Antonenkov V D, Sies H
Institut für Physiologische Chemie I, Heinrich-Heine-Universität Düsseldorf, Germany.
Biol Chem Hoppe Seyler. 1992 Nov;373(11):1111-6. doi: 10.1515/bchm3.1992.373.2.1111.
The capacity of rat liver cytosol to decrease Fe/ADP ascorbate-induced lipid peroxidation in microsomes was evaluated using the chemiluminescence technique and measuring the formation of thiobarbituric acid-reactive substances (TBARS). The inhibiting effect of dialysed cytosol depended on the ascorbate concentration and was highest in the range of 1.0mM. Precipitation of cytosolic proteins with ammonium sulfate at 53% saturation yielded an active antioxidative fraction. Gel-filtration on Sephadex G-200 led to the separation of at least two cytosolic compounds of approximate molecular masses of 60 kDa and > 400 kDa. Both factors were active at 1.0mM ascorbate in the presence of freshly prepared microsomes. No inhibition of lipid peroxidation was observed using microsomes stored for one month at -70 degrees C.
采用化学发光技术并测定硫代巴比妥酸反应性物质（TBARS）的形成，评估大鼠肝细胞溶质降低Fe/ADP抗坏血酸诱导的微粒体脂质过氧化的能力。透析后的细胞溶质的抑制作用取决于抗坏血酸浓度，在1.0mM范围内最高。用53%饱和度的硫酸铵沉淀细胞溶质蛋白得到一个具有活性的抗氧化部分。在Sephadex G-200上进行凝胶过滤可分离出至少两种分子量约为60 kDa和>400 kDa的细胞溶质化合物。在新鲜制备的微粒体存在下，这两种因子在1.0mM抗坏血酸时均具有活性。使用在-70℃下储存一个月的微粒体未观察到脂质过氧化的抑制作用。
