to carbon dioxide. Since the rate of formate oxidation is related to hepatic tetrahydrofolate content and the activites of folate dependent enzymes, studies were designed to determine hepatic concentrations of hepatic tetrahydrofolate and activites of folate dependent enzymes of human liver and livers of species considered insensitive to methanol poisoning. An excellent correlation between hepatic tetrahydrofolate and maximal rates of formate oxidation has been observed. In human liver, levels were only 50% of those observed for rat liver and similar to those found in monkey liver. Total folate was also lower (60% decreased) in human liver than that found in rat or monkey liver. Interestingly, mouse liver contains much higher hepatic tetrahydrofolate and total folate than rat or monkey liver. This is consistent with higher formate oxidation rates in this species. A second important observation has been made. 10-Formyltetrahydrofolate dehydrogenase activity, the enzyme catalyzing the final step of formate oxidation to carbon dioxide, was markedly reduced in both monkey and human liver. Thus, two mechanisms may be operative in explaining low formate oxidation in species susceptible to methanol toxicity, low hepatic tetahydrofolate levels and reduced hepatic 10-formyltetrahydrofolate dehydrogenase activity.
PMID:3574297 Johlin FC et al; Mol Pharmacol 31 (5): 557-61 (1987)
Formic acid, the toxic metabolite of methanol, has been hypothesized to produce retinal and optic nerve toxicity by disrupting mitochondrial energy production. It has been shown in vitro to inhibit the activity of cytochrome oxidase, a vital component of the mitochondrial electron transport chain involved in ATP synthesis. Inhibition occurs subsequent to the binding of formic acid to the ferric heme iron of cytochrome oxidase, and the apparent inhibition constant is between 5 and 30 mM. Concentrations of formate present in the blood and tissues of methanol-intoxicated humans, non-human primates and rodent models of methanol-intoxication are within this range. Studies conducted in methanol-sensitive rodent models have revealed abnormalities in retinal and optic nerve function and morphology, consistent with the hypothesis that formate acts as a mitochondrial toxin. In these animal models, formate oxidation is selectively inhibited by dietary or chemical depletion of folate coenzymes, thus allowing formate to accumulate to toxic concentrations following methanol administration. Methanol-intoxicated rats developed formic acidemia, metabolic acidosis and visual toxicity analogous to the human methanol poisoning syndrome.
WHO/International Programme on Chemical Safety; Environmental Health Criteria 196, Methanol (1997). Available from, as of July 19, 2017: https://www.inchem.org/pages/ehc.html
In addition to neurofunctional changes, bioenergetic and morphological alterations indicative of formate-induced disruption of retinal energy metabolism have been documented in methanol-intoxicated rats. Morphological studies, coupled with cytochrome oxidase histochemistry, revealed generalized retinal edema, photoreceptor and /retinal pigment epithelium/ (RPE) vacuolation, mitochondrial swelling and a reduction in cytochrome oxidase activity in photoreceptor mitochondria from methanol intoxicated rats. The most striking structural alterations observed in the retinas of methanol-intoxicated rats were vacuolation and mitochondrial swelling in inner segments of the photoreceptor cells. Photoreceptor mitochondria from methanol-intoxicated rats were swollen and expanded to disrupted cristae and showed no evidence of cytochrome oxidase reaction product. In contrast, photoreceptor mitochondria from control animals showed normal morphology with well-defined cristae and were moderately reactive for cytochrome oxidase reaction product. These findings are consistent with disruption of ionic homoeostasis in the photoreceptors, secondary to inhibition of mitochondrial function. Biochemical measurements also showed a significant reduction in retinal and brain cytochrome oxidase activity and ATP concentrations in methanol-intoxicated rats relative to control animals. Surprisingly, no differences from control values were observed in hepatic, renal or cardiac cytochrome oxidase activity or ATP concentrations in methanol-intoxicated rats. The reduction in retinal function, inhibition of retinal, optic nerve and brain cytochrome oxidase activity, depletion of retinal and brain ATP concentrations, and mitochondrial disruption produced in methanol-intoxicated rats are consistent with the hypothesis that formate acts as a mitochondrial toxin with selectivity for the retina and brain.
WHO/International Programme on Chemical Safety; Environmental Health Criteria 196, Methanol (1997). Available from, as of July 19, 2017: https://www.inchem.org/pages/ehc.html
For more Mechanism of Action (Complete) data for Methanol (6 total), please visit the HSDB record page.
Digital Content 
NEWS #PharmaBuzz
Market Place
REF. STANDARDS & IMPURITIES
ABOUT THIS PAGE
LOOKING FOR A SUPPLIER?
