Wolters H, van Tilburg C A, Konings A W
Int J Radiat Biol Relat Stud Phys Chem Med. 1987 Apr;51(4):619-28. doi: 10.1080/09553008414552151.
Radiation-induced lipid peroxidation in phospholipid liposomes was investigated in terms of its dependence on lipid composition and oxygen concentration. Non-peroxidizable lipid incorporated in the liposomes reduced the rate of peroxidation of the peroxidizable phospholipid acyl chains, possibly by restricting the length of chain reactions. The latter effect is believed to be caused by interference of the non-peroxidizable lipids in the bilayer. At low oxygen concentration lipid peroxidation was reduced. The cause of this limited peroxidation may be a reduced number of radical initiation reactions possibly involving oxygen-derived superoxide radicals. Killing of proliferating mammalian cells, irradiated at oxygen concentrations ranging from 0 to 100 per cent, appeared to be independent of the concentration of peroxidizable phospholipids in the cell membranes. This indicates that lipid peroxidation is not the determining process in radiation-induced reproductive cell death.
从辐射诱导的磷脂脂质体中脂质过氧化对脂质组成和氧浓度的依赖性方面进行了研究。脂质体中掺入的不可过氧化脂质降低了可过氧化磷脂酰链的过氧化速率,这可能是通过限制链反应的长度来实现的。后一种效应被认为是由双层中不可过氧化脂质的干扰引起的。在低氧浓度下,脂质过氧化减少。这种有限过氧化的原因可能是自由基引发反应的数量减少,可能涉及氧衍生的超氧自由基。在0%至100%的氧浓度范围内照射增殖的哺乳动物细胞,其杀伤似乎与细胞膜中可过氧化磷脂的浓度无关。这表明脂质过氧化不是辐射诱导生殖细胞死亡的决定性过程。