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北 海 道 大 学 脳 神 経 外 科*カ リ フ ォ ル ニ ア 大 学 サ ン フ ラ ン シ ス コ 校 脳 神 経 外 科 Addressreprintrequeststo:T.Aida,M.D.,DepartmentofNeurosurgery,HokkaidoUniversity,North-15,West-7,Kita-ku,SapporoO60. 受 稿1986年7月21日 受 理1986年11月27日 Abstract The cytotoxic and cytogenetic effects of 1 (4-amino-2-methyl-5-pyrimidinyl) methyl-3 (2-chloro ethyl)-3-nitrosourea hydrochloride (ACNU) treatment on two cell lines derived from human malignant glioma were studied. Compared to SF-126 cells, SF-188 cells were 7-fold more resistant to ACNU and were cross-resistant to 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU). In contrast to the results obtained with chloroethylnitrosoureas, SF-188 cells were more sensitive to nitrogen mustard (HN2) and cis-diamminedichloroplatinum (II) (cis-Pt) than were SF-126 cells. The number of sister chromatid exchanges (SCEs) induced by ACNU, BCNU, HN2, and cis-Pt was well correlated with cell survival in both cell lines. SF-188 cells had 70% fewer deoxyribonucleic acid (DNA) interstrand crosslinks with ACNU treatment than did SF-126 cells. Compared to SF 126 cells, the O6-methylguanine alkylation product was removed more rapidly from DNA in SF-188 cells treated with 3H-methylnitrosourea. These results suggest that DNA interstrand crosslinking may cause cell death and SCE induction in cells treated with ACNU and that one of the mechanisms of cellular resistance to ACNU is repair of O6-alkylguanine derivatives in DNA. This repair process prevents DNA interstrand crosslinks, which reduces both cytotoxic effects and SCE induction by ACNU.

Mechanisms of cellular resistance to ACNU in cell lines derived from human brain tumors.