N-methyl-N-nitrosourea (NMU)


OTHER NAMES:
1-methyl-1-nitrosourea
methylnitrosoure


ABBREVIATIONS:
MNU
NMU
NMH


DESCRIPTION: N-Nitroso-N-methylurea (NMU) is a highly reliable carcinogen, mutagen, and teratogen. NMU is an alkylating agent (SN1 type), and exhibits its toxicity by transferring its methyl group to nucleobases in nucleic acids.

Acute exposure to NMU in humans can result in skin and eye irritation, headache, nausea, and vomiting. NMU is reasonably anticipated to be a human carcinogen based on sufficient evidence of carcinogenicity in experimental animals. Various cancers induced in animal models include: squamous cell carcinomas of the forestomach, sarcomas and gliomas of the brain, adenocarcinomas of the pancreas, leukemia, and lymphomas. However, the actual potential for human exposure is quite limited, as the chemical is not produced or used in large quantities.

NMU is teratogenic and embryotoxic, resulting in craniofacial (cleft palate) and skeletal defects, increased fetal resorption, and fetal growth retardation. Exposure to NMU during pre-implantation, post-implantation, organogenesis, or by paternal exposure can result in these effects.

DNA DAMAGES:
3-methyl A (3meA)
O2-methyl T (O2meT)
3-methyl A (3-meA) in ssDNA
O2-methyl C (O2meC)
MePT
O4-methyl T (O4meT)


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NAME STRUCTURE PROTEINS DNA DAMAGE EFFECT(S) PATHWAY(S) RELATED
3-methyl A (3meA) AlkA
Tag
ANPG (MPG)
AP-site
A→T transversion
cell cycle arrest
cytotoxic
mutagenesis
point mutation
stalled replication fork
base excision repair (BER)
O2-methyl T (O2meT) AlkA cytotoxic base excision repair (BER)
3-methyl A (3-meA) in ssDNA AlkA AP-site
A→T transversion
cell cycle arrest
cytotoxic
mutagenesis
point mutation
stalled replication fork
transversion
base excision repair (BER)
O2-methyl C (O2meC) AlkA cytotoxic base excision repair (BER)
MePT Ada cytotoxic
stalled replication fork
direct reversal (DR)
O4-methyl T (O4meT) Ogt
Ada
MGMT
cytotoxic
mutagenesis
point mutation
substitution
T→C transition
transition
direct reversal (DR)

Last modification date: Aug. 28, 2011