1,N6-ethano A (EA)

FULL NAME: 1,N6-ethanoadenine


DESCRIPTION:
1,N6-ethanoadenine (EA) is the chemically reduced form of eA and forms through the reaction of adenine with the antitumor drug bis-chloroethylnitrosourea. EA can be weakly repaired by the E.coli enzyme AlkA and the corresponding human enzyme AAG, which suggested that BER is a means of repair of this adduct. The direct reversal repair enzyme AlkB easily alleviates the toxicity of EA in E.coli in vivo. In an AlkB-proficient cell, EA is almost non-toxic (i.e. easily bypassed) and not significantly mutagenic. However, in AlkB-deficient cells, EA is extremely toxic, showing an 86% reduction in replication. The adduct is weakly mutagenic causing A → C (2%), A → G (1%) and A → T (1%) mutations.

DAMAGE TYPE: DNA adduct


DNA DAMAGE SOURCE(S) (MAIN):
bischloroethyl nitrosourea (BCNU)


DNA DAMAGE EFFECT(S) (MAIN):
cell cycle arrest
stalled replication fork


DNA DAMAGE EFFECT(S) (MINOR):
A→C transversion
A→G transition
A→T transversion
mutagenesis
point mutation
substitution
transition
transversion


PATHWAYS:
base excision repair (BER)


DNA repair protein(s) related to damage:
AlkA
ANPG (MPG)


Last modification date: Aug. 29, 2011