Registration Dossier
Registration Dossier
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EC number: 203-471-2 | CAS number: 107-19-7
Additional toxicological data
Administrative data
- Endpoint:
- additional toxicological information
- Type of information:
- experimental study
- Adequacy of study:
- other information
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: acceptable publication
Data source
Reference
- Reference Type:
- publication
- Title:
- Cytochrome P450 2E1 metabolically activates propargyl alcohol: propiolaldehyde-induced hepatocyte cytotoxicity
- Author:
- Moridani MY, Khan S, Chan T, Teng S, Beard K & O’Brien PJO
- Year:
- 2 001
- Bibliographic source:
- Chemico-Biological Interactions, 130–132: 931–942.
Materials and methods
Test material
- Reference substance name:
- Prop-2-yn-1-ol
- EC Number:
- 203-471-2
- EC Name:
- Prop-2-yn-1-ol
- Cas Number:
- 107-19-7
- Molecular formula:
- C3H4O
- IUPAC Name:
- prop-2-yn-1-ol
Constituent 1
Results and discussion
Any other information on results incl. tables
Propargyl alcohol (2-propyn-1-ol), because of its structural similarity to allyl alcohol, was thought to be activated by alcohol dehydrogenase. However, it is a poor substrate compared to allyl alcohol.aIt was shown that; (1) propargyl alcohol-induced cytotoxicity was markedly enhanced in CYP 2E1-induced hepatocytes and prevented by various CYP 2E1 inhibitors but was only slightly affected when alcohol dehydrogenase was inhibited with methylpyrazole:DMSO or when catalase was inactivated with azide or aminotriazole, (2) hepatocyte GSHdepletion preceded cytotoxicity and was inhibited by cytochrome P450 inhibitors but not by catalase:alcohol dehydrogenase inhibitors. GSH conjugate formation during propargyl alcohol metabolism by microsomal mixed function oxidase in the presence of GSH was also prevented by anti-rat CYP 2E1 or CYP 2E1 inhibitors, (3) cytotoxicity was prevented when lipid peroxidation was inhibited with antioxidants, desferoxamine (ferric chelator) or dithiothreitol. Propargyl alcohol-induced cytotoxicity and reactive oxygen species formation were markedly increased in GSH-depleted hepatocytes. All of this evidence suggests that propargyl alcohol-induced cytotoxicity involves metabolic activation by CYP 2E1 to form propiolaldehyde that causes hepatocyte lysis as a result of GSH depletion and lipid peroxidation.
Applicant's summary and conclusion
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