Final Report on the Safety Assessment of Methyl Alcohol

Lanigan, Sean W.

doi:10.1080/109158101750300955

Cited by 11 publications

(1 citation statement)

References 81 publications

(124 reference statements)

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“…The increase in ROS and LPO due to methanol is associated with acidosis caused by methanol in the body [ 7 , 22 ]. Acidosis occurs when methanol is metabolized to formaldehyde, formate, and formic acid [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

Amelioration of oxidative damage parameters by carvacrol on methanol-induced liver injury in rats

et al. 2022

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The methanol metabolite that causes hepatotoxicity is formic acid, generating reactive oxygen radical formation and cell damage. Carvacrol is an antioxidant monoterpenic phenol produced from Thymus vulgaris. This study aimed to investigate the effects of carvacrol on methanolinduced oxidative liver damage in rats. Eighteen rats were divided into three groups.Methotrexate was administered orally for 7 days to methotrexate+methanol (MTM) and methotrexate+methanol+carvacrol (MMC) groups. Methotrexate was given before methanol to cause methanol poisoning. Distilled water was given to the healthy group (HG) as a solvent. At the end of the 7th day, 20% methanol was administered orally at a dose of 3 g/kg to the MTM and MMC groups. Four hours after methanol administration, 50 mg/kg carvacrol was injected intraperitoneally into the MMC group. Animals were sacrificed 8 hours after carvacrol injection. Biochemical markers were studied in the excised liver tissue and blood serum samples, and histopathological evaluations were made. Severe hemorrhage, hydropic degeneration, pycnosis, and mononuclear cell infiltration were observed in the liver of the MTM group. Additionally, the levels of malondialdehyde (MDA), total oxidant status (TOS), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were significantly higher, and total glutathione (tGSH) and total antioxidant status (TAS) were significantly lower in the MTM group compared to HG (p<0.001). Carvacrol prevented the increase in MDA, TOS, ALT and AST levels with methanol and the decrease in tGSH and TAS levels (p<0.001), and alleviated the histopathological damage.Carvacrol may be useful in the treatment of methanol-induced liver damage.

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Section: Discussionmentioning

confidence: 99%

Amelioration of oxidative damage parameters by carvacrol on methanol-induced liver injury in rats

et al. 2022

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Measurements in vivo of parameters pertinent to ROS/RNS using EPR spectroscopy

Khan

Swartz

2002

Oxygen/Nitrogen Radicals: Cell Injury and Disease

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Glutathione depletion modulates methanol, formaldehyde and formate toxicity in cultured rat conceptuses

2004

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The proposed use of methanol (H3COH) as an alternative to fossil fuels has prompted concern about potential health risks resulting from widespread environmental exposure. Methanol is teratogenic in rodents and, although the exact toxic species is not known, teratogenesis may result from the enzymatic biotransformation of H3COH to formaldehyde (CH2O) and formic acid causing increased biological reactivity and toxicity. A protective role for the antioxidant glutathione (GSH) has been described for H3COH, CH2O and formic acid toxicity in various biological systems but has yet to be evaluated in the developing conceptus. Whole embryo culture studies were conducted using GD 10-11 rat conceptuses to elucidate the relationship between H3COH and its metabolites and GSH status. Methanol exposure produced a decrease in normal growth parameters and a dose-dependent loss of viability. CH2O had deleterious effects on embryo growth and viability. Sodium formate (HCOONa) exposure resulted in a high mortality rate but viable embryos did not manifest any abnormalities. Methanol, CH2O, and HCOONa all produced a significant depletion of GSH in both embryo and VYS. Inhibition of GSH synthesis by L-buthionine-S,R-sulfoximine (BSO) treatment exacerbated H3COH, CH2O and HCOONa embryotoxicity. Interestingly, only H3COH/BSO and CH2O/BSO co-treatments caused increased malformation, while embryos treated with HCOONa/BSO did not produce any developmental deformities. These results implicate CH2O as the most embryotoxic H3COH metabolite, on a molar basis, in terms of causing dysmorphogenesis, alterations of normal growth parameters and embryolethality. HCOONa was selectively embryolethal and did not produce dysmorphogenesis. CH2O toxicity is potentiated by GSH depletion, indicating that GSH may be more directly involved in its detoxication in the embryo.

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Final Report on the Safety Assessment of Methyl Alcohol

Cited by 11 publications

References 81 publications

Amelioration of oxidative damage parameters by carvacrol on methanol-induced liver injury in rats

Amelioration of oxidative damage parameters by carvacrol on methanol-induced liver injury in rats

Measurements in vivo of parameters pertinent to ROS/RNS using EPR spectroscopy

Glutathione depletion modulates methanol, formaldehyde and formate toxicity in cultured rat conceptuses

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