Sonodynamic toxicity of gallium-porphyrin analogue ATX-70 in human leukemia cells

Sonodynamic toxicity of gallium-porphyrin analogue ATX-70 in human leukemia cells
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DOI:
10.2307/3579537
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发表时间:
1997-07-01
期刊:
影响因子:
3.4
通讯作者:
Riesz, P
Riesz, P
中科院分区:
医学3区
文献类型:
--
作者:
Miyoshi, N;Misik, V;Riesz, P

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相似文献

低浓度(大于或等于1μM)的镓卟啉类似物ATX-70显着增强暴露于50kHz超声的人白血病HL-525细胞的细胞毒性,这种ATX-70依赖性声敏化的机制尚不清楚,但我们已经确定了ATX-70分子的细胞外定位对于声敏化的要求。通过超声从 ATX-70 产生的短寿命有毒中间体与该机制有关,因为当对含有 ATX-70 的培养基进行超声处理并随后添加到细胞中时,没有发现细胞毒性。然而,我们无法通过亚硝基自旋捕获器、DBNBS 的 EPR 自旋捕获来证明自由基中间体的存在,并且 ATX-70 依赖性声毒性不能通过添加高达 70 mM POBN 和超声波照射期间的 DMPO 自旋陷阱。 (C) 1997 年,辐射研究会。
Low concentrations (greater than or equal to 1 mu M) 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. (C) 1997 by Radiation Research Society.