Lissi E A, Cáceres T, Llesuy S, Solari L, Boveris A, Videla L A
Departamento de Química, Facultad de Ciencia, Universidad de Santiago, Chile.
Free Radic Res Commun. 1989;6(5):293-301. doi: 10.3109/10715768909055154.
The characteristics of the visible luminescence that follows the lipid peroxidative process were investigated either in the autoxidation of rat brain homogenates or in the azo-bis-amidinopropane initiated lipid peroxidation of erythrocyte plasma membranes and liver microsomes. In these systems the luminescence decay observed after total inhibition of the lipid peroxidation is not an iron-catalyzed process, and follows a complex kinetics comprising fast and slow components. The slow component of the decay lasts for several hours at 27 degrees C and amounts to nearly half of the total intensity measured prior to the inhibition of the oxidative process by propyl gallate. The addition of thiols (diethyldithiocarbamate, penicillamine or dithiothreitol) to a lipid peroxidizing system inhibits the chain oxidation and catalyzes the dark decomposition of one (or several) of the luminescence precursors, following first order kinetics. The effect of temperature on the slow luminescence decay corresponds to an activation energy of 18.5 kcal/mol.
在大鼠脑匀浆的自氧化过程中，或在偶氮双脒丙烷引发的红细胞质膜和肝微粒体脂质过氧化过程中，研究了脂质过氧化过程之后可见发光的特性。在这些体系中，脂质过氧化完全抑制后观察到的发光衰减不是铁催化过程，而是遵循包含快速和慢速成分的复杂动力学。在27℃时，衰减的慢速成分持续数小时，几乎占没食子酸丙酯抑制氧化过程之前所测总强度的一半。向脂质过氧化体系中添加硫醇（二乙基二硫代氨基甲酸盐、青霉胺或二硫苏糖醇）会抑制链氧化，并按照一级动力学催化一种（或几种）发光前体的暗分解。温度对慢速发光衰减的影响对应的活化能为18.5千卡/摩尔。
