膜脂流动性影响离体大鼠肝细胞中5-羟硬脂酸的氮氧化物自由基衰变。

T Shima, T Nakashima, K Kashima, H Nishikawa
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引用次数: 3

摘要

我们研究了膜流动性对自旋标记大鼠肝细胞中5-羟硬脂酸氮氧自由基衰变速率的影响。5-羟基硬脂酸掺入离体大鼠肝细胞膜后EPR信号衰减的半衰期(t1/2)为12 min(平均值)。将自旋标记的肝细胞分离成膜段和胞浆段,膜段的t1/2延长2小时以上。然而,当细胞质组分加入到膜组分中时,自由基衰变反应恢复(t1/2为27 min)。肝细胞在37℃的95% O2流中孵育2小时,使t1/2延长106%,水溶性抗氧化剂含量减少18%。当测量温度从24℃变化到37℃时,t1/2缩短,序参量(S)降低,经磷脂酰胆碱(PC)处理的肝细胞t1/2和S分别降低14%和0.008。相反,经磷脂酰乙醇胺(PE)、PC+胆固醇和PE+胆固醇处理后,t1/2和S分别提高了14%和0.014、20%和0.018、29%和0.040。这些结果表明,5-羟硬脂酸在肝细胞膜上的氮氧自由基衰变是由细胞质组分中的抗氧化剂介导的,并且氮氧自由基的衰变速率不仅受水溶性抗氧化剂含量的影响,还受肝细胞膜脂流动性的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Membrane lipid fluidity affects the nitroxide radical decay of 5-doxyl stearic acids in isolated rat hepatocytes.

We investigated the effect of membrane fluidity on the nitroxide radical decay rate of 5-doxyl stearic acid in spin-labeled rat hepatocytes. The half-time (t1/2) for the EPR signal decay of 5-doxyl stearic acids incorporated into the membranes of isolated rat hepatocytes was 12 min (mean value). When spin-labeled hepatocytes were separated into membrane and cytosol fractions, the t1/2 of the membrane fraction was prolonged by more than 2 hrs. However, when the cytosolic fraction was added to the membrane fraction, the radical decay reaction recovered (t1/2 was 27 min). Incubation of hepatocytes with a stream of 95% O2 at 37 degrees C for 2 hrs prolonged t1/2 by 106% and was associated with a 18% decrease in water-soluble antioxidant content. When the measurement temperature was changed from 24 degrees C to 37 degrees C, t1/2 was shortened with a decrease in the order parameter (S). The t1/2 and S in hepatocytes treated with phosphatidylcholine (PC) were reduced by 14% and 0.008, respectively. Conversely, after treatment with phosphatidylethanolamine (PE), PC+cholesterol and PE+cholesterol, t1/2 and S increased by 14% and 0.014, 20% and 0.018 and 29% and 0.040, respectively. These findings suggest that the nitroxide radical decay of 5-doxyl stearic acids incorporated into hepatocyte membranes is mediated by the antioxidants in the cytosol fraction, and that the nitroxide radical decay rate is affected not only by water-soluble antioxidant content but also by the membrane lipid fluidity of the hepatocytes.

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