Wong K H, Koch C J, Wallen C A, Wheeler K T
Department of Radiology, Bowman Gray School of Medicine, Winston-Salem, North Carolina 27103.
Br J Cancer. 1991 Apr;63(4):484-8. doi: 10.1038/bjc.1991.116.
The acute toxicity, pharmacokinetics and hypoxic cytotoxicity of RSU-1069 were investigated using the subcutaneous (sc) rat 9L tumour model. The pharmacokinetics were studied after i.p. injection of RSU-1069 (20 mg kg-1 or 100 mg kg-1). For both doses, the elimination of RSU-1069 followed first-order kinetics in both plasma and unclamped tumours. After 100 mg kg-1, the peak plasma concentration of RSU-1069 was 40 micrograms ml-1; the elimination t1/2 was 39.3 +/- 11.1 min. After 20 mg kg-1, the peak plasma concentration was 3 micrograms ml-1; the elimination t1/2 was 47.8 +/- 6.3 min. In unclamped tumours, the peak concentration was 50 micrograms g-1 with an elimination t1/2 of 36.1 +/- 9.6 min for the 100 mg kg-1 dose, and 4 micrograms g-1 with an elimination t1/2 of 41.9 +/- 6.1 min for the 20 mg kg-1 dose. The tumour and plasma elimination half-times were not significantly different (P greater than 0.2) for the two doses. Clamping the tumour 30 min after administration of 100 mg kg-1 of RSU-1069 decreased the tumour elimination t1/2 to 10.9 +/- 1.4 min. After releasing the clamp, RSU-1069 returned rapidly to the unclamped tumour concentration. The unclamped tumour/plasma ratio reached a maximum of 4-6, then decreased to a constant value of about 2 for both doses, indicating that RSU-1069 accumulates in these 9L tumours. RSU-1069 kills hypoxic sc 9L cells more efficiently than oxic sc 9L cells; at a surviving fraction of 0.5, the SER was 4.8. For in vitro 9L cells, the SER was approximately 50 when the comparison was between those treated in 2.1% 0(2) and those treated in less than 7.5 x 10(-3)% 0(2); it was approximately 100 when the comparison was between those treated in 21% 0(2) and those treated in less than 7.5 x 10(-3)% 0(3). Tumours treated with RSU-1069 and clamped for various times exhibited biphasic cell-kill kinetics; at 50 mg kg-1, little additional cell kill was achieved after 40 min of clamping. Our data also indicate that RSU-1069 is 300-1000 fold more efficient than misonidazole or SR2508 for killing hypoxic sc 9L tumour cells in situ.
采用皮下接种大鼠9L肿瘤模型研究了RSU - 1069的急性毒性、药代动力学和缺氧细胞毒性。腹腔注射RSU - 1069(20mg/kg或100mg/kg)后研究其药代动力学。对于这两种剂量,RSU - 1069在血浆和未钳夹肿瘤中的消除均遵循一级动力学。100mg/kg剂量后,RSU - 1069的血浆峰值浓度为40μg/ml;消除半衰期为39.3±11.1分钟。20mg/kg剂量后,血浆峰值浓度为3μg/ml;消除半衰期为47.8±6.3分钟。在未钳夹肿瘤中,100mg/kg剂量的峰值浓度为50μg/g,消除半衰期为36.1±9.6分钟,20mg/kg剂量的峰值浓度为4μg/g,消除半衰期为41.9±6.1分钟。两种剂量的肿瘤和血浆消除半衰期无显著差异(P>0.2)。在给予100mg/kg的RSU - 1069后30分钟钳夹肿瘤,可使肿瘤消除半衰期降至10.9±1.4分钟。松开钳夹后,RSU - 1069迅速恢复到未钳夹肿瘤的浓度。未钳夹肿瘤/血浆比值最高达到4 - 6,然后两种剂量均降至约2的恒定值,表明RSU - 1069在这些9L肿瘤中蓄积。RSU - 1069杀伤皮下缺氧9L细胞比有氧皮下9L细胞更有效;在存活分数为0.5时,增敏比为4.8。对于体外9L细胞,当比较在2.1% O₂中处理的细胞和在小于7.5×10⁻³% O₂中处理的细胞时,增敏比约为50;当比较在21% O₂中处理的细胞和在小于7.5×10⁻³% O₂中处理的细胞时,增敏比约为100。用RSU - 1069处理并钳夹不同时间的肿瘤表现出双相细胞杀伤动力学;在50mg/kg时,钳夹40分钟后几乎没有额外的细胞杀伤。我们的数据还表明,RSU - 1069在原位杀伤皮下缺氧9L肿瘤细胞方面比米索硝唑或SR2508有效300 - 1000倍。