[The increasing mutagenic effect of nitrosoguanidine under the influence of modified bases during inhibition of repair AGT enzyme in mammalian somatic cells in vitro].
Gene mutations were studied on human cells SL68, XP12BE and chinese hamster cells Blld-ii-FAF28C1237. All the cells were sensitive to purine base analogs and were characterized by a high rate of O6-alkylguanine-DNA-transferase (AGT) activity. Inhibiting AGT activity by O6-benzylguanine considerably increases the frequency of mutants induced by the alkylating agent MNNG. Transitions of the GC-->AT type are the dominant mutations in the coding region of the hprt gene. The mechanism of DNA lesion repair by the AGT enzyme differs significantly from the excision repair.
Lukash
L L
LL
Lylo
V V
VV
Man'ko
V G
VG
Terent'ev
A G
AG
D000818:Animals; D001482:Base Composition / Q000235:genetics*; D002460:Cell Line; D002478:Cells, Cultured; D006224:Cricetinae; D004249:DNA Damage; D004260:DNA Repair; D005091:Exons; D005347:Fibroblasts / Q000187:drug effects / Q000201:enzymology; D017353:Gene Deletion; D006147:Guanine / Q000031:analogs & derivatives* / Q000378:metabolism / Q000494:pharmacology; D006801:Humans; D007041:Hypoxanthine Phosphoribosyltransferase / Q000235:genetics; D008769:Methylnitronitrosoguanidine / Q000633:toxicity*; D009153:Mutagens / Q000633:toxicity*; D019853:O(6)-Methylguanine-DNA Methyltransferase / Q000235:genetics / Q000378:metabolism*
D009153:Mutagens; C064976:O(6)-benzylguanine; D008769:Methylnitronitrosoguanidine; D006147:Guanine; D019853:O(6)-Methylguanine-DNA Methyltransferase; D007041:Hypoxanthine Phosphoribosyltransferase