Jana A K, Agarwal S, Chatterjee S N
Biophysics Division, Saha Institute of Nuclear Physics, Calcutta, India.
Radiat Res. 1990 Oct;124(1):7-14.
Ultrasonic radiation produced a dose-dependent linear increase in lipid peroxidation in the liposomal membrane as reflected in the measurements of conjugated dienes, lipid hydroperoxides, and malondialdehydes (MDA). Production of MDA was confirmed by spectrophotometric and spectrofluorometric methods including the detection of excitation (360 nm) and emission (435 nm) maxima characteristic of the MDA-glycine adduct formed after addition of glycine in the system. Ultrasound of frequencies 20 kHz (used for laboratory purposes) and 3.5 MHz (used for clinical purposes) produced MDA in an identical manner. Ultrasound-induced lipid peroxidation was enhanced synergistically by 2.5 X 10(2) microM ascorbic acid but inhibited significantly by 10(4) microM ascorbic acid. Ultrasound-induced production of MDA could not be inhibited to any significant degree by superoxide dismutase, histidine, dimethylfuran, or beta-carotene but was very significantly inhibited by cholesterol (93%), butylated hydroxytoluene (88%), alpha-tocopherol (85%), sodium benzoate (80%), dimethyl sulfoxide (80%), sodium formate (64%), and EDTA (64%). The scavenger studies indicated the functional role of OH radicals in the initiation of ultrasound-induced lipid peroxidation.
超声辐射使脂质体膜中的脂质过氧化呈剂量依赖性线性增加，这在共轭二烯、脂质氢过氧化物和丙二醛（MDA）的测量中得到体现。通过分光光度法和荧光分光光度法证实了MDA的产生，这些方法包括检测在系统中加入甘氨酸后形成的MDA - 甘氨酸加合物的特征激发（360 nm）和发射（435 nm）最大值。频率为20 kHz（用于实验室目的）和3.5 MHz（用于临床目的）的超声以相同方式产生MDA。超声诱导的脂质过氧化被2.5×10²微摩尔抗坏血酸协同增强，但被10⁴微摩尔抗坏血酸显著抑制。超氧化物歧化酶、组氨酸、二甲基呋喃或β - 胡萝卜素不能在任何显著程度上抑制超声诱导的MDA产生，但胆固醇（93%）、丁基化羟基甲苯（88%）、α - 生育酚（85%）、苯甲酸钠（80%）、二甲基亚砜（80%）、甲酸钠（64%）和乙二胺四乙酸（64%）能非常显著地抑制。清除剂研究表明OH自由基在超声诱导的脂质过氧化起始过程中的功能作用。
