Chia L S, Thompson J E, Dumbroff E B
Department of Biology, University of Waterloo, Waterloo, Ontario, Canada N2L 3G1.
Plant Physiol. 1981 Mar;67(3):415-20. doi: 10.1104/pp.67.3.415.
Chloroplast and microsomal membranes from the primary leaf of bean acquired increasing proportions of gel phase lipid as the tissue senesced. The lipid-phase transition temperature for microsomes rose from about 25 to 43 C and that for chloroplasts rose from below -30 C to about 52 C within 5 weeks of planting. This was accompanied by large increases (2- to 4-fold) in the sterol to phospholipid ratio of the membranes, which reflected breakdown of phospholipid. Changes in fatty acid saturation were of insufficient magnitude to account for the rise in transition temperature. All of these senescence-related changes in chloroplast and microsomal membranes were also induced by treating young, 2-week-old-plants with 10 milligrams per liter paraquat. Within 48 hours of treatment, the transition temperature rose from 25 to 57 C for microsomes and from below -30 to 24 C for chloroplasts. The membranes sustained only small changes in fatty acid saturation, comparable to those incurred during natural senescence, and there was a selective loss of phospholipid, resulting in augmented sterol to phospholipid ratios. Malondialdehyde, a product of lipid peroxidation, rose by 2- to 3-fold in both senescing and paraquat-treated leaves. Paraquat is known to form cation redicals that react with O(2) to produce O(2) (-) and has been implicated as an agent of lipid peroxidation. Accordingly, these observations suggest that membrane deterioration during natural senescence may be due in part to free radical damage.
随着菜豆初生叶组织衰老,叶绿体膜和微粒体膜中凝胶相脂质的比例不断增加。在种植后的5周内,微粒体的脂质相变温度从约25℃升至43℃,叶绿体的脂质相变温度从低于-30℃升至约52℃。与此同时,膜中甾醇与磷脂的比例大幅增加(2至4倍),这反映了磷脂的分解。脂肪酸饱和度的变化幅度不足以解释相变温度的升高。用每升10毫克百草枯处理2周龄的幼嫩植株,也会诱导叶绿体膜和微粒体膜发生所有这些与衰老相关的变化。处理后48小时内,微粒体的相变温度从25℃升至57℃,叶绿体的相变温度从低于-30℃升至24℃。膜的脂肪酸饱和度仅发生了微小变化,与自然衰老过程中发生的变化相当,并且磷脂发生了选择性损失,导致甾醇与磷脂的比例增加。脂质过氧化产物丙二醛在衰老叶片和经百草枯处理的叶片中均增加了2至3倍。已知百草枯会形成阳离子自由基,与O₂反应生成O₂⁻,并被认为是脂质过氧化的介质。因此,这些观察结果表明,自然衰老过程中的膜劣化可能部分归因于自由基损伤。