Simulation of the Effects of Leaf Senescence on Membranes by Treatment with Paraquat
Author(s) -
Loo Sar Chia,
John E. Thompson,
E. B. Dumbroff
Publication year - 1981
Publication title -
plant physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.554
H-Index - 312
eISSN - 1532-2548
pISSN - 0032-0889
DOI - 10.1104/pp.67.3.415
Subject(s) - phospholipid , paraquat , lipid peroxidation , chloroplast , senescence , membrane , microsome , biochemistry , chemistry , sterol , membrane lipids , malondialdehyde , biology , antioxidant , cholesterol , microbiology and biotechnology , in vitro , gene
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.
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