91598-91-3

Basic information

• Product Name: Acetamide, N-(6-hydroxy-1-pyrenyl)-
• Synonyms: Acetamide, N-(6-hydroxy-1-pyrenyl)-
• CAS NO: 91598-91-3
• Molecular Formula: C18H13 N O2
• Molecular Weight: 275.32
• Mol File: 91598-91-3.mol
• Article Data: 1

Chemical Properties

• Boiling Point: 599°Cat760mmHg
• Flash Point: 316.1°C
• Appearance: /
• Density: 1.422g/cm³
• Vapor Pressure: 6.06E-15mmHg at 25°C
• Refractive Index: 1.88
• CAS DataBase Reference: Acetamide, N-(6-hydroxy-1-pyrenyl)-(CAS DataBase Reference)
• NIST Chemistry Reference: Acetamide, N-(6-hydroxy-1-pyrenyl)-(91598-91-3)
• EPA Substance Registry System: Acetamide, N-(6-hydroxy-1-pyrenyl)-(91598-91-3)

Safety Data

• Hazardous Substances Data: 91598-91-3(Hazardous Substances Data)

Usage

Description

Acetamide, N-(6-hydroxy-1-pyrenyl)-, also known as 6-Hydroxy-N-acetyl-1-aminopyrene (OHNAAP), is a metabolite of 1-Nitropyrene (1-NP), a significant nitrated polycyclic aromatic hydrocarbon (NPAH) found in diesel exhaust particulate matter (DEP). It plays a crucial role in assessing exposure to DEP due to its association with direct-acting mutagenicity.

Uses

Used in Environmental Monitoring:
Acetamide, N-(6-hydroxy-1-pyrenyl)is used as a biomarker for monitoring exposure to diesel exhaust particulate matter (DEP). It serves as an indicator of the presence and potential health risks associated with DEP, allowing for better understanding and management of environmental pollutants.
Used in Public Health Research:
In the field of public health, Acetamide, N-(6-hydroxy-1-pyrenyl)is utilized for research purposes to study the effects of DEP exposure on human health. This helps in developing strategies for reducing exposure and mitigating the associated health risks.
Used in Occupational Health and Safety:
Acetamide, N-(6-hydroxy-1-pyrenyl)is employed as a tool in occupational health and safety to assess the exposure levels of workers in industries where DEP is prevalent. This aids in implementing necessary safety measures and guidelines to protect workers from potential health hazards.

InChI:InChI=1/C18H13NO2/c1-10(20)19-15-8-4-11-3-7-14-16(21)9-5-12-2-6-13(15)17(11)18(12)14/h2-9,21H,1H3,(H,19,20)

Upstream product

• 1767-28-8 1-hydroxy-6-nitropyrene 
• 108-24-7 acetic anhydride 
• 1732-30-5 6-hydroxy-1-aminopyrene 

Relevant articles and documents

Role of O-acetyltransferase in activation of oxidised metabolites of the genotoxic environmental pollutant 1-nitropyrene

The genotoxic environmental contaminant 1-nitropyrene is metabolised in mammalian systems by pathways more complex than the straightforward nitroreduction which accounts for most of its biological activity in bacteria. In order to evaluate the role of O-acetyltransferase (OAT) activity in generation of genotoxic intermediates from 1-nitropyrene, the mutagenicity of the major primary oxidised metabolites of 1-nitropyrene was characterised in the Ames Salmonella typhimurium plate incorporation assay with strain TA98, and with variants of TA98 deficient (TA98/1,8-DNP6) or enhanced (YG1024) in O-acetyltransferase. 1-Nitropyren-3-ol was more mutagenic in the absence than in the presence of S9, while 1-nitropyren-4-ol, 1-nitropyren-6-ol and 1-nitropyren-8-ol required S9 for maximum expression of mutagenicity. 1-Nitropyren-4-ol (176 rev/nmol without S9, 467 rev/nmol with S9 in TA98) and 1-nitropyren-6-ol (13 rev/nmol without S9, 266 rev/nmol with S9 in TA98) were overall the most potent nitropyrenol isomers assayed. 1-Acetamidopyren-8-ol and 1-acetamidopyrene 4,5-quinone were only minimally active. 1-Acetamidopyren-3-ol exhibited direct-acting mutagenicity. 1-Acetamidopyren-6-ol, previously shown to be a major contributor to mutagenicity in the urines of rats dosed with 1-nitropyrene (Ball et al., 1984b), was confirmed as a potent (359 rev/nmol) S9-dependent mutagen. Both the direct-acting and the S9-dependent mutagenicity of all the compounds studied was enhanced in the OAT-overproducing strain and much diminished (though not always entirely lost) in the OAT-deficient strain, showing that OAT amplifies expression of the genotoxicity of these compounds. 1-Acetamidopyren-6-ol required both S9 and OAT activity in order to exhibit any mutagenicity; this finding strongly implicates N-hydroxylation followed by O-esterification, as opposed to further S9-catalyzed ring oxidation, as a major route of activation for urinary metabolites of 1-nitropyrene.