Millar B C, Jinks S
Int J Radiat Oncol Biol Phys. 1982 Mar-Apr;8(3-4):795-7. doi: 10.1016/0360-3016(82)90737-4.
Overnight exposure of Chinese hamster cells, V-79-753B, to certain non-steroidal anti-inflammatory agents (NSAIA) including indomethacin (5 x 10(-5)M), benoxaprofen (5 x 10(-5)M) or aspirin (10(-4)M) protected against misonidazole-induced toxicity both in air and in hypoxia at 37 degrees C. In no instance was the radiosensitivity of cells affected by these treatments nor was there any effect on the amount of acute hypoxic cell radiosensitization produced by 1.0 mM misonidazole. There was no protection against misonidazole-induced toxicity when cells were pretreated with theophylline (10(-3)M). Protection against misonidazole-induced toxicity by benoxaprofen was not reversed by the addition of 1 microgram/ml prostaglandin E1 or F1 alpha. The results are discussed in terms of possible mechanisms.
将中国仓鼠细胞V - 79 - 753B在37℃下于空气中及低氧环境中过夜暴露于某些非甾体抗炎药(NSAIA),包括吲哚美辛(5×10⁻⁵M)、苯恶洛芬(5×10⁻⁵M)或阿司匹林(10⁻⁴M),可预防米索硝唑诱导的毒性。这些处理在任何情况下均未影响细胞的放射敏感性,对1.0 mM米索硝唑产生的急性低氧细胞放射增敏量也没有任何影响。当用茶碱(10⁻³M)预处理细胞时,对米索硝唑诱导的毒性没有保护作用。添加1微克/毫升前列腺素E1或F1α不会逆转苯恶洛芬对米索硝唑诱导毒性的保护作用。从可能的机制方面对结果进行了讨论。