In vitro simulation of senescence-related membrane damage by ozone-induced lipid peroxidation

Recent evidence indicates that as cells deteriorate, increasing proportions of the membrane lipids become crystalline (gel phase) at physiological temperature. Microsomal as well as chloroplast membranes from ageing bean (Phaseolus vulgaris) cotyledon and leaf tissue acquire regions of gel-phase lipid as senescence advances1–5. Gel-phase lipid has also been detected in microsomal membranes from aged batch cultures of green algae (Scenedesmus quadricauda)6, microsomal membranes from regressing corpus luteum of rat7 and plasma membranes of chick intestinal cells infected with an intracellular coccidial parasite8. These observations suggest that the presence of gel-phase lipid in membranes at physiological temperature may be a generalised feature of cell deterioration whether it is attributable to natural ageing or to some kind of infection. Moreover, the resulting mixture of liquid-crystalline-(fluid) and gel-phase lipid in the bilayer is likely tb render the membranes leaky9,10, and could thus readily account for the loss of cellular compartmentalisation that accompanies tissue senescence. The present study reports that phase changes occurring naturally during senescence of bean cotyledons1,2 can be simulated by exposing isolated membranes from young cotyledon tissue to ozone, a treatment that induces lipid peroxidation11. This finding has considerable bearing on previous observations which implicate atmospheric ozone as a source of crop damage by reason of its ability to induce premature plant senescence12, and lipid peroxidation as a major cause of membrane deterioration in ageing systems13,14.