Miyoshi N, Misík V, Riesz P
Radiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Radiat Res. 1997 Jul;148(1):43-7.
Low concentrations (> or = 1 microM) of the gallium-porphyrin analogue ATX-70 significantly enhanced cellular toxicity in human leukemia HL-525 cells exposed to 50 kHz ultrasound. The mechanism of this ATX-70-dependent sonosensitization is unknown, but we have established the requirement of extracellular localization of ATX-70 molecules for sonosensitization. Short-lived toxic intermediates produced from ATX-70 by ultrasound are implicated in the mechanism, since no cytotoxicity was found when medium containing ATX-70 was sonicated and subsequently added to the cells. However, we were unable to demonstrate the existence of radical intermediates by EPR spin trapping with the nitroso spin trap, DBNBS, and ATX-70-dependent sonotoxicity could not be ameliorated by the addition of up to 70 mM POBN and DMPO spin traps during ultrasound exposure.
低浓度（≥1微摩尔）的镓卟啉类似物ATX - 70能显著增强暴露于50千赫超声波下的人白血病HL - 525细胞的细胞毒性。这种依赖于ATX - 70的声敏化机制尚不清楚，但我们已经确定ATX - 70分子的细胞外定位是声敏化所必需的。超声作用于ATX - 70产生的短寿命毒性中间体与该机制有关，因为当含有ATX - 70的培养基被超声处理后再添加到细胞中时未发现细胞毒性。然而，我们无法通过用亚硝基自旋捕获剂DBNBS进行电子顺磁共振自旋捕获来证明自由基中间体的存在，并且在超声暴露期间添加高达70毫摩尔的POBN和DMPO自旋捕获剂并不能改善ATX - 70依赖的声毒性。
